Search

Qinglin Li,1,* Yan Wang,2,* Zhi Mao,1 Hongjun Kang,1 Feihu Zhou1,3 1Department of Critical Care Medicine, The First Medical Centre, Chinese PLA General Hospital, Beijing, 100853, People’s Republic of China; 2Department of Health Care, The Second Medical Centre, Chinese PLA General Hospital, Beijing, 100853, People’s Republic of China; 3Chinese PLA General Hospital National Clinical Research Center for Geriatric Diseases, Beijing, 100853, People’s Republic of China*These authors contributed equally to this workCorrespondence: Feihu ZhouDepartment of Critical Care Medicine, The First Medical Centre, Chinese PLA General Hospital, Beijing, 100853, People’s Republic of ChinaTel + 86-10-66938148Fax + 86-10-88219862Email feihuzhou301@126.comPurpose: We examined the relationship between different levels of serum sodium and mortality among elderly patients with acute kidney injury (AKI).Methods: We retrospectively enrolled elderly patients from Chinese PLA General Hospital from 2007, to 2018. All-cause mortality was examined according to eight predefined sodium levels: < 130.0 mmol/L, 130.0– 134.9 mmol/L, 135.0– 137.9 mmol/L, 138.0– 141.9 mmol/L, 142.0– 144.9 mmol/L, 145.0– 147.9 mmol/L, 148.0– 151.9 mmol/L, and ≥ 152.0 mmol/L. We estimated the risk of all-cause mortality using a multivariable adjusted Cox analysis, with a normal sodium level of 135.0– 137.9 mmol/L as a reference.Results: In total, 744 patients were suitable for the final evaluation. After 90 days, the mortality rates in the eight strata were 36.1, 27.8, 19.6, 24.4, 30.7, 48.6, 52.8, and 57.7%, respectively. In the multivariable adjusted analysis, patients with sodium levels < 130.0 mmol/L (HR: 2.247; 95% CI: 1.117– 4.521), from 142.0 to 144.9 mmol/L (HR: 1.964; 95% CI: 1.100– 3.508), from 145.0 to 147.9 mmol/L (HR: 2.942; 95% CI: 1.693– 5.114), from 148.0 to 151.9 mmol/L (HR: 3.455; 95% CI: 2.009– 5.944), and ≥ 152.0 mmol/L (HR: 3.587; 95% CI: 2.151– 5.983) had an increased risk of all-cause mortality. After 1 year, the mortality rates in the eight strata were 58.3, 47.8, 33.7, 38.9, 45.5, 64.3, 69.4, and 78.4%, respectively. Patients with sodium levels < 130.0 mmol/L (HR: 1.944; 95% CI: 1.125– 3.360), from 142.0 to 144.9 mmol/L (HR: 1.681; 95% CI: 1.062– 2.660), from 145.0 to 147.9 mmol/L (HR: 2.631; 95% CI: 1.683– 4.112), from 148.0 to 151.9 mmol/L (HR: 2.411; 95% CI: 1.552– 3.744), and ≥ 152.0 mmol/L (HR: 3.037; 95% CI: 2.021– 4.563) had an increased risk of all-cause mortality.Conclusion: Sodium levels outside the interval of 130.0– 141.9 mmol/L were associated with increased risks of 90-day mortality and 1-year mortality in elderly AKI patients.Keywords: serum sodium, acute kidney injury, elderly, mortality

Introducción. La hiponatremia es la alteración electrolítica más frecuente en pacientes con falla cardíaca crónica, que afecta hasta el 28% de pacientes en el ingreso hospilatario. Se ha demostrado que es un predictor independiente de mortalidad, estancia prolongada y rehospitalización. El objetivo es describir la frecuencia de hiponatremia en pacientes con falla cardíaca descompensada y su relación con la estancia hospitalaria y mortalidad. Metodología. Cohorte prospectiva en pacientes hospitalizados por el servicio de Medicina Interna en un hospital de cuarto nivel de Bogotá, Colombia, con diagnóstico de falla cardíaca descompensada entre abril de 2011 y marzo de 2012. Se midió el sodio al ingreso, a las 72 horas y al día séptimo de hospitalización. Se evaluó la relación de la hiponatremia al ingreso con la estancia hospitalaria y la mortalidad intrahospitalaria a 30 días. Resultados. Se incluyeron 162 pacientes, con promedio de edad de 72 años, 52.5% hombres. Cuarenta y uno (25.3%) presentaron hiponatremia al ingreso. Entre los pacientes que presentaron sodio normal al ingreso, 6 presentaron hiponatremia a las 72 horas y 2 a los 7 días. La mortalidad intrahospitalaria en la población total fue 9.2%, en el grupo de hiponatremia 12.2%, y 8.2% en los que no la tuvieron (p= 0.45). El promedio de estancia hospitalaria fue superior en los pacientes con hiponatremia, 6.6 vs. 8.4 días (p= 0.12). Discusión. La incidencia de hiponatremia al ingreso en este grupo de pacientes fue semejante a la reportada en la literatura. Conclusiones. Existe una tendencia hacia una mayor mortalidad y estancia hospitalaria en pacientes con hiponatremia, aun cuando no fue estadísticamente significativa. Introduction. Hyponatremia is the most common electrolyte disorder in patients with chronic heart failure affecting up to 28% of patients at admission. It has been shown to be an independent predictor of mortality, extended length of hospital stay and rehospitalization. The objective is to evaluate the presence of hyponatremia in patients with decompensated heart failure and describe its relationship with length of hospital stay and mortality. Methodology. A prospective cohort study in patients hospitalized at internal medicine service at a high level of complexity hospital in Bogotá, Colombia diagnosed with decompensated heart failure between April 2011 and March 2012. Sodium was measured on admission, 72 hours and at the seventh day of hospitalization. We evaluated the association between hyponatremia at hospital admission, mortality at 30 days and length of hospital stay. Results. 162 patients were included with an average age of 72 years, 52.5% male. Forty-one (25.3%) had hyponatremia at admission. Among the patients with normal sodium at admission, 6 had hyponatremia at 72 hours and 2 at the seventh day. In-hospital mortality in the total population was 9.2%, in the hyponatremia group 12.2%, and 8.2% in those who did not have it (p = 0.45). The average length of hospital stay was higher in patients with hyponatremia, 6.6 vs 8.4 days (p = 0.12). Discussion. The incidence of hyponatremia at admission in this group of patients was similar to that reported in the literature. Conclusions. The results showed a trend towards higher mortality and hospital stay in patients with hyponatremia, even though it was not statistically significant. Introdução. A hiponatremia é o desequilíbrio hidroeletrolítico mais frequente em pacientes com insuficiência cardíaca crônica, que afeta até 28% dos pacientes internados. Demonstrou ser um preditor independente de mortalidade, permanência prolongada e re-internação. O objetivo é descrever a frequência de hiponatremia em pacientes com insuficiência cardíaca descompensada e sua relação com internação hospitalar e mortalidade. Metodologia.Coorte prospectiva em pacientes internados pelo serviço de Medicina Interna em um hospital de quarto nível em Bogotá, Colômbia, com diagnóstico de insuficiência cardíaca descompensada, entre abril de 2011 e março de 2012. Foi medido o sódio na admissão, às 72 horas e no sétimo dia de internação. Foi avaliada a relação de hiponatremia na admissão com internação e a mortalidade hospitalar aos 30 dias. Resultados. Foram incluídos 162 pacientes, com idade média de 72 anos, 52,5% homens. Quarenta e um (25,3%) apresentaram hiponatremia na admissão. Entre os pacientes que apresentaram sódio normal na admissão, seis apresentaram hiponatremia às 72 horas, e dois aos sete dias. A mortalidade hospitalar na população total foi de 9,2%, no grupo de hiponatremia 12,2% e 8,2% naqueles que não apresentaram (p = 0,45). O tempo médio de internação foi maior nos pacientes com hiponatremia, 6,6 vs. 8,4 dias (p = 0,12). Discussão. A incidência de hiponatremia na admissão nesse grupo de pacientes foi semelhante à relatada na literatura. Conclusões. Existe uma tendência de maior mortalidade e permanência hospitalar em pacientes com hiponatremia, mesmo que não tenha sido estatisticamente significante.

Hyponatremia is a common finding in hospitalized patients. In this retrospective cohort study we assessed the characteristics and outcome of acute medical admissions with hyponatremia. Compared to the normal sodium group, those with hyponatremia were significantly older and the Charlson Comorbidity Index (CCI) was higher. The number of admissions to MCU/ICU between both groups was similar, but hyponatremic patients had a longer length of stay and both 28-day and one-year mortality were higher, even in patients with mild hyponatremia. Hyponatremia was independently associated with mortality after adjustment for age, CCI and polypharmacy, as was found in the subgroup with mild hyponatremia.

Trauma complicated by seawater immersion is a complex pathophysiological process with higher mortality than trauma occurring on land. This study investigated the role of vascular endothelial cells (VECs) in trauma development in a seawater environment. An open abdominal injury rat model was used. The rat core temperatures in the seawater (SW, 22°C) group and normal sodium (NS, 22°C) group declined equivalently. No rats died within 12 hours in the control and NS groups. However, the median lethal time of the rats in the SW group was only 260 minutes. Among the 84 genes involved in rat VEC biology, the genes exhibiting the high expression changes (84.62%, 11/13) on a qPCR array were associated with thrombin activity. The plasma activated partial thromboplastin time and fibrinogen and vWF levels decreased, whereas the prothrombin time and TFPI levels increased, indicating intrinsic and extrinsic coagulation pathway activation and inhibition, respectively. The plasma plasminogen, FDP, and D-dimer levels were elevated after 2 hours, and those of uPA, tPA, and PAI-1 exhibited marked changes, indicating disseminated intravascular coagulation (DIC). Additionally, multiorgan haemorrhagia was observed. It indicated that seawater immersion during trauma may increase DIC, elevating mortality. VECs injury might play an essential role in this process.

An elderly woman was transferred for biopsy of a pontine lesion. Her condition, including gait disturbances, truncal ataxia, and dysarthria-presumed to be due to severe alcohol abuse-had deteriorated during treatment of ambulatory-acquired pneumonia. No electrolyte abnormalities were noted during hospitalization. However, the neuroimaging findings were in line with central pontine myelinolysis, typically sparing the peripheral pontine fibers. Although extremely rare, pontine myelinolysis can occur in the presence of normal electrolyte levels. Thus, imaging findings should not be misinterpreted as pontine neoplasms, and patients should not undergo stereotactic biopsy-a procedure that could result in disastrous morbidity.

We investigated the effect of ovariectomy(oVx) on renal and systemic hemodynamic, electrolyte excretion and total and dephosphorylated Na(+),K(+)-ATPase α1 subunit (t-d-NKA) in normotensive Wistar rats under a normal sodium (NS, 0.24%) or high sodium (HS, 1%) intake versus intact female (IF). On NS intake, t-d-NKA was higher in oVx rats and overexpressed in the thick ascending limbs (P .01 vs. IF) and renal plasma flow was increased. On HS intake, oVx rats maintained a greater dephosphorylated NKA, excreted less sodium, and developed arterial hypertension (134 ± 4 vs. IF 112 ± 5 mm Hg, P .05). Sodium load caused salt-sensitive hypertension in oVx Wistar rats.

Objective: The objective of the present study was to determine the prevalence of exercise-associated hyponatraemia in hikers/trekkers along the Kokoda Trail. Methods: This was a cross-sectional study of 191 trekkers on the Kokoda Trail, Papua New Guinea. Blood was taken and analysed immediately using point-of-care technology 2 days walk from each end of the Trail. Results: The main outcome measure was hyponatraemia defined as serum sodium level less than 135 mmol/L. Three participants (1.6%, 95% CI 0.5–4.5%) were found to have mild hyponatraemia. The hyponatraemic group had a median estimated fluid intake on the day of testing that was almost double that of the normal sodium group (6 L vs 3.3 L). Conclusion: Exercise-associated hyponatraemia occurs in trekkers on the Kokoda Trail. Strategies for prevention of exercise-associated hyponatraemia should be delivered to trekkers via the trekking companies, chiefly focussing on only drinking in response to thirst.

This study reports the incidence and associated mortality of acquired hypernatraemia (Na > 150 mmol x l(-1)) in a general medical/surgical intensive care unit. Patients admitted over a 5-year period with normal sodium values were eligible for inclusion; exclusions were made for burn/neurosurgical diagnoses and for hypertonic saline therapy. From 3475 admissions (3317 patients), 266 (7.7%) episodes of hypernatraemia were observed. Hospital mortality was 33.5% in the hypernatraemic group and 7.7% in the normonatraemic group (p < 0.001). Acquired hypernatraemia was an independent risk factor for in-hospital mortality (OR 1.97, 95% CI 1.37-2.82, p < 0.001). Intermediate sodium levels (145-150 mmol x l(-1)) were associated with increased mortality (OR 1.42, 95% CI 1.02-1.98). Uncorrected sodium at discharge (p = 0.001) and peak sodium (p = 0.001) were better predictors of mortality than time to onset (p = 0.71) and duration of hypernatraemia (p = 1.0). Hypernatraemia avoidance is justified, but determinants of hypernatraemia and benefits of targeted treatment strategies require further elucidation.

Wir berichten über eine 84-jährige Patientin, die im Rahmen eines lokalisierten Herpes Zoster ein Syndrom der inadäquaten ADH-Sekretion (SIADH) mit schwerer Hyponatriämie entwickelt hat. Dies ist eine seltene, aber bekannte Komplikation der lokalisierten Varizella-Zoster-Infektion. Unter Trinkmengenrestriktion und Zufuhr salzreicher Nahrung zeigte sich eine Normalisierung des Serumnatriums, und gut ein Monat nach Spitalentlassung zeigte sich ohne Diät ein normaler Natriumwert.

The electronic properties of matched pairs of Cu(In x Ga 1 − x )Se 2 (CIGS) solar cells, with and without normal sodium levels, were studied by junction capacitance methods including admittance spectroscopy, drive level capacitance profiling (DLCP) and transient photocapacitance spectroscopy (TPC). The capacitance profiling measurements revealed a large deep defect density in the vicinity of the barrier interface that was likely responsible for the lower performance of the reduced Na samples. The metastable properties of CIGS solar cells were also examined, and these revealed marked differences between the two types of samples. These results directly address the predictions of theoretical microscopic models that have been proposed to account for metastable effects in CIGS.

We have previously shown that ovariectomy in adult Wistar rats under normal sodium (NS) intake results in an overexpression of total Na+, K+-ATPase α 1subunit (NKA). Upon high sodium (HS) intake ovariectomized (oVx) rats developed a defective NKA phosphorylation, a decrease in sodium excretion, and an increment in mean blood pressure (MBP). Since NKA phosphorylation is modulated by dopamine (DA), the aim of this study was to compare the intracellular response of the renal DA system leading to NKA phosphorylation upon sodium challenge in intact female (IF) and oVx rats. In IF rats HS caused an increase in urinary DA and sodium, in NKA phosphorylation state, in Cytochrome P4504A (CYP4A) expression and in 20-HETE production, while MBP kept normal. Blockade of D1R with the D1-like receptor antagonist SCH23390 in IFHS rats shifted NKA into a more dephosphorylated state, decreased sodium excretion by 50 % and increased MBP. In oVxNS rats, D1R expression was reduced and D3R expression was increased, and under HS intake sodium excretion was lower and MBP higher than in IFHS rats (both p

We have used atmospheric sodium profiles obtained at Sao Jose dos Campos over the period 1993–2004 to study the influence of sporadic layers on the average sodium distribution. All the profiles for the time period 19–22 h local standard time were individually classified as either normal or sporadic. Profiles were considered sporadic if they contained sharp increases above the background profile by more than a factor of 2, occurring on the topside of the layer, with a width of less than 5 km. For each night’s data, the averages of the normal and sporadic profiles were stored separately. A comparison between the long-term means of these two average profiles, for those days on which both normal and sporadic profiles were observed, showed no significant difference between them. This indicates that, on average, there is no additional sodium in the sporadic profiles. This analysis suggests that at least part of the topside of the normal sodium layer originates in a source that also gives rise to sporadic layers, which would occur when the source itself becomes layered. The most likely source is sodium-containing ions, which would be layered by the tide and/or gravity wave driven wind-shear mechanism generally accepted as being responsible for some types of ionospheric sporadic-E.

Salt and water are probably the most common therapeutic agents that we give to patients: used improperly, they can be lethal weapons. Rational management of fluid and electrolyte disorders requires that we think of salt (or saline) and water as drugs that have indications, contraindications, and appropriate doses. Such drug information, typically supplied in what Americans call the ‘package insert’, can be found in Tables 1 and 2. View this table: Table 1 Package insert for water View this table: Table 2 Package insert for saline Water is available in oral form or in parenteral preparations. Because it cannot be infused directly into a small vein without causing haemolysis, intravenous water is usually mixed with glucose. A 4% or 5% dextrose solution is used because the osmolality approximates that of plasma, and thus prevents haemolysis. However, after metabolism of the infused glucose, a solution containing only dextrose becomes equivalent to water. The concentration of salt (or in the case of 4% or 5% dextrose in water, the absence of any) determines the solution’s tonicity . It is useful to think of intravenous saline as a substitute for dietary salt. A ’normal’ hospital diet with no added salt provides about 4 g or 172 mmol of sodium. Ingested with water, it provides the equivalent of 1.1 l isotonic saline. A litre of isotonic or ‘normal’ (0.9%) saline contains 154 mmol of NaCI, equivalent to 9 g of salt or 3.6 g of sodium. The sodium concentration of isotonic saline is equivalent to the normal sodium concentration of plasma water. If glucose is added to isotonic saline, the solution becomes hyperosmolar but it is still isotonic ; after the glucose is metabolized, isotonic …

IntroductionA 71 year old gentleman presented with two discrete episodes of delirium with prominent psychotic features and catatonia, over a 3-year period. Symptomatically, he was suffering from fluctuating consciousness, paranoid ideation and both auditory and visual hallucinations. He went on to develop catatonia, demonstrating negativism and mutism and he also exhibited pseudoseizures. His symptoms resolved entirely after three weeks. He re-presented 3 years later with profound psychosis and hyponatraemia. On this occasion, he exhibited catalepsy, negativism, echolalia and mutism, which resolved when his sodium was corrected.Objectives/aimsTo illustrate 2 episodes of acute catatonia temporally associated with hyponatraemia in an otherwise healthy elderly gentleman.MethodsThis is a case study. Consent was sought from the patient to write up his case and distribute it for educational purposes. His medical inpatient notes, psychiatric inpatient notes, correspondence and bloods pertaining to both admissions were reviewed and analysed. A literature review was carried out using Pubmed.ResultsLow sodium levels were a common factor in his presentations and normal sodium levels were associated with a return to normal consciousness.ConclusionsWhile medical issues confounded his first presentation of hyponatraemia associated catatonia, his second presentation was directly related to hyponatraemia. Given the coincidence of hyponatraemia during his first admission, it would strongly suggest that low sodium levels were an important factor in this gentleman's presentation. Importantly, this is the first case in the literature to demonstrate catatonia related to hyponatraemia on two separate occasions in the same individual.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Nanofiltration is incorporated into the manufacturing processes of many protein biopharmaceuticals to enhance safety by providing the capacity to retain pathogens while allowing protein drugs to pass through the filter. Retention is mainly a function of size; however, the shape of the pathogen may also influence retention. The ability of the Viresolve® Pro nanofilter to remove different sized viruses during the manufacture of a Coagulation Factor IX (Alphanine® SD) was studied at varying ionic strength, a process condition with the potential to affect virus shape and, hence, virus retention. Eight viruses were tested in a scale-down of the nanofiltration process. Five of the viruses (EMCV, Reo, BVDV, HIV, PRV) were nanofiltered at normal sodium processing conditions and three (PPV, HAV and WNV) were nanofiltered at higher and lower sodium. Representative Reduction Factors for all viruses were ≥4.50 logs and removal was consistent over a wide range of ionic strength.

The understanding of hyponatremic disorders requires a knowledge of normal water balance and how this relates to the maintenance of normal sodium concentrations despite large variations of water intake. This chapter thus reviews the physiology of water homeostasis and describes the components of the normal renal diluting and concentrating mechanisms. The quantitation of water excretion is also reviewed in order to more appropriately approach the pathogenesis and treatment of disorders of water excretion. Emphasis is placed on the central role of vasopressin in the maintenance of water balance. Finally an overall approach to hyponatremic patients is put forth to be discussed in greater detail in forthcoming chapters.

The altitude of the sodium layer in the mesosphere and lower thermosphere is usually from 80 km to 105 km. In this paper, we report a set of double sodium layer (DSL) events observed by sodium lidar over Beijing, China. In these DSL events, the normal sodium layer and secondary sodium layer (SeSL) present separately. There were about 17 DSL events occurred in 319 observation nights during 2009 similar to 2011. All DSL events were observed in spring and summer. The SeSL appeared independently within the altitude range from 105 km to 130 km. The density of the SeSL is very high. The maximum ratio of peak density and the ratio of column density for the SeSL to the normal sodium layer are up to similar to 60% and similar to 47%, respectively. The SeSL lasted several hours, and then merged into the normal sodium layer. After the SeSL, a sporadic sodium layer occurred in the normal sodium layer. Citation: Wang, J., Y. Yang, X. Cheng, G. Yang, S. Song, and S. Gong (2012), Double sodium layers observation over Beijing, China, Geophys. Res. Lett., 39, L15801, doi:10.1029/2012GL052134.

Objective To investigate the relationship between specific immunocyte and pseudoanaphylactoid reactions (PR) induced by Shuanghuanglian injection (SHLI). Method ICR mice, SCID mice and BALB/C athymic mouse were divided into different test groups, the mice were intravenously injected with solutions of different concentration of SHLI, positive control Compound 48/80 and normal sodium. All test substances were mixed with 0. 4% Evans blue. The reaction and vascular permeability of the ears were observed and measured 30 min after SHLI injected. Result SHLI of 300, 600 mg x kg(-1) caused obvious vascular hyperpermeability in ICR mice, but the same dose of SHLI didn't cause vascular hyperpermeability in SCID mice and BALB/C athymic mouse. Conclusion SHLI in equivalent and 2 times the clinical dose can cause PR in ICR mice, but the same dose of SHLI can't cause PR in SCID mice and BALB/C athymic mouse, so specific immunocyte maybe take part in the SHLI-induced PR.

To evaluate the effect of salt responsiveness of blood pressure to the antihypertensive effect of calcium channel blockade, we studied 15 essential hypertensive patients who had previously been characterized with respect to salt sensitivity or resistance of blood pressure. After a placebo period, titration with verapamil in doses of 180 to 480 mg/day was begun until goal blood pressure responses were reached. The study population exhibited a significant (P < or = .007) reduction in systolic and diastolic blood pressure with treatment. There were no significant differences in the response to calcium channel blockade when the subjects were separated into salt-sensitive (n = 8) and salt-resistant (n = 7) subgroups. A significant (P < or = .05) correlation was observed between the age of the subjects and the blood pressure response. In this study verapamil lowered blood pressure in all subjects. We conclude that calcium channel blockade reduces blood pressure in essential hypertensive subjects during a normal sodium intake, independent of salt-sensitivity status.

We report on a sporadic sodium layer (SSL) event observed by our Na fluorescence lidar at Wuhan, China (31degreesN, 114degreesE) on 16 March 1999, and we reveal some special behaviour. From careful analysis of various sodium content variations of the layer during the development of this SSL event, it is found that besides the sodium injection mechanism as expected, another mechanism which we call atmospheric dynamics also made a noticeable contribution to this SSL formation. Computer simulations confirmed that under the combined action of a suitable sodium injection and a bi-direction vertical wind field, an SSL profile can be reproduced with a pronounced SSL peak on a normal sodium layer, as we observed in this event. From these results, it is emphasized that atmospheric dynamics is important for SSL formation.

To appropriately respond to an affective stimulus, we must be able to track its value across changes in both the external and internal environment. The nucleus accumbens (NAc) is a critical component of reward circuitry, but recent work suggests that the NAc encodes aversion as well as reward. It remains unknown whether differential NAc activity reflects flexible changes in stimulus value when it is altered due to a change in physiological state. We measured the activity of individual NAc neurons when rats were given intraoral infusions of a hypertonic salt solution (0.45 M NaCl) across multiple sessions in which motivational state was manipulated. This normally nonpreferred taste was made rewarding via sodium depletion, which resulted in a strong motivation to seek out and consume salt. Recordings were made in three conditions: while sodium replete (REP), during acute sodium depletion (DEP), and following replenishment of salt to normal sodium balance (POST). We found that NAc neurons in the shell and core subregions responded differently across the three conditions. In the shell, we observed overall increases in NAc activity when the salt solution was nonpreferred (REP) but decreases when the salt solution was preferred (DEP). In the core, overall activity was significantly altered only after sodium balance was restored (POST). The results lend further support to the selective encoding of affective stimuli by the NAc and suggest that NAc shell is particularly involved in flexibly encoding stimulus value based on motivational state.

In an attempt to compare various genetic strains of hypertensive rats, representative hypertensive strains and associated controls (male, 1-month-old, 6-10 of each strain and 18 strains in total) were collected at a single center (National Institutes of Health; NIH, United States), maintained under the same experimental conditions with normal sodium NIH open formula diet and studied by a single investigator using standard techniques. Animals were measured for blood pressure (BP) by a tail-cuff method without anesthesia and body weight (BW) at 10 and 12 weeks of age and killed to measure organ weights. Hypertension was severe (190 mmHg) in spontaneously hypertensive rats (SHR) and their stroke-prone substrains at 12 weeks of age but mild to moderate (145-160 mmHg) in the rest of the hypertensive strains (Dahl's, Milan, Lyon, Sabra, and New Zealand Strains). Regarding organ size, partial correlation analysis showed that organ weights, except for brain and adrenal glands, are good functions of BW and that weight of the left ventricle (LV) was the only one significantly linked to BP levels. A bivariate regression model for LV weight was obtained as follows: LV(mg) = 1.478 BW(g) + 2.13BP(mmHg) - 51(R = 0.878, P0.001). The presence of some genetic factor regulating relative organ size independently of BW and BP was suggested in LV weight as well as in the weight of the other organs. Among the strains, MHS was found to be unique for the smallest kidney size and New Zealand strains for the greatest relative LV size when adjusted to allow for the influence of BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth responses to three different media, temperatures, and sodium chloride concentrations in the media were determined for 13 salmonid and 14 non-salmonid fish cell lines. Most cell lines showed better growth in Eagle's MEM than in Medium 199 or in Leivobitz L-15 medium. Nine salmonid cell lines grew well in the normal sodium bicarbonate buffer in Eagle's MEM, while 11 non-salmonid cell lines grew better in Eagle's MEM buffered with either HEPES-bicarbonate or Tris-bicarbonate. Optimum temperature for growth ranged from 15 to 20℃ for almost all salmonid cells and 20 to 30℃ for non-salmonid cells. Most of the cell lines showed highest growth in commercial medium preparations with the lowest concentrration of sodium chloride (0.116M) examined. However, three of the six cell lines derived from rainbow trout, Oncorhynchus mykiss, and cell lines from eels, Anguilla japonica, showed optimum growth response at a higher sodium chloride concentration of 0.171M in the medium.

The crucial physiologic role of such transport is illustrated by cystic fibrosis. In that lethal genetic disease, transepithelial sodium absorption and chloride secretion are respectively increased and decreased, and pulmonary mucus is dehydrated. Mechanisms that regulate normal sodium and chloride movement are discussed, as are the derangements in cystic fibrosis.

Disorders of sodium balance can result in seizures. In electroconvulsive therapy (ECT) practice, it is customary to obtain electrolytes, including sodium, before treatment. A question that arises is whether the patient with mild disturbances of sodium can safely be treated with ECT or whether normalization of serum sodium is needed first. In this series, 207 patients were treated with ECT and had a serum sodium performed within a week before the first treatment. A few patients were mildly hypernatremic or hyponatremic. We found no correlation between baseline sodium and seizure threshold or seizure duration at the first treatment session. We conclude that although it is ideal to have normal sodium values before ECT, mild abnormalities do not necessarily presage prolonged seizures or lower seizure thresholds in ECT.

Lifetime elevation of sodium chloride intake elicits hypertension in rats infused intracerebroventricularly with angiotensin II (AII) at doses that are subpressor in rats fed normal sodium diets. T...

The Na+/K+ pump is a ubiquitous P-type ATPase that binds three cytoplasmic Na+ ions deep within its core where they are temporarily occluded before being released to the extracellular surface. The 3Na+/2K+-exchange transport cycle is completed when two extracellular K+ ions bind and become temporarily occluded within the protein and subsequently released to the cytoplasm. Coupling of Na+-ion occlusion to phosphorylation of the pump by ATP and of K+-ion occlusion to its dephosphorylation ensure the vectorial nature of net transport. The occluded-ion conformations, with binding sites inaccessible from either side, represent intermediate states in these alternating-access descriptions of transport. They afford protection against potentially catastrophic effects of inadvertently allowing simultaneous access from both membrane sides. The marine toxin, palytoxin, converts Na+/K+ pumps into nonselective cation channels, possibly by disrupting the normal strict coupling between opening of one access pathway in the Na+/K+ ATPase and closing of the other. We show here that gating of the channels in palytoxin-bound Na+/K+ pumps in excised membrane patches is modulated by the pump's physiological ligands: cytoplasmic application of ATP promotes opening of the channels, and extracellular replacement of Na+ ions by K+ ions promotes closing of the channels. This suggests that, despite the presence of bound palytoxin, certain partial reactions of the normal Na+/K+-transport cycle persist and remain capable of effecting the conformational changes that control access to the pump's cation-binding sites. These findings affirm the alternating-access model of ion pumps and offer the possibility of examining ion occlusion/deocclusion reactions in single pump molecules.

A prospective study was conducted over a 2-year period to detect the effect of feeding practice, in particular the role of artificial milk formulae, in children admitted with hypernatraemic dehydration (serum sodiumor = 150 mmol/L) caused by acute gastro-enteritis, and to record morbidity and mortality in these patients. A control group was selected from infants and children admitted with gastro-enteritis but normal sodium levels. Sixty-seven children aged 18 days to 18 months (mean 6.9 months) were studied and represented 4.6% of all children admitted during the study with acute gastro-enteritis. Their mean serum sodium level was 161 mmol/L, the highest being 194 mmol/L. Twenty-four infants (36%) with hypernatraemic dehydration were on evaporated cow's milk powder compared with ten (15%) in the control group (p0.01). Five hypernatraemic infants (7.5%) were breastfed compared with 40 (60%) isonatraemic controls (p0.00001). Six children from the hypernatraemic group developed convulsions and two died. Hypernatraemic dehydration remains an important and serious complication in infants with gastro-enteritis in our area. Artificial milk feeding, particularly the use of evaporated cow's milk powder, is a predisposing factor for hypernatraemia in infantile gastro-enteritis. This study emphasises the importance of breast-feeding and the need to educate mothers to avoid giving evaporated cow's milk formulae to babies under 1 year of age if breast-feeding is not possible.

Aim: Treatment-related hypertension and neutropenia are biomarkers of outcome in patients with mRCC. Other biomarkers are needed. Methods: Baseline Heng risk group status and time-dependent biomarkers within the first 12 weeks after treatment initiation were analyzed with univariate and multivariate Cox proportional hazard model in a complete national cohort of all Danish mRCC patients receiving first line tyrosinekinase-inhibitors (TKI) or interleukin-2 based immunotherapy (IT) from 2006 – 2010. Measurements were made day 1 of each cycle after the first cycle. Results: 735 patients received first line TKI (59%) or IT (41%). Overall median survival (OS) was 14.0 months and median OS for baseline Heng favourable, intermediate and poor risk groups were 33.4, 18.5 and 5.8 months, respectively (p LLN and LDH OS per biomarker profile within 12 weeks treatment for baseline Heng risk group status Favourable Intermediate Poor Biomarker profile N OS 95% CI p value N OS 95% CI p value N OS 95% CI p value Good 40 38.9 29.7-NA 0.112 175 25.7 20.9-33.6 67 12.8 10.7-19.8 Poor 17 28.7 23.4-NA 77 12.0 7.9-16.5 86 6.4 5.2-10.8 This table contains 462 patients with complete data; OS = Overall Survival (months); N = Number; CI = Confidence interval; NA = Not applicable. Conclusions: Hypertension, neutropenia, thrombocytopenia, normal sodium, and LDH within the first 12 weeks of treatment are independent biomarkers of favourable outcome in mRCC and provide additional prognostic information for patients in Heng intermediate and poor risk groups. These biomarkers seem independent of treatment type. Disclosure: A.V. Soerensen: has received research funding from Pfizer; R. Sandin: is a fulltime employee at Pfizer and has stock ownership; F. Donskov: has received a research grant from Novartis and GSK. All other authors have declared no conflicts of interest.

The present study was performed to compare the resting level of arterial blood pressure when monitored for 24 h/day in outbred Swiss Webster (SW) and inbred C57BL/ 6J, A/J, C3HeB/FeJ, and SWR/J mice. Mean arterial pressure (MAP) and heart rate (HR) varied throughout the day, with maximal values observed in the hours of darkness. Systolic (SAP), MAP, and diastolic (DAP) arterial blood pressure averaged 122 +/- 2, 112 +/- 2, and 102 +/- 2 mm Hg, respectively, in conscious SW mice (N = 6). No differences were detected in the 24-h averages of MAP between SW, C57BL/6J (N = 7), A/J (N = 5), C3HeB/FeJ (N = 5), or SWR/J (N = 7) mice maintained on a normal sodium diet. Average daily heart rate (HR) was highest in the C3HeB/FeJ (665 +/- 15 beats/min) and lowest in the C57BL/6J (594 +/- 9 beats/min). The MAP was significantly increased in SW mice administered L-NAME (133 +/- 2 mm Hg, N = 5) and significantly decreased in SW mice administered captopril (99 +/- 2 mm Hg, N = 5). These studies demonstrate similar levels of resting arterial pressure in different mouse strains under baseline conditions.

The contribution of endogenous dopamine (DA) to the natriuresis accompanying various sodium challenges is reviewed. Data are presented suggesting that DA participates in the control of sodium excretion produced by a normal sodium diet, increments in sodium consumption, and an acute infusion of isoosmotic saline. In contrast, the natriuresis accompanying a high sodium diet in the dog and extracellular fluid volume expansion with hypoosmotic saline or a very large volume of isoosmotic saline is independent of DA activity. Thus, the evidence suggests that DA contributes to the natriuresis produced by some, but not all, forms of sodium loading.

Objectives To investigate the effect of myocardial remodelling in rabbit with adriamycin-induced heart failure. To explore the mechanism of simvatatin to treat the chronic heart failure. Methods Fourty-eight male rabbits weighed 2.5∼3.0 kg, were randomly divided into four groups: control group, n = 12(CON group); chronic heart failure group (CHF group), n = 12; early-simvasatin treatment group (E-SIM group), n = 12; later simvasatin group (L-SIM group), n = 12. The control group received peritoneal injection with normal sodium once a week for ten weeks. Adriamycin was given to the other three groups with the dosage of 3 mg/kg diluted to 2 mg/ml with normal sodium once a week,all for ten times. At the meantime the E-SIM group of rabbits received simvastatin 0.3 mg/kg/d for twelve weeks; After two weeks, the L-SIM group of rabbits received the same dose simvastatin for ten weeks. In the course of experiment, observing the general state of health of the rabbit regularly such as the mental state, action, collar pattern, food intake, weight and ascite. Afer twelve weeks later, all rabbit were sactificed after hemodynamics surveyed and echocardiography performed. Morphological characteristics were measured with HE staining and Masson staining. Results Compared with the control group, the left ventricle enlarged and left ventricular ejact fraction dropped in the CON group, E-SIM group and L-SIM group (P Conclusions Simvastatin can inhibit cardiac remodeling and improve chronic heart failure, used earlier the effect was better.

Source Citation DiNicolantonio JJ, Di Pasquale P, Taylor RS, Hackam DG. Low sodium versus normal sodium diets in systolic heart failure: systematic review and meta-analysis. Heart. 2012 Aug 21. [Ep...

We compare the electronic properties of Cu(In1−xGax)Se2 (CIGS, x=0.3) companion films with standard and nearly absent sodium levels. The films were examined over a wide range of metastable states produced by light-soaking. Admittance spectroscopy revealed that the activation energy of the dominant deep defect (hole trap) decreased monotonically from 300 to 60 meV with light-soaking time for samples with normal sodium, but remained nearly fixed (∼350 meV) for samples without sodium. Drive-level capacitance profiling indicated that the deep defect densities increased under light-soaking by roughly a factor of 20 for both samples and annealed at identical rates; however, the relative increases between the defect and hole carrier densities were dramatically different.

The treatment of hyponatraemia is controversial because of the risk of causing central or extrapontine myelinolysis (EPM). Rapid correction with hypertonic saline to a low normal sodium level has its proponents; others feel that slow correction to below normal sodium values is preventative. Most investigators feel that overcorrection should be avoided. It is not known whether the magnitude of serum sodium change is more important than the actual rate of correction. We present three patients with hyponatraemia ranging from 103 to 105 mmol/l who were corrected slowly with normal saline, corrected quickly with hypertonic saline, or rapidly overcorrected with hypertonic saline. All became comatose and died; all had EPM with or without central pontine myelinolysis (CPM). The rate of correction, the solution used, or the magnitude of correction did not seem to protect against demyelination. In a review of 67 reported CPM cases since 1983, no patients documented as having CPM or EPM by radiological studies or necropsy were treated with water restriction only. A group of 27 hyponatraemic patients treated only with water restriction and 35 with diuretic cessation alone did not develop CPM or EPM. This may be a reasonable approach to patients with symptomatic hyponatraemia and normal renal function.

Although sodium disturbances are common in hospitalised patients, few studies have specifically investigated the epidemiology of sodium disturbances in the intensive care unit (ICU). The objectives of this study were to describe the incidence of ICU-acquired hyponatraemia and hypernatraemia and assess their effects on outcome in the ICU.We identified 8142 consecutive adults (18 years of age or older) admitted to three medical-surgical ICUs between 1 January 2000 and 31 December 2006 who were documented to have normal serum sodium levels (133 to 145 mmol/L) during the first day of ICU admission. ICU acquired hyponatraemia and hypernatraemia were respectively defined as a change in serum sodium concentration to below 133 mmol/L or above 145 mmol/L following day one in the ICU.A first episode of ICU-acquired hyponatraemia developed in 917 (11%) patients and hypernatraemia in 2157 (26%) patients with an incidence density of 3.1 and 7.4 per 100 days of ICU admission, respectively, during 29,142 ICU admission days. The incidence of both ICU-acquired hyponatraemia (age, admission diagnosis, Acute Physiology and Chronic Health Evaluation (APACHE) II score, length of ICU stay, level of consciousness, serum glucose level, body temperature, serum potassium level) and ICU-acquired hypernatraemia (baseline creatinine, APACHE II score, mechanical ventilation, length of ICU stay, body temperature, serum potassium level, level of care) varied according to patients' characteristics. Compared with patients with normal serum sodium levels, hospital mortality was increased in patients with ICU-acquired hyponatraemia (16% versus 28%, p0.001) and ICU-acquired hypernatraemia (16% versus 34%, p0.001).ICU-acquired hyponatraemia and hypernatraemia are common in critically ill patients and are associated with increased risk of hospital mortality.

The advent of ion-selective electrodes made possible the potentiometry of sodium in serum and plasma. These methods were based on dilution of serum, as done in flame photometry, and the results were identical. Analysis of whole blood precludes dilution and so "direct" potentiometry was developed. Results by this technique are variable but tend to compensate for the spurious hyponatremias found by the "indirect" dilution methods due to displacement of volume by lipids and protein. However, there is no unambiguous theoretical basis on which to choose between the various direct ion-selective-electrode techniques and instruments. As an alternative, I propose use of current indirect methods, with numerical correction for the shift in normal sodium values in the presence of abnormal lipid and (or) protein. A table was constructed for making such corrections.

Role of aldosterone in the control of sodium excretion in patients with advanced chronic renal failure. The factors that regulate sodium and potassium excretion in patients with chronic renal failure have not been fully clarified. The role of aldosterone in the control of sodium and potassium excretion was therefore examined in eight normokalemic patients with chronic renal failure (mean creatinine clearance, 14.3 ml/min). With a normal sodium intake (120 to 151 mEq/24 hr), plasma aldosterone levels were above normal in five of the eight patients and in five of six patients with a creatinine clearance of less than 15 ml/min. Aldosterone levels were further increased in all eight patients by assumption of an upright posture (from a mean of 523 to 1,454 pg/ml, P < 0.01). When seven of the patients were placed on a low sodium diet (10 to 20 mEq/24 hr), mean plasma aldosterone levels increased from 587 to 2,393 pg/ml; (P < 0.02). The low sodium diet was also associated with a fall in mean body of 2.1 kg and a decrease in plasma sodium concentration from 140 to 131 mEq/liter (P < 0.005) in all patients. To further define the physiologic role of the high aldosterone levels, we administered the aldosterone antagonist, spironolactone (300 mg/24 hr), to the patients while they were on a normal sodium diet. The administration of spironolactone was associated with a significant natriuresis, as mean sodium excretion increased from 142 to 173 mEq/24 hr (P < 0.02) and mean body wt decreased by 1.4 kg (P < 0.02). With the administration of spironolactone, the mean potassium excretion decreased from 47 to 41 mEq/24 hr (P < 0.05) as plasma potassium rose from 4.6 to 5.4 mEq/liter (P < 0.01). We conclude that (1) many normokalemic patients with advanced renal failure (creatinine clearance < 15 ml/min) are in a state of hyper-aldosteronism, (2) nevertheless, the secretion of aldosterone in these patients can be stimulated further by posture and volume depletion, and (3) aldosterone plays a physiologic role not only in the maintenance of serum potassium concentration but also as an antinatriuretic force in advanced chronic renal failure.

A strong appetite for salt seems to be a normal link in the complex mechanisms that serve to maintain a normal sodium content of the organism. Experiments with rats have helped to unravel many aspects of the endocrine mechanisms that are involved in regulating sodium balance and salt appetite, but more work is needed to understand the mechanisms that induce salt appetite in different species.

Plasma levels of immunoreactive atrial natriuretic peptides (IrANP) have been measured in 8 normotensive subjects during alterations in dietary sodium intake. Subjects were studied on their normal sodium intake (2 days) then on a low sodium intake (7 days, 10 mmols Na+/day) and subsequently on a high sodium intake (14 days, 350 mmols Na+/day with the diets being given in a fixed order. Plasma levels (mean +/- S.E.M.) of IrANP on a normal sodium diet were 7.3 +/- 0.9 pg/ml; 4.5 +/- 0.8 on the 7th day of a low sodium intake and 10.8 +/- 1.3; 16.6 +/- 3.3; 15.5 +/- 4.2; 15.6 +/- 2.3 pg/ml respectively or the 1st, 3rd, 10th and 14th day on the high sodium intake. Changes in plasma IrANP were closely associated with changes in urinary sodium excretion. These results suggest that in normal subjects the atrial natriuretic peptides may play an important role in the adaptation to increases in dietary sodium intake both on a short and on a longer term basis.

A study was made of the responses of the renin-angiotensin-aldosterone system (RAAS) produced in hyper- and hypothyroid rats maintained in a state of sodium depletion, as part of a wider study to effect a comparison with results previously obtained for the same parameters in rats maintained on a normal sodium diet and during experimental alterations of thyroid function. In hyperthyroid rats maintained on sodium deficient and normal sodium diet, and in euthyroid animals on a sodium deficient regimen, elevations of both plasma renin concentration (PRC) and serum aldosterone concentration (AC) were observed, while the plasma renin substrate (PRS) was decreased. In hypothyroid rats with normal sodium intake, PRC and AC were observed to be decreased relative to similar sodium-deficient animals. Relationships were observed between PRC and AC, and between AC and urinary sodium excretion. These results suggest that: i) Sodium depletion is a more effective stimulus than the thyroid hormones on the RAAS. ii) Aldosterone changes in sodium depletion are mediated by the RAS. iii) Sodium depletion appeared to induce a decrease in the hepatic synthesis of angiotensinogen.

To study the mechanisms underlying renin and aldosterone increase during low sodium diet, eight normal subjects were studied during normal sodium diet (5 g of NaCl per day) for 5 days, after 4 days of low sodium diet, and, on continuing low sodium diet, after randomized treatment with oxprenolol (100 mg), indomethacin (200 mg) and oxprenolol + indomethacin (100 + 200 mg) each given for 24 h with a 48 h interval between each treatment. Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Both oxprenolol and indomethacin significantly reduced PRA to values similar to those during normal sodium intake, while the combination of the two drugs showed a net additive effect on PRA. PRA decrements after either oxprenolol or indomethacin were significantly related to PRA values after low sodium diet while no correlation was present between PRA values after oxprenolol and indomethacin. Aldosterone excretion showed a trend similar to that of PRA, being related to PRA on normal and low sodium diet, and to a lesser extent after drug treatment. These studies suggest that both the sympathetic nervous system and prostaglandins may play a permissive role in the regulation of renin and aldosterone of normal subjects on low sodium diet.

Plasma aldosterone level (PAL) and deoxycorticosterone level (PDL) were determined in 5 subjects of normal sodium intake and 5 subjects of low sodium intake after the intramuscular administrations of ACTH (Upjohn, Cortrosyn) 40 IU, using radioligand methods. PAL and PDL reached their peaks at one hour after the administrations of ACTH, and then decreased in their normal ranges. Pretreated with the oral administrations of Dexamethasone 2 mg/day for 2 days, these subjects had, when ACTH were injected, such a similiar pattern in PAL and PDL as the peak of one hour and the consecutive falling without the pretreating of Dexamethasone. PAL and PDL of these subjects were not different between normal sodium intake and low sodium intake during the course of the experiment.

The renin-angiotensin-aldosterone system was studied in fifty healthy children aged 4-16 years under normal sodium and potassium intake. The plasma renin activity (PRA) and plasma aldosterone (PA) decreased with age: r = -0.30, P less than 0.05 for plasma renin activity and r = -0.33, P less than 0.05 for plasma aldosterone. Significant negative correlation was obtained between plasma renin activity and the 24-h urinary sodium excretion; r = -0.40, P less than 0.01. This relationship remained significant when the daily urinary sodium excretion was corrected for 1.73 m2 body surface area (BSA); r = -0.40, P less than 0.01. Using the multivariance analysis, plotting the plasma renin activity against the two combined parameters (24-h urinary sodium excretion and age), no improvement was obtained (r = 0.38, P greater than 0.05). This finding suggests that during childhood, sodium rather than age has a major modulatory role on plasma renin activity. With advancing age the plasma aldosterone showed a significant positive correlation coefficient with plasma renin activity(r = 0.29, P less than 0.05). Multivariance analysis between plasma aldosterone and the two combined parameters, Plasma renin activity and age, significantly improved the correlation coefficient (r = 0.42, P less than 0.05) suggesting that both plasma renin activity and age play a dominant modulatory role in the control of plasma aldosterone during childhood. Neither 24-h urinary sodium excretion, nor 24-h urinary potassium excretion, improved the multiple correlation coefficient with plasma aldosterone when added to plasma renin activity and age.

To determine factors mediating the aldosterone secretory response to orthostasis, we examined the effect of angiotensin-converting enzyme inhibition (CEI) on orthostasis in eight normal subjects and 10 normotensive patients with primary glomerulonephritis ingesting a normal sodium intake. On standing with CEI, the mean plasma aldosterone concentration (PAC) did not change [68.6 +/- 3.9 (+/- SE) and 63.4 +/- 6.9 pg/ml] in normal subjects, while PAC rose significantly from 72.3 +/- 7.5 to 129.5 +/- 13.2 pg/ml (P less than 0.001) in the glomerulonephritis patients without a concurrent rise in plasma angiotensin II, serum potassium, plasma ACTH, or mean blood pressure. There was a good correlation (r = -0.7064; P less than 0.03) between the changes in PAC and the changes in fractional sodium excretion in the patients. Pretreatment with indomethacin blunted the rise in PAC from 159.0 +/- 21.5 to 63.3 +/- 10.2 pg/ml upon standing with CEI, without a concurrent change in circulating 6-keto prostaglandin F1 alpha (from 57.7 +/- 9.5 to 56.0 +/- 11.1 pg/ml) in 4 patients. These results suggest that the aldosterone secretory response to orthostasis in patients with glomerulonephritis is dependent on factors blunted by pretreatment with indomethacin in addition to angiotensin II.

The work to be described consists of following the changes in oxidation reduction potential as glucose solutions is progressively added to an alkaline solution of Hg(II)-EDTate. Preliminary work appears to show that normal sodium hydroxide provides the best alkaline medium for the purpose. The titrations are carried out at 70–80° C. It was also found that there was no need for rigid exclusion of air. The response of the more important carbohydrates upon titration with this reagent are studied and their reduction values ascertained.

Because accurate diagnosis of the alkaline reflux gastritis syndrome has been elusive, surgical treatment has had a high failure rate, particularly with respect to relief of pain. We have used intragastric infusion of alkali as a provocative test in 147 patients with symptoms and endoscopic findings suggestive of bile gastritis and in 19 asymptomatic control subjects. Subjects received saline solution, 0.1 normal hydrochloric acid, and 0.1 normal sodium hydroxide solutions, as well as their own gastric aspirates in random blinded fashion by a nasogastric tube. There were no complications. A positive test result was defined as pain with sodium hydroxide but not with saline solution or hydrochloric acid infusion. All of the control subjects had negative test results. A total of 87 percent of the symptomatic patients have been followed (mean 4.3 years, minimum 1 year); 47 of those 128 had a Roux-Y gastrojejunal reconstruction to divert duodenal contents from the stomach. Correlation of the test results and the subsequent clinical status showed 87 percent of those with negative test results improved spontaneously or with other treatment versus 15 percent if the test results were positive (p less than 0.001), and 78 percent of those with positive test results had lasting relief of pain after surgical diversion versus a 30 percent success rate if the test results were negative (p less than 0.01). We conclude that positive alkali infusion test results predict that symptoms will likely respond best to surgical diversion of duodenal contents, and that negative test results should be a strong deterrent to surgical diversion. The test is safe, simple, and deserves further trial.

In 12 conscious dogs on a normal sodium diet the renal venous-arterial plasma renin activity-difference as a function of mean renal artery pressure (renin stimulus-response curve; RSRC) as well as long-term mean arterial blood pressure (MAP; pressure-histograms) were measured repeatedly. The RSRC has 1) a threshold pressure (Pth), 2) a flat section above Pth (plateau-level), and 3) a steep slope below Pth. From dog to dog the slope varied from -0.20 to -0.54 ng AI/ml/h/mmHg and Pth from 78.4 to 107.1 mmHg. In every dog MAP was higher than Pth (MAP-Pth:12.8 +/- 1.58 mmHg). Dogs with a higher Pth regularly showed a higher MAP (r = 0.76; P less than 0.005). Due to its normal variability arterial pressure occasionally falls below Pth and thus causes renin release. Therefore MAP will stabilize at a level above Pth. The pressor effect (MAP-Pth) of this feedback system should depend on the sensitivity of the pressure-dependent renin release mechanism (slope of RSRC). Accordingly we observed a close correlation between the slope of the RSRC and the MAP-Pth difference (r = 0.93; P less than 0.0001). We conclude that in healthy dogs the level of long-term blood pressure can be explained almost completely by Pth and the slope of the pressure-dependent renin release. Our findings may offer new perspectives to the pathogenesis of hypertension.