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Purpose: The aim of this study was to determine how sodium hydrogen carbonate (NaHCO 3 ) ingestion during a 1-h recovery period after a 200-m front-crawl swim affects blood-gas levels, acid-base balance, and performance during a successive trial., Methods: Fourteen national-level male swimmers (age: 21 ± 3 years, body mass (BM):77 ± 10 kg, stature: 181 ± 7 cm) performed four maximal 200-m front-crawl tests. On one of the two days, the swimmers swam two 200-m tests with a 1-h recovery break, during which they drank water (WATER); on the other day, they performed the same protocol but consumed 0.3 g min -1 NaHCO 3 solution during the recovery break (NaHCO 3 )., Results: The ingestion of NaHCO 3 before the second test had no effect on swim time despite a greater [ HCO 3 - ] (19.2 ± 2.3 mmol L -1 ) than that measured during the first test (NaHCO 3 ) (14.5 ± 1.1 mmol L -1 ) and the other two tests (WATER) (12.7 ± 2.4 and 14.8 ± 1.5 mmol L -1 ; F = 18.554; p = 0.000) and a higher blood pH (7.46 ± 0.03) than that measured during the first test (NaHCO 3 ) (7.39 ± 0.02) and the other two tests (WATER) (7.16 ± 0.04 and 7.20 ± 0.05); (F = 5.255; p = 0.004). An increase in blood pCO 2 (0.2 ± 0.3 kPa) between both tests (NaHCO 3 ) compared to unchanged pCO 2 values (- 0.1 ± 0.3 kPa) between the other two tests (WATER) (t = - 2.984; p = 0.011; power = 0.741) was confirmed., Conclusions: NaHCO 3 ingestion during the recovery period between two 200-m front-crawl time trials had a strong buffering effect that did not positively affect performance. An increase in pCO 2 may have counterbalanced this impact., (© 2024. The Author(s).)

Purpose: Enteric-coated sodium bicarbonate (NaHCO 3 ) can attenuate gastrointestinal (GI) symptoms following acute bicarbonate loading, although the subsequent effects on exercise performance have not been investigated. The purpose of this study was to examine the effects of enteric-coated NaHCO 3 supplementation on high-intensity exercise performance and GI symptoms., Methods: Eleven trained male cyclists completed three 4 km time trials after consuming; a placebo or 0.3 g∙kg -1 body mass NaHCO 3 in enteric-coated or gelatin capsules. Exercise trials were timed with individual peak blood bicarbonate ion concentration ([HCO 3 - ]). Blood acid-base balance was measured pre-ingestion, pre-exercise, and post-exercise, whereas GI symptoms were recorded pre-ingestion and immediately pre-exercise., Results: Pre-exercise blood [HCO3 - ] and potential hydrogen (pH) were greater for both NaHCO 3 conditions (P < 0.0005) when compared to placebo. Performance time was faster with enteric-coated (- 8.5 ± 9.6 s, P = 0.044) and gelatin (- 9.6 ± 7.2 s, P = 0.004) NaHCO 3 compared to placebo, with no significant difference between conditions (mean difference = 1.1 ± 5.3 s, P = 1.000). Physiological responses were similar between conditions, although blood lactate ion concentration was higher with gelatin NaHCO 3 (2.4 ± 1.7 mmol∙L -1 , P = 0.003) compared with placebo. Furthermore, fewer participants experienced GI symptoms with enteric-coated (n = 3) compared to gelatin (n = 7) NaHCO 3 ., Discussion: Acute enteric-coated NaHCO 3 consumption mitigates GI symptoms at the onset of exercise and improves subsequent 4 km cycling TT performance. Athletes who experience GI side-effects after acute bicarbonate loading may, therefore, benefit from enteric-coated NaHCO 3 supplementation prior to exercise performance.

Although they are ureotelic, marine elasmobranchs express Rh glycoproteins, putative ammonia channels. To address questions raised by a recent study on high environmental ammonia (HEA) exposure, dogfish were intravascularly infused for 24 h at 3 ml kg(-1) h(-1) with isosmotic NaCl (500 mmol l(-1), control), NH4HCO3 (500 mmol l(-1)), NH4Cl (500 mmol l(-1)), or HCl (as 125 mmol l(-1) HCl + 375 mmol l(-1) NaCl). While NaCl had no effect on arterial acid-base status, NH4HCO3 caused mild alkalosis, NH4Cl caused strong acidosis, and HCl caused lesser acidosis, all predominantly metabolic in nature. Total plasma ammonia (T(Amm)) and excretion rates of ammonia (J(Amm)) and urea-N (J(Urea-N)) were unaffected by NaCl or HCl. However, despite equal loading rates, plasma T(Amm) increased to a greater extent with NH4Cl, while J(Amm) increased to a greater extent with NH4HCO3 due to much greater increases in blood-to-water PNH3 gradients. As with HEA, both treatments caused large (90%) elevations of J(Urea-N), indicating that urea-N synthesis by the ornithine-urea cycle (OUC) is driven primarily by ammonia rather than HCO3(-). Branchial mRNA expressions of Rhbg and Rhp2 were unaffected by NH4HCO3 or NH4Cl, but v-type H(+)-ATPase was down-regulated by both treatments, and Rhbg and Na(+)/H(+) exchanger NHE2 were up-regulated by HCl. In the kidney, Rhbg was unresponsive to all treatments, but Rhp2 was up-regulated by HCl, and the urea transporter UT was up-regulated by HCl and NH4Cl. These responses are discussed in the context of current ideas about branchial, renal, and OUC function in this nitrogen-limited predator.

CO2 exposure elicits multiple changes in the acid-base balance and hematology of avian embryos, but the time-specific, dose-dependent effects of graded increases in extrinsic CO2 in a normoxic environment are poorly understood. Consequently, we exposed day 15 chicken embryos to 1, 3, 5, 6 or 10% CO2 in 20% O2. We hypothesized that both the magnitude of hypercapnic respiratory acidosis and the resultant metabolic compensation within 24 h of exposure to <10% CO2 are proportional to ambient CO2 concentration ([CO2]). We also predicted that regulation of hematological respiratory variables is graded according to [CO2]. Time-course (2, 6 and 24 h) changes were determined for acid-base disturbances and hematological respiratory variables; hematocrit (Hct), red blood cell concentration ([RBC]), hemoglobin concentration, mean corpuscular volume (MCV) and other mean corpuscular indices. Both the decrease in uncompensated pH, which indicates uncompensated respiratory acidosis, and the compensatory pH increase, a sign of metabolic compensation, increased with [CO2]. The partial metabolic compensation across all CO2 gas mixtures was ~17, 46 and 53% compensation at 2, 6 and 24 h, respectively. Hematological responses were nearly identical across the entire range of [CO2], with Hct decreasing across the time course of CO2 exposure due to a decrease in MCV from 2 to 24 h and a decrease in [RBC] at 24 h. Even though hematological regulation was not graded, chicken embryos were able to compensate and survive exposure to <10% CO2.

The oceanic carbonate system is changing rapidly due to rising atmospheric CO(2), with current levels expected to rise to between 750 and 1,000 μatm by 2100, and over 1,900 μatm by year 2300. The effects of elevated CO(2) on marine calcifying organisms have been extensively studied; however, effects of imminent CO(2) levels on teleost acid-base and respiratory physiology have yet to be examined. Examination of these physiological processes, using a paired experimental design, showed that 24 h exposure to 1,000 and 1,900 μatm CO(2) resulted in a characteristic compensated respiratory acidosis response in the gulf toadfish (Opsanus beta). Time course experiments showed the onset of acidosis occurred after 15 min of exposure to 1,900 and 1,000 μatm CO(2), with full compensation by 2 and 4 h, respectively. 1,900-μatm exposure also resulted in significantly increased intracellular white muscle pH after 24 h. No effect of 1,900 μatm was observed on branchial acid flux; however, exposure to hypercapnia and HCO(3)(-) free seawater compromised compensation. This suggests branchial HCO(3)(-) uptake rather than acid extrusion is part of the compensatory response to low-level hypercapnia. Exposure to 1,900 μatm resulted in downregulation in branchial carbonic anhydrase and slc4a2 expression, as well as decreased Na(+)/K(+) ATPase activity after 24 h of exposure. Infusion of bovine carbonic anhydrase had no effect on blood acid-base status during 1,900 μatm exposures, but eliminated the respiratory impacts of 1,000 μatm CO(2). The results of the current study clearly show that predicted near-future CO(2) levels impact respiratory gas transport and acid-base balance. While the full physiological impacts of increased blood HCO(3)(-) are not known, it seems likely that chronically elevated blood HCO(3)(-) levels could compromise several physiological systems and furthermore may explain recent reports of increased otolith growth during exposure to elevated CO(2).

The aim of the present study was to examine the effect of sodium bicarbonate ingestion on consecutive "all out" sprint tests, analyzing the acid-base status and its influence on performance and perceived effort. Ten elite bicycle motocross (BMX) riders (20.7 ± 1.4 years, training experience 8-12 years) participated in this study which consisted of two trials. Each trial consisted of three consecutive Wingate tests (WTs) separated by 15 min recovery. Ninety minutes prior to exercise subjects ingested either NaHCO(3) (-) (0.3 g kg(-1) body weight) or placebo. Blood samples were collected for the assessment of blood acid-base status: bicarbonate concentration ([HCO(3) (-)]), pH, base excess (BE) and blood lactate concentration ([La(-)]). Performance variables of peak power (PP), mean power (MP), time to peak power and fatigue index were calculated for each sprint. Significant differences (p < 0.05) were observed in acid-base variables [pH before WT1: 7.47 ± 0.05 vs. 7.41 ± 0.03; [HCO(3) (-)] before WT1: 29.08 ± 2.27 vs. 22.85 ± 0.24 mmol L(-1) (bicarbonate vs. placebo conditions, respectively)], but there were not significant differences in performance variables between trials [PP WT1: 1,610 ± 373 vs. 1,599 ± 370 W; PP WT2: 1,548 ± 460 vs. 1,570 ± 428 W; PP WT3: 1,463 ± 361 vs. 1,519 ± 364 W. MP WT1: 809 ± 113 vs. 812 ± 108 W; MP WT2: 799 ± 135 vs. 799 ± 124 W; MP WT3: 762 ± 165 vs. 782 ± 118 W (bicarbonate vs. placebo conditions, respectively)]. Rating of perceived effort (RPE) was not influenced nor ratings of perceived readiness. Sodium bicarbonate ingestion modified significantly the blood acid-base balance, although the induced alkalosis did not improve the Wingate test performance, RPE and perceived readiness across three consecutive WTs in elite BMX cyclists.

Background: Several reports have confirmed the efficacy of Intralipid® (containing soya bean oil, egg phospholipids, glycerin and water) in the therapy of systemic local anesthetic intoxication. Pretreatment with Intralipid® shifted the dose-response to bupivacaine-induced asystole in rats. Whether intravenous anesthesia with propofol in the widely used medium chain triglyceride lipid emulsion increases the therapeutic range of systemically administered bupivacaine or not is unknown and was investigated in this study., Methods: A total of 30 piglets aged 2-6 weeks and weighing 4.5-6.5 kg were randomized into 2 groups and anesthetized with sevoflurane (group S) alone or with propofol 10 mg/kg body weight (BW)/h plus sevoflurane (group PS). After 60 min of steady state anesthesia arterial blood was sampled for assessment of blood gases, acid-base state and triglyceride plasma concentrations. Thereafter bupivacaine 0.125% was continuously infused by an infusion syringe pump through a central venous line at a rate of 4 mg/kg BW/min until invasively measured mean arterial pressure (MAP) was reduced by 50% of initial value. The bupivacaine infusion was stopped, blood for assessment of bupivacaine plasma concentration was drawn and the spontaneous hemodynamic course was observed. Resuscitation was not attempted. Results are presented as median and range. The Mann-Whitney U-test was used to assess differences between the two groups for triglyceride as well as for bupivacaine plasma concentrations measured at MAP 50%. A p-value≤0.05 was considered to be significant., Results: Baseline conditions (arterial blood pH, plasma protein and triglyceride plasma concentrations) did not differ significantly between the two groups. After 1 h of anesthesia, triglyceride plasma concentrations were significantly increased in group PS (median 0.69 mmol/l) compared to the corresponding baseline values (median 0.14 mmol/l; p<0.001) and to the 1 h values of group S (median 0.16 mmol/l; p<0.001). The total amount of bupivacaine administered was 9 mg/kg BW in both groups (6-13 mg/kg BW in group S, 5-13 mg/kg BW in group PS). Resulting bupivacaine plasma concentrations were 180 μmol/l (83-686 μmol/l) in group S and 185 μmol/l (130-465 μmol/l) in group PS. However, the total amount of bupivacaine administered and bupivacaine plasma concentrations at MAP 50% did not reveal statistically significant differences between the two groups but a huge variability of both parameters within each group was observed. None of the 30 piglets spontaneously recovered and they died from pulseless electrical activity or from asystolic cardiac arrest. The time from MAP 50% until cardiac arrest demonstrated a large variability but did not reveal significant differences between the two groups. The time to cardiac arrest was similar in both groups., Conclusion: Medium/long chain triglyceride lipid emulsion (50:50) as widely used in propofol solutions did not increase therapeutic safety in cases of intravascular bupivacaine administration in this piglet model.

The purpose of the present study was to compare the acute hormonal response to a short-term high-intensity training (HIT) versus a high-volume endurance training (HVT) and to investigate the effects of acid-base status on cytokines involved in angiogenesis (VEGF and bFGF). Eleven subjects participated in three experimental trials. Two times subjects performed four 30-s "all-out" exercise bouts on a cycle ergometer separated by 5-min rest each, at which subjects either received bicarbonate (HIT (B)) or a placebo (HIT (P)) before the exercise. The third exercise trail consisted of a constant load exercise for 1 h at 50% peak power output (PPO). Venous blood samples were taken under resting conditions, 10, 60, and 240 min after each exercise condition to determine VEGF and bFGF serum concentrations. Capillary blood samples were taken to determine lactate concentrations and blood gas parameters. Mean pH values were significantly higher during HIT (B) compared to HIT (P). Serum VEGF concentration was significantly increased 10-min post-exercise in both HIT interventions. HVT showed no significant effects on VEGF levels. The diminished acidosis during HIT (B) had no effects on the VEGF response. There were no significant changes in bFGF in response to HIT or HVT. The present study suggests that HIT is a stimulus for exercise-induced VEGF secretion. These findings might be relevant for the arrangement of training, due to the fact that most of the training is often performed at low intensities possibly leading to an insufficient stimulus for VEGF secretion and angiogenesis.

Intravenous administration of fluids, electrolytes and glucose are the most common interventions in hospitalized pediatric patients. Parenteral fluid administration can be life-saving, however, if used incorrectly it also carries substantial risks. Perioperatively, adequate hydration, prevention of electrolyte imbalances and maintenance of normoglycemia are the main goals of parenteral fluid therapy. Conceptionally, the distinction between maintenance requirements, deficits and ongoing loss is helpful. Although the pathophysiological basis for parenteral fluid therapy was clarified in the first half of the 20th century, some aspects still remain controversial. In newborn infants, rational parenteral fluid therapy must take into account large insensible fluid losses, adaptive changes of renal function in the first days of life and the fact that neonates do not tolerate prolonged periods of fasting. In older infants the occurrence of iatrogenic hyponatremia with the use of hypotonic solutions has led to a critical reappraisal of the validity of the Holliday-Segar method for calculating maintenance fluid requirements in the postoperative period. Pragmatically, only isotonic solutions should be used in clinical situations which are known to be associated with increases in antidiuretic hormone (ADH) secretion. In this context, it is important to realize that in contrast to lactated Ringer's solution, the use of normal saline can lead to hyperchloremic acidosis in a dose-dependent fashion. Although there is no convincing evidence that colloids are better than crystalloids, there are clinical situations where the use of the more expensive colloids seems justified. It may be reasonable to choose a solution for fluid replacement which has a composition comparable to the composition of the fluid which must be replaced. Although hypertonic saline can reduce an elevated intracranial pressure, this therapy cannot be recommended as a routine procedure because there is currently no evidence that this intervention improves long-term outcome in pediatric patients with traumatic brain injury.

Objective: Development of a two-buffer model which simulates the acid-base properties of blood and allows comparison of the different acidbase concepts according to Stewart and to Siggaard-Andersen., Methods: The two-buffer model consisted of different aqueous solutions of bicarbonate/CO(2) (pCO(2), sCO(2), pK(1)), HEPES buffer (A(tot), pK(a)) and electrolytes. These were used to calculate the pH from the independent variables according to Stewart - strong ion difference (SID), pCO(2) and total concentration of the weak acids (A(tot)) - from which all other dependent variables (cHCO(3)(-), cA(-), BB, BE) were obtained and compared with the measured values., Results: The normal pH (7.408) was calculated from the normal values for SID (48 mmol/l), pCO(2) (40 mmHg) and A(tot) (45.2 mmol/l) and agreed perfectly with the measured value (7.409+/-0.001). This was also valid for all calculated and measured pH values when the SID was varied: non-respiratory alkalosis ( upward arrow) or acidosis ( downward arrow), pCO(2):respiratory acidosis ( upward arrow) or alkalosis ( downward arrow) and A(tot):hyperproteinemic acidosis ( upward arrow) or hypoproteinemic alkalosis ( downward arrow) were varied and the sum of the buffer bases (BB) was always equal to the SID. All changes and hence BE were also equal, providing that A(tot) was normal. This was not the case, however, if A(tot) was outside the normal range, when BE was then the difference from the normal BB at the respective reference point. Whereas the deviation of the measured pCO(2) was acceptable (1.74+/-0.86 mmHg), this was not the case for the SID (-6.18+/-3.58 mmol/l) calculated from the measured ion concentrations (Na, K, Ca, Cl)., Conclusions: Despite controversial discussions, both concepts are much closer than might be expected. Whereas in the Stewart approach the focus of analysis is on plasma, with the Siggaard-Andersen approach it is on blood. Hence, a combined analysis of the blood gases (pH, pCO(2), pO(2), sO(2), cHb, BE) and of the strong ion gap (SIG) may be useful.

Mechanisms of acid release and intracellular pH (pH(i)) homeostasis were analysed in goldfish (Carassius auratus) gill cells in primary culture. The rate of acid secretion was measured using a cytosensor microphysiometer, and pH(i) was determined using the fluorescent probe 2',7'-bis-(3-carboxypropyl)-5-(and-6)-carboxyfluorescein (BCPCF). Amiloride, a Na(+) channel and Na(+)/H(+) exchanger (NHE) inhibitor, had no effect on pH(i), but acid secretion of the gill cells was significantly impaired. In the presence of amiloride, the intracellular acidification (achieved using the NH(4)Cl pulse technique) was more severe than in the absence of amiloride, and recovery from the acidosis was slowed down. Accordingly, acid secretion of gill cells was severely reduced in the absence of extracellular Na(+). Under steady-state conditions, 4,4'-diisothiocyanatodihydro-stilbene-2,2'-disulfonic acid (DIDS), a HCO(3)(-)-transport inhibitor, caused a slow acidification of pH(i), and acid secretion was significantly reduced. No recovery from intracellular acidification was observed in the presence of DIDS. Bafilomycin A(1), an inhibitor of V-ATPase, had no effect on steady-state pH(i) and recovery from an intracellular acidification, whereas the rate of acid secretion under steady-state conditions was slightly reduced. Immunohistochemistry clearly revealed the presence of the V-ATPase B-subunit in goldfish gill lamellae. Taken together, these results suggest that a Na(+)-dependent HCO(3)(-) transport is the dominant mechanism besides an NHE and V-ATPase to control pH(i) in goldfish gill cells.

Separated plasma and whole blood non-bicarbonate buffering capacities, together with plasma and gill carbonic anhydrase activities and endogenous plasma carbonic anhydrase inhibitor activity were investigated in three species of fish: the brown bullhead (Ameirus nebulosus), a teleost; the longnose skate (Raja rhina), an elasmobranch; and the spotted ratfish (Hydrolagus colliei), a chimaeran. The objective was to test the hypothesis that species possessing gill membrane-bound carbonic anhydrase and/or plasma carbonic anhydrase activity would also exhibit high plasma nonbicarbonate buffering capacity relative to whole blood non-bicarbonate buffering capacity and would lack an endogenous plasma carbonic anhydrase inhibitor. Separated plasma non-bicarbonate buffering capacity constituted > or = 40% of whole-blood buffering in all three species. In addition, all species lacked an endogenous plasma carbonic anhydrase inhibitor. Separated plasma from skate and ratfish contained carbonic anhydrase activity, whereas bullhead plasma did not. Examination of the subcellular distribution and characteristics of branchial carbonic anhydrase activity revealed that the majority of branchial carbonic anhydrase activity originated from the cytoplasmic fraction in all species, with only 3-5% being associated with a microsomal fraction. The microsomal carbonic anhydrase activity of bullhead and ratfish was significantly reduced by washing, indicating the presence of carbonic anhydrase activity that was not integrally associated with the membrane pellet, microsomal carbonic anhydrase activity in skate was unaffected by washing. In addition, microsomal carbonic anhydrase activity from skate and ratfish but not bullhead gills was released to a significant extent from its membrane association by treatment with phosphatidylinositol-specific phospholipase C. The results obtained for skate are consistent with published data for dogfish, suggesting that the possession of branchial membrane-bound carbonic anhydrase activity may be a generalised elasmobranch characteristic. Ratfish, which also belong to the class Chondrichthyes, exhibited a similar pattern. Unlike skate and ratfish, bullhead exhibited high plasma non-bicarbonate buffering capacity and lacked an endogenous carbonic anhydrase inhibitor in the absence of plasma and gill membrane-bound carbonic anhydrase activities.

Nitrite influx into crayfish showed saturation kinetics, supporting a carrier-mediated uptake. Addition of 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS: at 10(-5), 10(-4) and 10(-3) M) and bumetanide (at 10(-5) M and 10(-4) M) to the ambient water did not significantly affect nitrite influx. Rather than suggesting that neither Cl-/HCO3- exchange nor K+/Na+/2Cl- cotransport were involved in the transport, this may reflect that the gill cuticle has a low permeability to the pharmacological agents, or that the sensitivity of the transport mechanism to the inhibitors is low. Nitrite accumulation in the haemolymph was significantly decreased during hypercapnic conditions compared to normocapnic conditions. This supports the idea that an acid-base regulatory decrease in Cl-(influx)/HCO3- (efflux) induced by hypercapnia should decrease NO2- uptake if NO2- and Cl- share this uptake route. The respiratory acidosis caused by exposure to hypercapnia alone was partially compensated by HCO3- accumulation in the haemolymph. Combined exposure to hypercapnia and nitrite improved pH recovery, mainly by augmenting the [HCO3-] increase, but also by decreasing haemolymph PCO2. Exposure to nitrite in normocapnic water induced an initial increase in haemolymph [HCO3-] and later also a decrease in PCO2. Thus, the improved acid-base compensation during combined hypercapnia and nitrite exposure was an amplification of this nitrite-induced response. Haemolymph base excess rose much more than haemolymph [Ca], suggesting that transfer of acid-base equivalents between animal and water was more important than H+ buffering by exoskeletal CaCO3 in mediating the increase in haemolymph [HCO3-].

The influence of a CO2/HCO3(-)-buffered medium on intracellular pH regulation of gill pavement cells from freshwater rainbow trout was examined in monolayers grown in primary culture on glass coverslips; intracellular pH (pHi) was monitored by continuous spectrofluorometric recording from cells loaded with 2',7'-bis(2-carboxyethyl)-5(6)-carboxy-fluoroscein. When cells in HEPES-buffered medium at normal pH = 7.70 were transferred to normal CO2/HCO3(-)-buffered medium ¿PCO2 = 3.71 mmHg, [HCO3-] = 6.1 mmol l(-1), extracellular pH (pHe) = 7.70¿, they exhibited a brief acidosis but subsequently regulated the same pHi (approximately 7.41) as in HEPES. Buffer capacity (beta) increased by the expected amount (5.5-8.0 slykes) based on intracellular [HCO3-], and was unaffected by most drugs and treatments. However, after transfer to high PCO2 = 11.15 mmHg, [HCO3-] = 18.2 mmol l(-1) at the same pHe = 7.70, the final regulated pHi was elevated (approximately 7.53). The rate of correction of alkalosis caused by washout of this high PCO2, high-HCO3- medium was unaffected by removal of extracellular Cl-. Removal of extracellular Na + lowered resting pHi and greatly inhibited the rate of pHi recovery from acidosis. Bafilomycin A1 (3 micromol l(-1)) had no effect on these responses. However amiloride (0.2 mmol l(-1)) inhibited recovery from acidosis caused by washout of an ammonia prepulse, but did not affect resting pHi, the latter differing from the response in HEPES where amiloride also lowered resting pHi. Similarly 4-acetamido-4'- isothiocyanatostilbene-2,2'-disulfonic acid, sodium salt (0. 1 mmol l(-1)) did not affect resting pHi but slowed the rate of recovery from acidosis, though to a lesser extent than amiloride. Removal of extracellular Cl(-1) also slowed the rate of recovery but greatly increased beta by an unknown mechanism; when this was taken into account, H+ extrusion rate was unaffected. These results are consistent with the presence of Na+ -(HCO3)N co-transport and/or Na+-dependent HCO3(-)/Cl(-) exchange, in addition to Na+/H+ exchange, as mechanisms contributing to "housekeeping" pHi regulation in gill cells in CO2/HCO3(-) media, whereas only Na+/H+ exchange is seen in HEPES. Both Na(+)-independent Cl-/HCO3(-) exchange and V-type H(+)-ATPase mechanisms appear to be absent from these cells cultured in isotonic media.

Macrobrachium rosenbergii that had been exposed individually for 24 h to 0 (control), 2, 5, 10 mg/L nitrite-N (nitrite as nitrogen) at 4. 3 and 7.7 pH levels were examined for hemolymph nitrite-N, oxyhemocyanin, protein, acid-base balance, ion concentrations, and ammonia-N (ammonia as nitrogen) excretion. Hemolymph oxyhemocyanin, protein, pH, HCO3- , TCO2, osmolality, and ion concentrations were inversely related to ambient nitrite-N concentration and were lower at pH 4.3. However, hemolymph nitrite-N, PO2 and PCO2 levels, and ammonia-N excretion were directly related to ambient nitrite-N, and were higher at pH 4.3. Ambient nitrite-N and pH level interacted to cause changes in hemolymph nitrite-N, oxyhemocyanin, protein, PO2, and pH levels. It is concluded that for M. rosenbergii following nitrite exposure, the incorporated nitrite causes a decrease of pH and an increase of PO2 in the hemolymph where it reduces oxyhemocyanin level; disturbs nitrogen excretion, ion regulation, and respiratory gas exchange; and may lead to a decrease of oxygen-carrying capacity, which are affected more at low pH.

Objective: A new portable device for blood gas analyses (BGA) has been examined for prehospital application., Methods: After a 1 h introduction to the procedure, two physicians used the blood gas analyzer in the emergency medical system in Graz, Austria, for 7 months. The indications for prehospital BGA were prolonged cardiopulmonary resuscitation, mechanical ventilation, hyperventilation for reducing increased intracranial pressure, respiratory failure and metabolic disorders. All patients tested were also checked with pulse oximetry and capnography. TECHNICAL SPECIFICATION: The device measures pO2, pCO2 and pH using the fluorescence method. The innovation of a single-use cassette system makes it unnecessary to do any calibrations or transport any test substances. The storage battery measures eight samples without recharge. The time spent on one measurement is 3-6 min., Results: We took 49 samples from 24 patients and found 16 indications for therapeutical intervention, such as buffering metabolic acidosis and adjusting mechanical ventilation by means of BGA. In all cases the analyzer worked reliably., Conclusions: One advantage of BGA over the non-invasive methods pulse oximetry and capnography is that it does not interfere with factors like peripheral vasoconstriction or inequality of the pulmonary ventilation/ perfusion ratio. Moreover, it is the only method for controlled buffering of acid-base disturbances. This means more security in diagnostics and therapeutical interventions for the patient in danger of dying. The device has proved to be a useful addition to the monitoring methods for prehospital application.

In male patients with idiopathic recurrent calcium urolithiasis (RCU) the effects of oral potassium sodium citrate (PSC) on acid-base, citrate and mineral metabolism were investigated. There were 17 normocitraturic and 15 hypocitraturic patients. The examination time points in our clinical laboratory were prior to medication and after 3, 6 and over 12 months of medication. Urine collection periods were over 24 h, 2 h--after an overnight fast--3 h postprandially. Acceptance by the patients was poor, a large number refusing to take PSC for 12 months. Compliance of the patients continuing with the study was adequate as assessed by the urinary excretion of potassium and sodium. No unwanted side effects were observed. After 3 months of PSC medication a compensated metabolic alkalosis developed; in the urine calcium was decreased, while citrate, pH and oxalate were increased, as were hydroxyapatite supersaturation and calcium phosphate particles. After more than 12 months of PSC medication, citrate and pH tended toward the pretreatment baseline values, while hydroxyapatite supersaturation and calcium had already returned to pretreatment values. Despite ongoing PSC intake, patients with pre-existing hypocitraturia had lower urinary citrate than patients with previous normocitraturia, while the concomitant pH and hydroxyapatite supersaturation in the urine of the former remained at levels close to those of the latter. Under the influence of PSC, parathyroid gland function remained unchanged, but serum levels of bone alkaline phosphatase and osteocalcin were low, and urinary hydroxyproline was high.(ABSTRACT TRUNCATED AT 250 WORDS)

The objectives of this study were to use pulmonary function tests, blood gas measurements and bronchoalveolar lung lavage (BAL) to characterize lesions in the respiratory tract of young adult male Wistar rats as a result of a 5-day exposure (6 h/day) to 0, 1.1, 6.2, 15 or 26 mg n-butyl isocyanate (n-BIC)/m3 air. Further objectives were to probe the diagnostic sensitivities of these procedures in comparison with more traditional evaluations (clinical observation, lung weight, histopathology). Measurements were performed during post-exposure weeks 2 and 5. Most rats exposed to 26 mg/m3 died or were sacrificed in a moribund state during post-exposure week 2. All other rats survived the exposure regimen. In rats exposed to 15 and 26 mg/m3 a significant decrease in body weight, laboured breathing, hypoactivity, nasal discharge, cyanosis, and hypothermia were observed. Pulmonary function measurements revealed increased total lung capacity (TLC) and residual volume (RV), decreased forced expiratory flow rates and quasi-static compliance in rats exposed to 26 mg/m3. At the end of the observation period rats exposed to 6.2 and 15 mg/m3 air were hyperresponsive to an acetylcholine bronchoprovocation aerosol. Arterial blood gas measurements revealed an arterial hypoxia and an increase in venous admixture, suggesting a severe mismatch of the ventilation-perfusion relationship. Biochemical and cellular components in BAL fluid (BALF) indicated a concentration dependent and protracted increase of polymorphonuclear leucocytes and further inflammatory parameters. In the 1.1 mg/m3 group BALF parameters were not significantly elevated. The major histopathological lesions of the lung were thickening of septa, emphysema, and intra-alveolar oedema in rats exposed to 26 mg/m3.(ABSTRACT TRUNCATED AT 250 WORDS)

In idiopathic recurrent calcium urolithiasis (RCU) in men (n = 37) the metabolic effects of oral tripotassium citrate (PC) were investigated in a longitudinal field study. The patients were either normo- (n = 22) or hypocitraturic (n = 15). Laboratory examinations were performed before, and after 3, 6, and more than 12 months of medication. Acceptance of PC was poor, mainly because of the salty taste of the tablet preparation chosen, and a number of participants dropped out of the study. In the remaining participants, compliance was acceptable when evaluated on the basis of urinary potassium and undesired side effects did not occur. In the short term (up to 3 months), PC evoked compensated metabolic alkalosis (pH and citrate in urine increased; blood gases remained normal), a drop in urinary calcium, together with increasing oxaluria, hydroxyapatite supersaturation, and calcium phosphate crystalluria. In the long term (greater than 12 months) PC urinary pH and citrate "dissociated", in that pH returned to pretreatment baseline values, whereas citrate stayed at high levels. In normocitraturics but not in hypocitraturics, urinary urea and sodium increased with PC. Hypocitraturics appeared to be less sensitive to the effects of PC, as reflected by the relatively small rise in urinary pH and citrate, and they maintained higher mean levels of indicators of bone metabolism (osteocalcin, alkaline phosphatase, hydroxyproline) despite continuous administration of PC. It was concluded that although the PC tablet preparation was effective it may not be an ideal anti-stone drug treatment in the long term and that, especially in hypocitraturics, the intrinsic metabolic defect of RCU may not be sufficiently well controlled.

A well known complication following surgical intervention is metabolic alkalosis. In general this acid-base disturbance is treated in our intensive care units by application of arginine-hydrochloride. In an experimental study on rats in vivo we determined the influence of this substance on the acid-base status of the extra- and intracellular body compartment. It was found that the extracellular bicarbonate decreases but there is nearly no influence on intracellular buffering. The "mean whole body pHi", an overall estimate of the intracellular pH as complementary to the in vivo determined extracellular plasma pH, was determined with DMO (5,5-dimethyl-2,4-oxazolidinedione) and shown to increase significantly after application of arginine-HCl. From this result it is concluded that arginine-hydrochloride should no longer be used for clinical therapy of metabolic alkalosis.

10 adult, female Göttingen minipigs were anaesthetized with isoflurane under controlled ventilation. A mixture of O2: N2O = 1:3 was used to vaporize isoflurane in an inspiratory concentration of 1.75-2.0 Vol%. Electrocardiogram, blood pressure, cardiac output and central venous pressure were continuously monitored. To determine the maximum rate of rise of intraventricular pressure (dp/dt max) as an indirect measure of myocardial contractility we placed a micro-tip manometer in the left ventricle before and during (30 min value) the experiment. Acid-base balance was controlled by collecting arterial blood samples anaerobically. We found a negative chronotropic and marked inotropic effect of isoflurane on the heart-muscle. This probably is the main cause for the depression of arterial pressure, though peripheral vasodilatation has some effect. All cardiovascular changes were fully reversible within a few minutes of completing anaesthesia. After only 15 min all animals were fully conscious and data values had returned to control levels. Because of its deficient metabolism and toxicity isoflurane seems to be well qualified for use in experimental medicine in minipigs, especially when the animals require long or multiple exposure. But we recommend the use of isoflurane in combination with a basic anaesthesia, for example NLA or Ketamine to reduce cardiovascular depression.

The effects of intravenously injected 4-dimethylaminophenol and Co2EDTA on peripheral circulation, respiration, acid-base balance, and several other physiological and biochemical parameters were studied on dogs. DMAP increased the respiratory minute volume and mean arterial pressure, diminished the lactate-to-pyruvate ratio, and induced an increase in arterial oxygen pressure caused by liberation of oxygen from oxyhemoglobin during the formation of ferrihemoglobin. A study in vitro of the fate of the oxygen during the reaction between DMAP and oxyhemoglobin showed that only 30--40% of the oxygen released by the formation of ferrihemoglobin appeared in the gas phase. Co2EDTA caused circulatory depression, hyperventilation, and metabolic acidosis resulting in a decrease in base-excess and pH. The concentrations of lactate, pyruvate, potassium, and urea nitrogen and the hemoglobin content were increased by Co2EDTA. The side effects of Co2EDTA in therapeutic doses were more serious than those of DMAP. Thus the latter is superior in the therapy of cyanide poisoning, all the more since it detoxifies more cyanide.

In all cases, statistical parameters of a H+-activities ought to be evaluated from data of pH values. Owing to the fact that the lower range of variability of the concentratons of H-ions is limited by zero, the values ought to be transformed into a logarithmic scale. In order to facilitate comprehension, the handling of transformations for the statistical evaluation of random samples is first explained by the example of the tidal volume of newborns and infants. In the second part of the paper, statistical parameters of several significant random samples of pH data are computed from various transformation systems and are contrasted in order to allow comparisons. Thus it becomes apparent that, under certain circumstances, the method of computing mean and standard deviations from a H+-activities may result in a characterization of random samples that are implausible.

The effects of a combination of etomidate (1.0 mg/kg bw) and fetanyl (0.005 mg/kh bw) on haematology, blood gases, acid-base balance and haemodynamics were investigated in 8 mongrel dogs. The only significant change in haematology was leucopenia. Blood gas values and acid-base balance initially showed a depression of respiration and a tendency to slight metabolic acid dosis. Decreased heart rate caused diminution of cardiac output, while systemic and pulmonary resistance as well as stroke volume were not altered significantly.

Twenty male volunteers were exposed to 95 ppm trichloroethylene for 4 h. Immediately before and aftere xposure and 4 h and 20 h after cessation, some serum-enzymes, the cytoenzymological activity of the alkaline and acid phosphatases and the naphthol-AS-D-esterase in neutrophil granulocytes and the acid-base equilibrium were investigated. Compared with the control experiment, the activities of the three neutrophil enzymes increased during trichloroethylene exposure with high significance. No significant changes of the serum-enzymes and the acid-base equilibrium could be found.

In 9 animals 500 ml of blood was replaced with 500 ml of Fluosol DA 20%. An average of 19.2 ml per kg body weight of emulsion, i.e. 3.883 gm per kg body weight of fluorocarbons was given. On the eighth day following exchange transfusion the animals were killed and tissue samples taken from liver and lung for electron microscopy and chemical analysis. Biochemical parameters were measured in central venous blood prior to transfusion and on the 2nd, 3rd, 6th and 8th days. One animal died on the sixth day of study, hence only the results obtained from the remaining 8 animals were analysed. On removing the lungs a marked firmness of consistency and failure to collapse was noted. Electron microscopy revealed numerous phagocytic cells packed with foam-like substance, partly occluding the pulmonary capillaries. On chemical analysis a residue of 23.95 mg fluorocarbon per gm of lung tissue was found. Acid-base analysis of central venous blood showed a compensated respiratory acidosis on the 6th and 8th day. The hepatic reticulo-endothelial system was found to be laden with numerous vacuoles, to such a degree that the sinusoids were all practically fully occluded. Neither cell necrosis nor inflammatory reactions were observed.

The cardiovascular, blood gas, acid-base and metabolic changes occurring during operative stress were studied in 10 elderly, metabolically healthy patients, suffering from idiopathic trigeminal neuralgia, who underwent electrocoagulation of the gasserian ganglion under neuroleptanalgesia. In a group of 12 patients undergoing the same operative procedure and anesthesthetic management, we investigated the effects of administration of a beta blocking agent on these parameters. Intraoperative rises of blood pressure and tachycardia were prevented by intravenous administration of 0.4 mg Pindolol (Visken), whereas increases in the blood glucose levels at the end of the operation were the same. The increase of glycerol, free fatty acids and ketone bodies was markedly reduced after pretreatment with the beta blocker compared with the controlgroup. In the patients without beta blocker treatment pH and standard bicarbonate at the end of the operation were lower as the result of the stimulation of ketogenesis.

Acidosis induced increase in renal calcium excretion was produced by means of ammonium chloride load in 12 control persons and in 76 patients with recurrent oxalate lithiasis. This increase is more marked in stone patients - even in those with normocalciuria - than in control persons. The calcium excretion is especially increased in patients with renal hypercalciuria. This might result from the primary nature of the renal defect. The acid load did not prove useful in the diagnosis of hyperparathyroidism.

Thermoregulatory, cardiac, and blood gas responses of muskrats to CO2 inhalation were examined during recovery from controlled dives in 3 degrees C water. It was shown that CO2 levels previously recorded in the winter lodges of this species are sufficient to reduce postdive oxygen consumption and rate of rewarming in unrestrained animals. Postdive exposure to 5-10% CO2 reduced recovery of abdominal and subcutaneous temperature (Tb) in the middorsal lumbar region, but did not affect interscapular warming overlying brown adipose tissue. Depressed recovery of deep Tb was matched by a prolonged acidosis in restrained muskrats breathing 5-10% CO2 following 90-s submergence in 3 degrees C water. This occurred despite a comparatively high whole body buffer value (delta H+/delta PaCO2) of 0.53 nM X l-1 X mmHg-1. Protracted recovery of arterial pH did not appear to involve retention of CO2 accumulated during diving, since in all trials, PaCO2 returned to the predive baseline within 5 min of surfacing. Perturbations in PaO2, like PaCO2, were restored within 5 min of surfacing, irrespective of inspired gas mixture. Predive exposure to 5-10% CO2 had no discernible effect on establishment of bradycardia in diving muskrats. Compared to predive values, postimmersion heart rate was significantly reduced in 5-10% CO2, but not in control runs.

We determined in two groups of patients with normal circulation and metabolism during operations on the retina and vitreous body the concentration of plasma catecholamines. The intensity of stress was compared between electrostimulation anaesthesia and neuroleptanaesthesia. Venous blood was sampled 1) before premedication, 2) 30' after premedication, 3) at the start of surgery, 4) 45' after the start of surgery, 5) 30' after extubation. Plasma catecholamines (adrenaline and noradrenaline) were determined using a modified trihydroxyindol-spectrofluoremetric method (combined "Batch-technique"). There was no relevant difference between the two techniques of anaesthesia when using the concentrations of plasmacatecholamines as an indicator of stress resulting from operation and anaesthesia.

Dichlorphenamide as well as Diamox lowers intraocular pressure. For adequate treatment of acute glaucoma only 20% of commonly used Diamoxdosis is requested to reach comparable pressure release two hours later. After one hour control intraocular pressure of 60% from patients with Dichlorphenamide treatment was found below 40 mm Hg since in Diamoxgroup there were only 30% below 40 mm Hg. Different effects of Dichlorphenamide and Diamox after one hour use is demonstrated in respect of serum electrolytes and base excess as well. Essential side effects after a single dosis of 200 mg Dichlorphenamide or in combination with Diamox for acute glaucoma treatment could not be observed.

Results obtained during animal investigations cannot be directly applied to patients because of the anatomical and physiological differences present. Experience has shown that cases of sudden cardiac arrest can only be effectively helped if cardiac massage and artificial ventilation are carried out as soon as possible, and that no sodium bicarbonate need be given when resuscitation measures are begun immediately, or very soon after arrest. In this situation it is better to use adrenaline only, in order to improve organ perfusion. The examples presented show that giving bicarbonate can alter potassium kinetics. Very low serum potassium concentrations are often measured during and following successful resuscitation, and giving too large an amount of buffer solution can worsen this hypokalaemia and lead to a further arrest. The infusion of sodium bicarbonate and the rapid increase in blood sugar levels during resuscitation can lead to a marked rise in serum osmolality which in turn can jeopardize the return of cerebral function. Because in the presence of reduced cerebral perfusion, high blood glucose levels increase the degree of cerebral lactacidosis blood glucose levels should be measured and corrected as necessary.

Perioperative effects of buprenorphine during and after combined anesthesia for gynecological laparotomies were compared to those of morphine. In a controlled, randomized study two similar groups of patients received flunitrazepam (0.016 mg/kg) and either buprenorphine (0.008 mg/kg) or morphine (0.333 mg/kg); all patients were ventilated with a N2O/O2-mixture. To maintain adequate anesthesia, additional injections of buprenorphine or morphine and a volatile anesthetic agent (enflurane, less than 1.0 vol.%) were administered as needed. In some patients in both groups the injection of thiopental (1-2 mg/kg) became necessary for induction of anesthesia. Hemodynamic parameters showed a slight but not significant increase during intubation and remained stable intraoperatively (Figs. 1 and 2). The frequencies of additional intraoperative injections of buprenorphine or morphine and modalities of enflurane administration were similar in both groups. Based on an awakeness score, recovery from anesthesia was similar in both groups (Fig. 3). All patients were pain-free for a long period postoperatively (pain score 1-2, duration 6-10 h) (Fig. 4). In both groups respiratory depression could be demonstrated by means of ventilatory CO2 response (Figs. 6 and 7). The respiratory depression was of no clinical importance and seems to have been due to the combination of a long-acting benzodiazepine with an opiate. There were no differences in the occurrence of nausea and vomiting in both groups. Buprenorphine seems to be an alternative to morphine in combined anesthesia.

In order to demonstrate pharmacokinetic and pharmacodynamic interactions between fentanyl and buprenorphine, 3 groups of patients (n = 30) were compared, receiving either fentanyl (0.005 mg/kg b.w.) or buprenorphine (0.01 mg/kg b.w.) or both opioids as analgesic during surgery for disc protrusion. For a period of 4 h haemodynamic parameters were monitored and blood samples were taken for determination of the following concentrations: ADH, ACTH, cortisol, glucose, unbound glycerol, fentanyl and buprenorphine. Blood gas analyses were performed up to 2 h postoperatively. Although in all groups haemodynamic parameters were constant, there was an increase in factors related to operative stress (cortisol, glucose, unbound glycerol, postoperative acidosis) after the combination of both opioids, while postoperative ventilatory parameters in this group were not improved by the partial agonist buprenorphine. Plasma levels were not affected by combined application, except for a slight elevation of buprenorphine concentrations during additional use of fentanyl. Buprenorphine, at least in higher dosages, seems to antagonize analgesia induced by fentanyl, although respiratory depression is even more pronounced. It may be assumed, that with partial agonists the relation of agonistic and antagonistic activity may be different, depending on the dosage used and on the respective pharmacologic effect observed during investigation.

A total of 19 patients (aged 17-66 years) with priapism received primarily conservative treatment in the form of aspiration of blood from the cavernous bodies and subsequent intracavernous (i.c.) administration of the alpha-adrenergic drug metaraminol. In 15 patients the priapism was due to i.c. injection of vasoactive agents; 1 patient each it had developed after hemodialysis, during oral prazosin medication, and in conjunction with Fabry's disease; and in 1 patient the etiopathogenesis was unknown. Treatment of priapism with metaraminol was successful in the first 15 patients and in 2 patients with priapism due to hemodialysis and oral prazosin medication. Therapy failed in long-lasting priapism associated with Fabry's disease and in priapism of unknown etiopathogenesis. Penile detumescence took place in the first 15 patients 3 min to 2.5 h after the injection of 2-4 mg metaraminol. Hemodialysis- and prazosin-linked priapism was treated with 5 and 2 mg metaraminol, respectively; in these patients erection subsided within 15 and 4 min after onset of therapy. In a further 2 patients in whom therapy had failed Al-Ghorab shunts were constructed, with the subsequent postoperative complication of erectile impotence. Injection of metaraminol must be carried out under strict supervision of the patient's circulatory system: doses of 4 mg metaraminol or more led to an increase in blood pressure and heart rate. In 15 patients with priapism induced by i.c. application of vasoactive agents, the analysis of blood gas parameters demonstrated a severe hypercapnia (70.3 +/- 10.0 mm Hg) and acidosis (pH 7.08 +/- 0.08) 5-10 h after the onset of erection, but severe hypoxia (37.0 +/- 16.6 mm Hg) was not found until erection had lasted for more than 10 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Whereas the impact of colloids and crystalloids on hypoxia and edema has been extensively debated with respect to pulmonary function, their corresponding effects on the systemic circulation have been largely ignored. Manifest edema of the intestine and skin develops, however, when the serum colloid osmotic pressure (COP) is lowered to 15 mm Hg or less by crystalloid infusions. Hypoxia of wounds, which may be aggravated by crystalloids, impairs healing and antibacterial defense, and its has been speculated that edema and/or hypoxia of the intestine may be associated with postoperative gastrointestinal dysfunction. We therefore studies the relationship between lowering and restoration of the COP, the pO2 of the intestinal surface and skin, and tissue edema. We generated an acute hypoproteinemic fluid overload reducing the COP from around 20 to 10 mm Hg in 56 rabbits by means of a 50% plasma loss and excess replacement with Ringer's lactate. We measured the COP with a membrane having a cut-off level of 20,000 d, the cardiac output (with derivation of further hemodynamic data) with an electromagnetic flow probe around the ascending aorta, and the tissue pO2 (pO2t) in mm Hg with the Dortmund 8-channel surface electrode. After 30 min without infusion (Fig. 1), we assigned 14 animals each at random to 4 treatment groups: (1) no treatment (O); (2) 20% albumin 7.5 ml/kg (A); (3) furosemide 2 mg/kg i.v. given three times at 30-min intervals (F); and (4) the combination of both agents (AF). During the infusion-free interval, the cardiac output and pO2t fell by 20%-30% of baseline (Table 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Of 66 patients undergoing hypotensive anaesthesia for oto-rhino-laryngological surgery, a sufficient low-pressure state was obtained in only 72% of patients when nitroglycerine was used. The cumulative nitroglycerine-consumption varied between 4.0 and 98.6 mg (0.05-1.698 mg/kg body weight). In 40 cases a normal or weak nitroglycerine-effect was accentuated by dihydralazine and the extend and time course of the interaction were investigated. The exceedingly marked additional effect of this substance indicates a mutual potentiation of both drugs. The maximum of the dihydralazine-action appeared after 25-35 minutes. In 16 further cases dihydralazine was given intravenously before the nitroglycerine infusion as a premedication, whereby always constant and satisfactory hypotension could be produced. A disadvantage of these combinations, occurring in several cases, was the decreased manoeuvrability of hypotension. The continuation of the long-term sodium nitroprusside-hypotension by using nitroglycerine was succesful. Even after nitroglycerine application longer than 3 hours (up to 6 hours) the acid-base-status remained normal.

Etomidate 0,3 mg/kg body weight and fentanyl 0,1 mg were given intravenously to two groups of patients--different by age--whilst spontanously breathing room-air. The effects on arterial blood pressure, heart rate and blood gases (arterial) were measured. In neither group did arterial blood pressure and heart rate changed appreciably but a significant fall of pO2 was found. There was only a small influence on acid-base-metabolism.

The influence of HCl infusion on extra- and intracellular acid-base status of liver, brain, heart, and skeletal muscle of nephrectomized rats was investigated in vivo. The present results showed that a decrease of extracellular plasma pH was followed by similar changes of the intracellular pH of the investigated tissues and a loss of bicarbonate from extracellular and intracellular body compartment. The results lead to the conclusion that HCl seems to be a suitable agent for correction of severe metabolic alkalosis.

Adult carp were subjected to 1 mM environmental nitrite for 48 h and nitrite uptake and changes in blood respiratory properties, extracellular electrolyte composition and acid-base status were examined. A constant influx of nitrite caused an accumulation of NO2- in plasma to 5.4 mM in 48 h. The fraction of methaemoglobin rose with plasma [NO2-] to 83%, and the arterial oxygen content decreased to extremely low values. Arterial PO2 increased as a compensation to this O2-shortage, whereas the O2 saturation of the functional (unoxidized) haemoglobin decreased, revealing a reduction in its O2 affinity. Blood haematocrit decreased as a result of red cell shrinkage, which caused very high red cell haemoglobin (Hb) concentrations. The erythrocytic nucleoside triphosphate (NTP) concentration showed a parallel increase whereby NTP/Hb, as well as the relative contributions of ATP and GTP to NTP, remained unchanged. Plasma [Cl-] declined by 15 mM in 48 h, offsetting the plasma [NO2-] increase, minor changes in plasma [HCO3-] and a considerable increase in plasma [lactate]. Arterial pH and [HCO3-] rose slightly during the first 24 h of nitrite exposure, but returned to control values at 48 h. The rise in plasma [lactate] was not reflected in an extracellular metabolic acidosis. Plasma [K+] increased by 94% in 48 h, revealing an uncompensated extracellular hyperkalemia, whereas plasma [Na+] decreased, and plasma [Ca++] was unchanged. Plasma osmolality remained essentially constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypotension at 70 mm Hg was induced with sodium nitroprusside in 6 hemodiluted and 6 control dogs. In contrast to the control dogs, the reduction in mean arterial pressure was not primarily due to the peripheral resistance reduction, but the result of a hazardous fall in cardiac output.