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African American (AA) individuals are at a greater risk for the development of cardiovascular complications, such as hypertension, compared with European Americans (EAs). Higher vagally mediated heart rate variability (HRV) is typically associated with lower blood pressure (BP) and total peripheral resistance (TPR). However, research has yet to examine the differential impact of HRV on longitudinal hemodynamic activity between AAs and EAs. We sought to rectify this in a sample of 385 normotensive youths (207 AAs, 178 EAs; mean age 23.16 ± 2.9 yr). Individuals participated in two laboratory evaluations spanning approximately 6 yr. Bioimpedance was used to assess HRV at time 1 and cardiac output at both time 1 and time 2. Mean arterial pressure (MAP) was measured at both time points via an automated BP machine. TPR was calculated as MAP divided by cardiac output. Results showed AAs to have higher BP and higher TPR at time 2 compared with EAs, independent of several important covariates. Also, higher HRV at time 1 significantly predicted both lower TPR and BP at time 2 among EAs only; these associations were attenuated and not significant in AAs. HRV did not significantly predict cardiac output at time 2 in the full sample or split by ethnicity. Our findings highlight that AAs show TPR mediated long-term increases in BP irrespective of resting HRV, providing a physiological pathway linking AAs with a greater risk for mortality and morbidity from hypertension and potentially other cardiovascular disease. NEW & NEWSWORTHY African Americans and European Americans differ in hemodynamics underlying long-term blood pressure regulation. Over 6 yr, African Americans show total peripheral resistance-mediated increases in blood pressure compared with European Americans. Higher heart rate variability predicts lower blood pressure and total peripheral resistance 6 yr later in European Americans but not African Americans.

Hypertension, affecting a third of the world’s population is associated with many vascular changes in blood vessels, which include rise of peripheral resistance and arterial stiffness. As there are very few studies done on Indian hypertensive women, this project was taken up to determine the prevalence of arterial stiffness in them. In this study, arterial stiffness is determined by assessing the carotid–femoral pulse wave velocity (C-F PWV). Fifty hypertensive female subjects between the ages 25 and 75 years were selected as subjects after informing the procedure and taking their consent. PWV was obtained from blood (BP) and electrocardiogram (ECG) recordings. They showed that subjects belonged to 3 categories depending on the level of their blood pressure—normal, grade I, and grade II hypertensives. PWV increased progressively with level of hypertension (p values = 0.0171 and

Pseudohypoaldosteronism type I is caused by a peripheral resistance to aldosterone and can present with electrolyte abnormalities, poor growth, or dehydration. Although a rare disease, several case reports have been published regarding Pseudohypoaldosteronism type I in neonates and infants. We report a case of failure to thrive and hyponatremia in an infant with hypoplastic left heart syndrome who was subsequently found to have Pseudohypoaldosteronism type I.

Objective The aim was to determine the main differences in the external structure of the body and the of central hemodynamics parameters in of high-level sports skills volleyball players of the juvenile age with the role of libero, hitters and setters. Patients and methods Materials and methods: 116 volleyball players of high level athletic skill of the youth age from 16 to 20 years old. The control group included 140 practically healthy girls who were not engaged in sports of the corresponding age. Anthropometric investigation was performed according to Bunak's V.V. and Martirosov's E.G. method, rheographic - according to the method of Ronkin M.A. and Ivanov L.B. The reliability of the difference between independent quantitative values was determined using Mann-Whitney U-test. Results Results: It was established that volleyball players have significantly higher total, longitudinal, circumferential dimensions of the body, width of distal epiphyses, transverse diameters of the chest and pelvis in comparison with girls, who are not involved in sport. According to the most parameters of the body external structure the hitters are predominate than setters and libero. In hitters and setters, most anthropo-somatotypological parameters are larger than in nonathletes. The stroke and minute volumes, the impact index, the volume velocity of the blood and the capacity of the left ventricle in volleyball players are significantly higher. Specific peripheral resistance is significantly lower than that of girls who are not involved in sports. Between the volleyball players of different positions in the value of the central hemodynamics parameters, there were no significant differences, except for the impact index, which is significantly higher in libero than in the hitters. Conclusion Conclusions: The external structure of the body, anthropometric parameters and indicators of central hemodynamics depend of volleyball player's position and have some peculiarities.

BACKGROUND: Peripheral resistance to thyroid hormones is a type of unresponsiveness of the peripheral cells or tissues to FT3 and/or FT4. Generalised resistance to thyroid hormones affects the pituitary gland and most of the peripheral tissues. Selective pituitary resistance or central resistance to thyroid hormones include unresponsiveness of the pituitary gland, but the peripheral tissues are responsive. Selective peripheral resistance involves peripheral tissue or cellular resistance to thyroid hormones, but the pituitary gland is responsive.CASE PRESENTATION: We present a rare case of a female patient with partial peripheral resistance to thyroid hormones due to a point mutation coding for the beta subunit of the integrin molecule α(V)β(3) and concomitant Hashimoto`s thyroiditis. Clinically, the patient`s symptoms were in favour of hypothyroidism, and the laboratory results were in favour of the secondary hyperthyroid state. PCR protein amplification detected a point mutation coding for the membrane receptor, which mediates a signal via the MAPK pathway when bonded with thyroid hormones.CONCLUSION: Peripheral resistance to thyroid hormones is a very rare condition and can often be misdiagnosed due to the broad spectrum of clinically similar differential diagnostic entities. Molecular analysis is required to confirm the exact underlying cause for the impaired peripheral sensitivity to thyroid hormones syndrome.

This article presents a clinical observation of a patient with a giant atherosclerotic abdominal aortic aneurysm and comorbid uncorrected coronary artery disease. Taking into account the threat of aneurysm rupture, we have chosena surgical intervention using methods that reduce the risk of cardiovascular events in the perioperative period: the distal-first technique allowed us to reduce the aortic clamping time, and the use of temporary axillofemoral bypass grafting reduced peripheral resistance and stress on myocardium.

BackgroundSeveral studies indicate that hypertension causes major changes in the structure of the vessel wall by affecting the regulation of blood supply to the tissues. Recently, it has been observed that capillary blood flow is also considerably influenced by the structural arrangement of the microvascular networks that undergo rarefaction (reduction of the perfused vessel number). Therefore, this study aimed to assess the geometric arrangements of the pial arteriolar networks and the arteriolar rhythmic diameter changes in spontaneously hypertensive rats (SHRs).MethodsFluorescence microscopy was utilized to observe in vivo the pial microcirculation through a closed cranial window. Pial arterioles were classified according to Strahler’s method. The arteriolar rhythmic diameter changes were evaluated by a generalization short-time Fourier transform.ResultYoung SHRs showed four orders of vessels while the adult ones only three orders. The diameter, length, and branching number obeyed Horton’s law; therefore, the vessels were distributed in a fractal manner. Larger arterioles showed more asymmetrical branches than did the smaller ones in young SHRs, while in adult SHRs smaller vessels presented asymmetrical branchings. In adult SHRs, there was a significant reduction in the cross-sectional area compared with the young SHRs: this implies an increase in peripheral resistance. Young and adult age-matched normotensive rats did not show significant alterations in the geometric arteriolar arrangement with advancing age, both had four orders of arteriolar vessels, and the peripheral resistance did not change significantly. Conversely, the frequency components evaluated in arteriolar rhythmic diameter changes of young and adult SHRs showed significant differences because of a reduction in the frequency components related to endothelial activity detected in adult SHRs.ConclusionIn conclusion, hypertension progressively causes changes in the microarchitecture of the arteriolar networks with a smaller number of vessels and consequent reduced conductivity, characteristic of rarefaction. This was accompanied by a reduction in the formation and release of independent and dependent – endothelial nitric oxide components regulating arterial vasomotion.

Herein we report in a sample of healthy young men ( n = 14) and women ( n = 12) that hyperinsulinemia induces time-dependent decreases in total peripheral resistance and its contribution to the maintenance of blood pressure. In the same participants, we observe profound vasodilatory effects of insulin in the lower limb despite concomitant activation of the sympathetic nervous system. We hypothesized that this prominent peripheral vasodilation is possibly due to the ability of the leg vasculature to escape sympathetic vasoconstriction during systemic insulin stimulation. Consistent with this notion, we demonstrate in a subset of healthy men ( n = 9) and women ( n = 7) that systemic infusion of insulin blunts sympathetically mediated leg vasoconstriction evoked by a cold pressor test, a well-established sympathoexcitatory stimulus. Further substantiating this observation, we show in mouse aortic rings that insulin exposure suppresses epinephrine and norepinephrine-induced vasoconstriction. Notably, we found that such insulin-suppressing effects on catecholamine-induced constriction are diminished following β-adrenergic receptor blockade. In accordance, we also reveal that insulin augments β-adrenergic-mediated vasorelaxation in isolated arteries. Collectively, these findings support the idea that sympathetic vasoconstriction can be attenuated during systemic hyperinsulinemia in the leg vasculature of both men and women and that this phenomenon may be in part mediated by potentiation of β-adrenergic vasodilation neutralizing α-adrenergic vasoconstriction.

Instructed reappraisal has previously been associated with a challenge-oriented cardiovascular response profile, indexed by greater cardiac output (CO) and lower total peripheral resistance (TPR), in response to a single stress exposure. The present study builds on this research by employing a stress habituation paradigm where participants completed a speech task twice; in which prior to the second task participants heard reappraisal instructions (i.e., view feelings of stress arousal as something that is beneficial) or control instructions. This paradigm allowed us to (a) test if reappraisal aids cardiovascular habituation to recurrent stress, and (b) examine if reappraisal leads to a within-participant change in CO/TPR responding from an uninstructed task to an instructed reappraisal task. Habitual use of reappraisal was assessed using the Emotion Regulation Questionnaire. The analyses report upon 173 young adults (121 women, 52 men). Cardiovascular parameters were measured continuously using the Finometer Pro. All participants demonstrated similar cardiovascular habituation during the second stress exposure (lower SBP, CO, and HR); suggesting reappraisal did not aid cardiovascular habituation to recurrent stress. Reappraisal instructions did not lead to a challenge-oriented response compared to both the control group and responses to the uninstructed task. This study is the first to examine the relationship between instructed reappraisal and cardiovascular habituation and identifies that habitual use of reappraisal does not interact with reappraisal instructions to influence cardiovascular responses to stress.

Background: In many cases, Ilomedin® infusions are applied as part of a perioperative measure in patients with peripheral arterial occlusive disease because it makes a relevant vasodilatatory effect in patients with type 2 diabetes mellitus and with/without peripheral neuropathy. Aims: A prospective case–control study was performed to investigate the effect of prostanoids on peripheral resistance in patients with type 2 diabetes mellitus and patients without type 2 diabetes mellitus, as well as the role of peripheral neuropathy in patients undergoing arterial reconstruction. Methods: Sixty patients undergoing arterial reconstruction were enrolled. Sufficient data were collected on 38 patients. Prior to surgery, peripheral nerve conduction velocity was measured. Blood flow volume at the common femoral artery was assessed intraoperatively using a Doppler flowmeter at four time points: at baseline before arterial reconstruction (T0), after reconstruction (T1), after 5 (T2) and 10 min (T3) after intra-arterial application of 3000 ng of Ilomedin. Peripheral resistance units were calculated as a function of mean arterial pressure and flow volume using the following formula: peripheral resistance unit = mean arterial pressure (mm Hg) / flow volume (mL/min). Results: Ilomedin produced an immediate and significant drop of peripheral resistance in patients without type 2 diabetes mellitus as well as in patients with type 2 diabetes mellitus. Patients with peripheral neuropathy showed a less pronounced effect to Ilomedin compared to individuals with normal nerve conduction velocity.

Hypertension is a condition characterized by pressure and/or volume overloads and echocardiography is helpful and feasible to understand hemodynamic mechanisms. Echocardiographic information is sometimes critical and susceptible of modifying decision making. In this review, we provide detailed descriptions of the parameters that can be derived from a standard transthoracic echocardiogram, including some more recent techniques. We will also explain how each parameter might have impact in the evaluation of the hypertensive patient and give indications on when to refer patients to echo-labs, which parameters are critical and which ones might be redundant, and how to use the information obtained in the report. Cardiac geometry, LV systolic and diastolic function, LV pump performance, output impedance and left atrial function are parameters that might be altered in arterial hypertension, but not necessarily doctors need the whole information for decision making. The critical measures are provided.

In hypertension, the increase in peripheral resistance occurs at the level of microcirculation. It was clearly demonstrated that wall thickness is increased in relation to internal lumen and that this alteration significantly contributes to peripheral resistance. The increased media/lumen ratio may impair organ flow reserve. This may be important in the maintenance and, probably, also in the progressive worsening of hypertensive disease. The presence of structural alterations represents a prognostically relevant factor, in terms of development of target organ damage and incidence of cardiovascular events, thus allowing a prediction of hypertension complications.

This paper presents the first two studies to explore the effect of challenge and threat states on endurance exercise capabilities. In study one, relationships between cardiovascular markers of challenge and threat states, ratings of perceived exertion (RPE), and exercise tolerance were explored during moderate- and severe-intensity cycling. Cardiovascular reactivity more reflective of a challenge state (i.e., relatively higher cardiac output and/or lower total peripheral resistance reactivity) predicted lower RPE throughout moderate- but not severe-intensity cycling. Building on these findings, study two experimentally manipulated participants into challenge, threat, and neutral groups, and compared 16.1 km time-trial performances, where pacing is self-regulated by RPE. Participants completed familiarisation, control, and experimental visits while physiological (oxygen uptake), perceptual (RPE), and performance-based (time to completion [TTC] and power output [PO]) variables were assessed. When compared to the threat group, the challenge group demonstrated cardiovascular responses more indicative of a challenge state, and delivered faster early-race pacing (PO) at similar RPE. Although there were no significant differences in TTC, results revealed that augmentations in PO for the challenge group were facilitated by tempered perceptions of fatigue. The findings suggest that an individual’s pre-exercise psychophysiological state might influence perceived exertion and endurance exercise capabilities.

Background/Aims: Intradialytic hypertension (IH) occurs frequently in some hemodialysis patients and increases mortality risk. We simultaneously compared pre-dialysis, post-dialysis and changes in extracellular volume and hemodynamics in recurrent IH patients and controls. Methods: We performed a case-control study among prevalent hemodialysis patients with recurrent IH and hypertensive hemodialysis controls. We used bioimpedance spectroscopy and impedance cardiography to compare pre-dialysis, post-dialysis, and intradialytic change in total body water (TBW) and extracellular water (ECW), as well as cardiac index (CI) and total peripheral resistance index (TPRI). Results: The ECW/TBW was 0.453 (0.05) pre-dialysis and 0.427 (0.04) post-dialysis in controls vs. 0.478 (0.03) and 0.461 (0.03) in IH patients (p=0.01 post-dialysis). The ECW/TBW change was -0.027 (0.03) in controls and -0.013 (0.02) in IH patients (p=0.1). In controls, pre- and post-dialysis TPRI were 3254 (994) and 2469 (529) dynes/sec/cm2/m2 vs. 2983 (747) and 3408 (980) dynes/sec/cm2/m2 in IH patients (p=0.002 post-dialysis). There were between-group differences in TPRI change (0=0.0001), but not CI (p=0.09). Conclusions: Recurrent intradialytic hypertension is associated with higher post-dialysis extracellular volume and TPRI. Intradialytic TPRI surges account for the vasoconstrictive state post-dialysis, but intradialytic fluid shifts may contribute to post-hemodialysis volume expansion.

In this work we studied the interrelations of violation regional hemodynamics and microcirculation of a fabric blood groove of a mucous membrane of a mouth in 70 patients with the chronic heart failure (CHF) and inflammatory diseases of a parodontium. The microcirculatory bed is a peculiar model of the regulatory processes happening in vessels of various calibers. The received results show that patients with initial stages of chronic heart failure have a decrease in haemodynamics indicators of speed of a fast and slow blood filling in the pool of internal sleepy are followed by increase of linear speed of a bloodgroove, increase in an index of a pulsation and peripheral resistance in the field of a transitional fold of the sky and interdental nipples of fabrics of a parodontium. The microcirculatory bed is a peculiar model, the regulatory processes happening in vessels of various calibers. The received results reflect mechanisms of regulation and compensation for maintenance of microcircula tion of a fabric bloodgroove of a parodontium in patients with CHF.

Preeclampsia affects 2% of pregnant women and is one of the main causes of prenatal maternal mortality and morbidity. Recent studies with two-dimensional echocardiography have shown that PE is characterized by a marked reduction on maternal cardiac output and increased peripheral resistance. However, studies on the maternal hemodynamic adaptation during PE and the available information about central maternal hemodynamics are scarce. The main purpose of this study is to develop a computational model, in order to obtain relevant hemodynamic parameters of the maternal circulation, formed by the common iliac, the internal and external iliac and the uterine arteries. The first stage of this work consists on creating the geometric model. This model require many approximations and generalizations in order to optimize the numerical calculation of the hemodynamic parameters by Computational Fluid Dynamics (CFD), but it is the best representation of the morphology and anatomy of the maternal circulatory system. In order to represents the maternal system, four different models were created, to simulate no-pregnant women and 21, 30 and 36 weeks of pregnancy. The numerical simulations performed by ANSYS®-Fluent software correlate the main hemodynamic parameters, such as flow, velocity and arterial pressure, with the variation of uterine morphological data. A variation on the velocity and pressure was verified on each geometrical model, and their corresponding inlet flow.

Hypertension is caused by increased cardiac output and/or increased peripheral resistance. Areas covered: The various mechanisms affecting cardiac output/peripheral resistance involved in the development of essential hypertension are covered. These include genetics; sympathetic nervous system overactivity; renal mechanisms: excess sodium intake and pressure natriuresis; vascular mechanisms: endothelial cell dysfunction and the nitric oxide pathway; hormonal mechanisms: the renin-angiotensin-aldosterone system (RAAS); obesity, obstructive sleep apnea (OSA); insulin resistance and metabolic syndrome; uric acid; vitamin D; gender differences; racial, ethnic, and environmental factors; increased left ventricular ejection force and hypertension and its association with increased basal sympathetic activity - cortical connections. Expert commentary: Maximum association of hypertension is found with sympathetic overactivity which is directly or indirectly involved in different mechanisms of hypertension including RAAS, OSA, obesity, etc.. It is not overt sympathetic activity but disturbed basal sympathetic tone. Basal sympathetic tone arises from hypothalamus; possibly affected by cortical influences. Therefore, hypertension is not merely a disease of circulatory system alone. Its pathogenesis involves alteration in ANS (autonomic nervous system) and likely in cortical-hypothalamic connections. Assessment of ANS and cortical-hypothalamic connections may be required for better understanding of hypertension.

Patients with peripheral arterial disease (PAD) have an exaggerated pressor response to dynamic exercise of the affected limb. We tested the hypothesis that this response is mediated by an increase in total peripheral resistance (TPR). We measured heart rate, blood pressure, stroke volume, cardiac output (CO), and total peripheral resistance (TPR) during exercise in 9 subjects with PAD and 9 age matched controls using continuous finger arterial pressure monitoring (Finometer). Finometer derived values were adjusted to values obtained by echocardiography, and brachial pressure at baseline. The average age and ABI was 65 ± 7 and 1.06 ± 0.07 in controls, and 66 ± 7 and 0.64 ± 0.08 in PAD. Participants performed dynamic plantar flexion at progressive workloads of 2 to 12kg (increased by 1kg/min until onset of fatigue/pain) using their symptomatic leg or leg with lower ABI. Those who reached 12kg continued exercise at a constant load until onset of fatigue/pain or a maximum of 4 minutes. Participants were then asked to perform an isometric handgrip exercise at 30% of maximum voluntary contraction (MVC) until fatigue. Results are shown in Table 1. There were no differences in hemodynamic parameters at baseline. The average weight at end of plantar flexion was 12.0 ± 0.2 and 9.2 ± 2.5 kg (p

SummarySmoking has many harmful effects on human body. It is well known that smoking is one of the most important risk factors for cardiovascular diseases. Though the ingredients from cigarette smoke stimulate the release of vasoconstrictor and reduce the release of vasodilator substances, the goal of this study was to investigate the acute effects of smoking on arterial blood pressure, heart rate and blood vessel flow.The investigation was conducted on forty healthy volunteers divided into two groups of twenty non-smokers (control group), and twenty smokers (experimental group). The group of smokers was examined before and after smoking four cigarettes during one hour. Blood pressure and electrocardiograph (ECG) were measured by common methods. Brecht’s and Boucke’s methods of plethysmography were used to evaluate the peripheral circulation.There were no differences in measured systolic and diastolic blood pressure and recorded ECG between non-smokers and smokers, neither between smokers before and after smoking. However, heart rate was increased by 29.57% after smoking in comparison to the value before smoking.Evaluation of plethysmographic parameters showed that amplitude was significantly decreased. Parameters of peripheral resistance were very increased: ductility was decreased by over 20%.It can be concluded that acute smoking does not significantly affect the level of blood pressure, although it increases heart rate. The shape of plethysmograms showed decreased systolic filling and decreased diameters of blood vessels.

Specificities of the changes in the systemic hemodynamics indices in the spontaneously hypertensive line SHR rats have been studied in comparison with the normotensive line WKY rats. It was demonstrated that an increase in blood pressure observed in the young hypertensive male rats, which have completed puberty (8 weeks old), is associated with the development of the hyperkinetic type arterial hypertension, which is characterized by increased cardiac minute output. It has been shown that SHR line male rats reveal the establishment of stable arterial hypertension due to a significant increase in the total peripheral resistance with the simultaneous recovery of the cardiac minute output by the 25th week of life. SHR line rats at the age of 15 weeks may be regarded as being in the period of transition from the hyperkinetic type arterial hypertension to stable arterial hypertension.

The study proposes an extension of cardiac baroreflex (cBR) sequence analysis, traditionally performed over spontaneous fluctuations of heart period and systolic arterial pressure, to typify peripheral resistance baroreflex (prBR) from spontaneous variations of peripheral resistances and diastolic arterial pressure. The prBR baroreflex sensitivity (BRS prBR ) and percentage of prBR sequences (SEQ% prBR ) were computed along with analogous quantities assessed over cBR (i.e. BRS cBR and SEQ% cBR ). The cBR and prBR were typified in healthy subjects at rest (REST) and during light bicycle ergometer exercise at 10 percent of the maximal effort (EXE). Both cBR and prBR were affected by EXE: indeed, BRS cBR and SEQ% prBR were significantly reduced. Moreover, while BRS cBR and BRS prBR were not significantly associated, SEQ% cBR and SEQ% prBR were, and the correlation coefficient was positive. This study suggests that prBR can be typified from spontaneous variabilities along with the more traditional cBR, thus enlarging the possibility of monitoring human cardiovascular control mechanisms.

BACKGROUND Cardiovascular reflexes that regulate blood pressure (BP) adapt during repeated exposure to +Gz acceleration separated by short (< 20 s) breaks, but whether this effect is preserved with longer intervals remains unknown. METHODS There were 17 subjects who completed 5 repeated gradual onset (0.1 G x s(-1)) runs (GOR1-5) to 60 degrees peripheral light loss (PLL) on a human centrifuge, separated by 2 min. Heart rate (HR) and BP were measured before and during each GOR and noninvasive estimation of cardiac output (CO) was used to calculate total peripheral resistance (TPR). RESULTS Mean resting (+/- SE) systolic BP (138 +/- 4 vs. 128 +/- 3 mmHg) and TPR (13.9 +/- 1.2 vs. 12.7 +/- 1.0 mmHg x L(-1) x min(-1)) were elevated after GOR1 and remained elevated thereafter. Compared with that before GOR1, resting HR was decreased (5-6 bpm) before GOR2-5. Resting CO decreased from 8.3 +/- 0.6 L x min(-1) before GOR1 to a nadir of 7.2 +/- 0.5 L x min(-1) before GOR4 and GOR5. The change in HR under increased +Gz decreased from +39 +/- 3 bpm during GOR1 to +31 +/- 3 bpm during GOR4 and GOR5, but the decrease in eye level BP under +Gz was unaffected. RGT did not change across the five GORs. CONCLUSIONS Increased resting BP and TPR following a single +Gz exposure suggest alterations in the cardiovascular system expected to confer improved tolerance during subsequent exposures. However, these changes were insufficient to improve +Gz tolerance measured during repeated GORs separated by 2 min.

We examined the effects of acute and chronic exercise under hypobaric hypoxia on cardiovascular responses/adaptations to test the hypothesis that cardiovascular adaptations are more effective after exercise under hypobaric hypoxia than under normobaric normoxia. First, we found that a decrease in peripheral resistance and blood pressure (BP) concomitant with an increase in stroke volume (SV) and cardiac output (CO) could be more effectively induced by chronic exercise under hypobaric hypoxia, than under normoxia. Also, the decrease in peripheral resistance and BP might be attributable to a decrease in arterial stiffness and enhanced vasodilatory activity. Second, the effects of acute hypoxic exposure and exercise on arterial stiffness and vasodilatory activity were examined. Arterial stiffness decreased after acute exercise alone, but not after acute hypoxic exposure alone. However, vasodilatory activity was enhanced by hypoxic stimulus, and to greater extent after hypoxic exercise. These findings suggested that stimulation with concomitant exercise and hypoxia could bring about more beneficial vascular responses. Finally, the time course of cardiovascular adaptations to hypobaric hypoxic exercise were accessed, and we found that a significant decrease in BP, accompanied by an increase in SV and CO, occurs within one week of starting the exercise; and that there is a significant decrease in arterial stiffness by the end of the second week. These changes in cardiovascular responses persisted until the end of the training period. Our findings suggest that exercise under hypobaric hypoxia brings about more rapid and effective beneficial cardiovascular adaptations than that under normoxia.

This double-blind study tested the effects of pulsating electromagnetic field (PEMF) therapy sessions on the changes in peripheral cardiovascular function in a group of aging adults after 12 weeks of treatment. Each therapy session involved 15 min of exposure to low-frequency PEMF with asymmetrical waveforms emitted by the Impulser™ Pro mattress. The treatment was provided 5 days per week for a total of 60 sessions. Resting blood pressure and arterial stiffness index were determined for peripheral cardiovascular function. Fifty-four older men and women (mean age 59.8 ± 3.5 yrs) completed the entire protocol involving either the PEMF or a sham treatment. The results include statistically significant reductions in systolic and pulse blood pressure, while no significant difference in diastolic pressure or the index of arterial stiffness was observed. These findings suggest that the PEMF treatment might be linked to improvements in peripheral resistance or circulation.

Mental stress can trigger myocardial infarction, with poor vascular responses to stress implicated as a pathway. Vascular stress reactivity can be assessed by different methods, such as total peripheral resistance (TPR) and forearm blood flow (FBF). Little is known about how these vascular assessments are linked. This was examined in two separate studies. Healthy men (Study 1: N = 29, Study 2: N = 23) completed rest and mental arithmetic (Study 1: 8 min, Study 2: 16 min). In both studies, heart rate, mean arterial pressure, and FBF increased in response to stress. In Study 1, no changes in TPR were seen, but Study 2 found stress-induced increases in TPR. FBF was not linked to TPR at any time (all ps > .05). It appears that limb vasculature and TPR responses to stress do not give the same information about impairments of the vasculature. These findings are relevant to the interpretation of prior research findings and the design of future studies on stress and vascular responses.

UNLABELLED Space Shuttle astronauts wore an inflatable antigravity suit during reentry and landing, and astronauts and cosmonauts wear an elastic-compression garment (with lacing) during Soyuz re-entry and landings and in the first few days of recovery. However, neither garment is an ideal countermeasure to spaceflight-induced orthostatic intolerance. Our laboratory has been investigating an elastic graded compression garment (GCG) that applies graduated pressures from the feet to the abdomen for use following International Space Station missions and possibly during exploration missions. METHODS Before and after Shuttle missions, 14 astronauts participated in a 3.5-min stand test. The stand test was conducted without garments preflight. On landing day, 7 astronauts wore the GCG while 7 astronauts did not (controls). Heart rate and blood pressure were measured in all astronauts during prone rest and standing. Stroke volume and cardiac output were measured only in GCG subjects. RESULTS No astronauts in either group became presyncopal during the stand test preflight or postflight. The change in heart rate from prone to standing was lower in the GCG subjects on landing day than in the control subjects. Within the GCG subjects only, the increase in total peripheral resistance from prone to standing was higher after spaceflight. CONCLUSIONS The GCG prevented tachycardia and increased total peripheral resistance with standing after spaceflight. The GCG shows promise as a countermeasure against post-spaceflight orthostatic intolerance, can be easily donned, and is relatively comfortable to wear, but has not been validated after long-duration spaceflight.

The purpose in this article is to investigate the measurement method and normal values of the total peripheral resistance (TPR) and total peripheral resistance index (TPRI) measured by the reconstructed impedance cardiogram (RICG). Methods The cardiac output and cardiac index of 180 normal adults is measured by means of the RICG. The computed formula of the TPR and TPRI are deduced, and the TPR and TPRI are calculated. The subjects are divided to the different groups according to the sex and age. The TPR and TPRI are calculated statistically. Results The TPR and TPRI are increased with the increase of the age, and there is significant difference between the young and elder groups (P0.05). The normal value of the TPR is less than 1650 dyn.s.cm-5, and that of the TPRI is less than 2650 dyn.s.cm-5.m2. Conclusion The TPR and TPRI measured by the RICG can reflect the hemodynamic changes of the normal or abnormal body.

PURPOSE: The dynamics of the postulated phenomenon of exercise baroreflex resetting is poorly understood, but can be investigated using closed-loop procedures. To shed light on some mechanisms and temporal relationships participating in the resetting process, we studied the time course of the relationship between the R-R interval (RRi) and arterial pressure with a closed-loop approach. METHODS: On ten young volunteers at rest and during light exercise in supine and upright position, we continuously determined, on single-beat basis, RRi (electrocardiography), and arterial pressure (non-invasive finger pressure cuff). From pulse pressure profiles, we determined cardiac output (CO) by Modelflow, computed mean arterial pressure (MAP), and calculated total peripheral resistance (TPR). RESULTS: At exercise start, RRi was lower than in quiet rest. As exercise started, MAP fell to a minimum (MAPm) of 72.8 ± 9.6 mmHg upright and 73.9 ± 6.2 supine, while RRi dropped. The initial RRi versus MAP relationship was linear, with flatter slope than resting baroreflex sensitivity, in both postures. TPR fell and CO increased. After MAPm, RRi and MAP varied in opposite direction toward exercise steady state, with further CO increase. CONCLUSION: These results suggest that, initially, the MAP fall was corrected by a RRi reduction along a baroreflex curve, with lower sensitivity than at rest, but eventually in the same pressure range as at rest. After attainment of MAPm, a second phase started, where the postulated baroreflex resetting might have occurred. In conclusion, the change in baroreflex sensitivity and the resetting process are distinct phenomena, under different control systems.

Background With the development of left ventricular assist device (LVAD), the long-term support has been paid more attention by various researchers. According to previous researches, the combination of LVAD and pharmacological therapy can significantly improve the heart rate recovery and survival rate of patient. However, the effect of pharmacological therapy on the cardiovascular hemodynamic states with LVAD support is still unclear. Methods In this study, pharmacokinetic model of captopril is established to describe the relationship between plasma–drug concentration and time. Then, combination model, consisting of pharmacokinetic model of captopril and lumped parameter model of cardiovascular system with BJUT-II VAD support, is established to mimic the effect of pharmacological therapy on cardiovascular hemodynamics. BAI control strategy and HR control strategy for BJUT-II VAD are chosen to evaluate their performance by the combination model. Results The simulation results demonstrate that the concentration of captopril could affect the pressure and heart rate by changing the peripheral resistance, and then affect the performance of BJUT-II VAD in a short duration. Under the regulation of control strategies of BJUT-II VAD, the hemodynamic states of cardiovascular system returned to the standard value in 10 s. Conclusion This study could provide useful information about how to design coupled strategy of LVAD support and pharmacological therapy.

Caribbean vervets ( Chlorocebus aethiops sabeus ) develop hypertension (HT; Systolic Blood Pressure ≥ 140 mmHg) in over 30% (125/345) of the outbred population. Elevated total peripheral resistance in HT increases cardiac afterload, which may lead to left ventricular hypertrophy (LVH) and cardiac remodeling. We hypothesize that prolonged spontaneous HT is associated with LVH, cardiac and aortic fibrosis, as well as differential transcription of myocardial contractile proteins. Vervets were characterized as HT (SBP = 170 ± 25.3 mmHg; n=125) or normotensive (NT, SBP = 99 ± 14.5 mmHg; n=148) using forearm plethysmography (ketamine sedated;15 mg/kg i.m.). Cardiomyocyte cross-sectional area was greater in HT compared to NT animals (HT 283 ± 52 μm 2 , n=9 vs NT 114 ± 8 μm 2 , n=10; p2 , n=9 vs NT 12.22 ± 0.80% or 0.16/1.27 mm 2 , n=10; p>0.05). Aortic adventia collagen area was greater in HT compared to NT vervets (HT 66.12 ± 4.22% or 0.60/0.90 mm 2 , n=6 vs NT 54.53 ± 2.21% or 0.56/1.02 mm 2 , n=10; p

In experiments on anaesthetized dogs with modeling of experimental ischemia (90 min) and reperfusion (180 min), the cardioprotective influence of the pharmacological preconditioning caused by intragastric (with a help of catheter) introduction of medicinal form (tablets) of new fluorine-containing opener of ATP-sensitive potassium channels flocalin was shown. Flocalin was introduced in a dose 2.2 mg/kg, which in the conditions of physiological norm has a minimum influence on the parameters of cardiohemodynamic. The conducted research allowed to define the changes of these parameters during development of antiischemic protective effect of pharmacological preconditioning, caused by the medicinal form of flocalin, and describes basic cardioprotective mechanisms, related to the changes of cardiohemodynamic in the dynamics of ischemia-reperfusion of myocardium. In our opinion, to positive influences of flocalin, which are possibly related to cardioprotective action, it is possible to add the prevention of an increase of general peripheral resistance, resistance of coronal vessels of heart, and relative preservation of myocardium contractility in the period of reperfusion. Also these positive effects can be explained by moderate decrease of blood pressure that decreases the loading on the damaged heart and allows to preserve cardiac emission in the first period of ischemia. One of the major indexes of development of protective mechanism of pharmacological preconditioning caused by preischemic introduction of medicinal form of flocalin is the diminishing of infarct size of myocardium in experiments with ischemia-reperfusion of myocardium on 42.53% +/- 2.91% versus control experiments.

Echocardiography was performed at every six months in hypertensives well controlled on metoprolol, 100 mg twice a day. After six months' treatment blood pressure was reduced from 177/110 mm Hg to 147/88 (p less than 0.02). LV wall thickness (septum + posterior wall) was unchanged 2.10 cm (2.14), and a significant drop in cardiac output (CO) to 5.0 l/min (6.1, p less than 0.02) was recorded (pretreatment values in brackets). After 24 months' treatment LV wall thickness was reduced to 1.94 cm (p less than 0.02), total peripheral resistance (TPR) to 17.3 mm Hg/l/min (23.4, p less than 0.02) and CO increased to 6.7 l/min (6.1, n.s.). After six months' treatment, there was thus a drop in BP with a significant drop in CO and unchanged TPR. After 24 months' treatment, however, CO was back to the pretreatment level and the drop in BP was entirely caused by a drop in TPR which was probably secondary to a reduction in the wall thickness of the arterial resistance vessels as judged by the relationship between the reduction in wall thickness in the LV and the reduction in TPR during the treatment.

Eighteen young females performed two kinds of mental tasks, an Internally-Generated Mental Arithmetic task (IGMA: serial subtraction) and an Externally-Presented Mental Arithmetic task (EPMA: continual subtraction). Both tasks were equal in establishing active coping, but EPMA made participants attend more to an external stimulus. The expected reaction patterns were vascular-dominant (blood pressure elevation mainly due to an increase in total peripheral resistance) for only EPMA, or cardiac-dominant (mainly due to an increase in cardiac output) for both IGMA and EPMA. The results showed that vascular-dominant patterns were evoked during EPMA, while mixed (moderate increases in both cardiac output and total peripheral resistance) reaction patterns were evoked during IGMA. Post-task questionnaires confirmed that attention to an external stimulus was required much more in EPMA than in IGMA. These results indicate that the vascular-dominant reaction pattern was evoked in the state where attention to an external stimulus was heightened. The implications of the present findings are discussed in term of how to interpret the hemodynamic reaction patterns during mental stress.

In a prospective, randomized and controlled study, 29 patients received i.v. verapamil, 5-10 mg/h for two days, at a mean of eight hours after onset of myocardial infarction. In a control group, 25 patients received no specific treatment. In all patients, left ventricular end-diastolic pressure was initially less than 15 mm Hg. The two groups were comparable as to age, infarct site and haemodynamics (measured via Swan-Ganz catheter). CK and CKMB peaks were significantly lower in the verapamil than the control group (CK 547 vs 703 U/1, P less than 0.05; CKMB 51 vs 68 U/1, P less than 0.025), as well as infarct weight (CK = 48 vs 65 g-equivalent; P less than 0.03; CKMB = 31 vs 49 g-equivalent; P less than 0.005). Arterial blood pressure was lower by 10 mm Hg than in the control group. Peripheral resistance and filling pressure remained unchanged. In patients without left ventricular failure verapamil reduces the infarct size by about 30%. The most prominent haemodynamic change is a reduction in blood pressure.

Background Even if sodium sensitivity represents a risk factor at any blood pressure ( BP ) level, limited evidence is available that it may influence cardiovascular control in normotensives, particularly in white individuals. Therefore, the aim of the study was to investigate whether sodium sensitivity alters hemodynamic or autonomic responses to salt in normotensives. Methods and Results We evaluated the Sodium‐Sensitivity Index ( SS ‐Index) in 71 white normotensives after 5 days of high‐ and low‐sodium diets. We measured BP continuously at the end of each period, estimating hemodynamic indices from BP waveform analysis, and autonomic indices from heart rate ( HR ) and BP variability. According to the SS ‐Index distribution, we defined 1 sodium‐sensitive group ( SS , with SS ‐Index >15 mm Hg/[mmol·day]), 1 sodium‐resistant group, (unresponsive to sodium load with −15≤ SS ‐Index ≤+15), and 1 inverse sodium‐sensitive group, responsive to sodium by decreasing BP , with SS ‐Index SS ‐Index. After sodium loading, a significant decrease in systemic peripheral resistances, HR , spectral indices of BP modulation, and a significant increase of indices of HR vagal modulation were found in the inverse sodium‐sensitive group but not in SS normotensives. Moreover, the highest SS ‐Indices were associated with the lesser vagal HR decelerations. Conclusions Our data suggest that salt sensitivity in white normotensive individuals is associated with impaired vasodilation and altered autonomic response to dietary salt. Such dysfunction may critically contribute to induce a BP response to dietary salt.

Athletes sometimes collapse either during or after exercise. Conditions that cause collapse during exercise may be life-threatening and account for 10-15% of all exercise-related medical encounters at endurance sporting events. These conditions are not always 'sports-specific' and are managed according to the usual clinical care guidelines. The majority (85%) of exercise-related collapse occurs after athletes have completed the event and key features are that patients are fully conscious and they have no clinical evidence for other serious medical conditions, but they have postural hypotension (blood pressure usually100mm Hg) with unexpectedly low heart rates (100 beats per minute). The cause of the postural hypotension appears to be the combination of physiological changes induced by exercise that tend to maintain a state of abnormally low peripheral vascular resistance for some hours after exercise. The most appropriate treatment for these patients is the supine position with the legs and pelvis above the level of the heart. Additional therapeutic interventions should be reserved for those who fail to respond adequately (blood pressure100mm Hg; normal heart rate) to this simple treatment.

The analysis of the hemodynamics accompanying correction of renal anemia by rhEPO shows that--although they behave qualitatively as in nonuremic anemic patients--cardiac output and peripheral resistance may change inadequately and thereby cause a rise of blood pressure. The underlying mechanisms are not yet fully understood but to a great part may be related to preexisting pathology due to a history of longlasting hypertension. In some patients the development of hypertension may only represent a temporary phenomenon of hemodynamic dysregulation. To avoid cardiovascular complications the following should be considered: Patients with a history of hypertension, even if they are normotensive in the anemic state, are at a higher risk of developing hypertension during therapy with rhEPO. Hypertensive complications may be rare events when anemia is corrected slowly. In case of the development or aggravation of hypertension a reduction of the target hematocrit is indicated.

Introduction: Vascular pathophysiology is a hallmark of hypertension (HTN)-linked cardiovascular disease, as increased peripheral resistance leads to vascular remodeling. Consistent with this is th...

A quantitative scale for identifying cardiac versus vascular reactor, balance of blood pressure equivalents (BE), was newly advocated and compared with a very recently advocated one, hemodynamic profile (HP), by Gregg, Matyas and James (2002). BE was defined as “(ΔQ/Q0)P0′ − (ΔR/R0)P0.” Here, P0, Q0, and R0 were mean blood pressure (P), cardiac output (Q), and total peripheral resistance (R) during baseline, and ΔQ and ΔR were the difference scores of Q and R from baseline to stress, respectively. This was named as BE because the two terms in the formula indicated changes in Q and R in their blood pressure equivalents. Comparisons of the BE and HP scales were carried out, theoretically, in a newly introduced pressor space, on orthogonality with the extent of elevation of P (ΔP); and then, practically, by using hypothetical data. In summary, it was shown that data points in the neighborhood in the pressor space can be judged as having not so different hemodynamic balance whether the BE or HP scale was used. As a merit, the BE scale seemed helpful to an intuitive understanding of the hemodynamics during stress. As a demerit, it cannot maintain the quasi-orthogonal relationship with ΔP when Q or R changes profoundly in the face of stress.

Although initially recognised for their GH-releasing properties, the cardiovascular system has been recognised as a potentially important target for GH secretagogues (GHS). Moreover, a limited number of studies also indicate cardiovascular effects of ghrelin. So far reported cardiovascular effects of GHS and/or ghrelin include lowering of peripheral resistance, possible improvement of contractility and cardioprotective effects both in vivo and in vitro. Taken together, these results offer an interesting perspective on the future where further studies aiming at evaluating a role of GHS and ghrelin in the treatment of cardiovascular disease are warranted.

The military antishock trouser (MAST) is an inflatable garment that surrounds the lower portion of the body (legs and abdomen). It is primarily used as an emergency garment to stop bleeding in the lower extremities, increase peripheral resistance to better perfuse the upper body, and increase blood flow to the brain and other vital organs. The MAST garment consists of three chambers, which can be inflated separately or together with a simple foot pump to 100 mmHg. MAST garments are designed to be applied rapidly in the field, and they use Velcro straps to secure the leg and abdominal chambers on a patient. MAST is most often used for rapid transport of patients with hypovolemia resulting from shock or trauma.

Blood pressure (BP) and cardiovascular hemodynamics were assessed at baseline and after caffeine administration in a 4-week, placebo-controlled, double-blind, randomized, crossover trial of caffeine tolerance formation. Half of the subjects developed tolerance to the pressor effect of caffeine, whereas the other half continued to show increases in BP after caffeine ingestion (F = 16.7, p

Endothelium-dependent vasodilation decreases in patients with congestive heart failure (CHF). Whether this decreased vasodilation occurs simultaneously in different vascular beds has not been elucidated. We studied the vasomotor reactivity in both coronary and peripheral resistance vessels in a rat CHF model produced by ligating the left coronary artery. Variations in vessel diameter in response to vasoactive drug administration were measured using an in vitro system of coronary resistance vessels from cardiac muscle and peripheral resistance vessels from cremaster muscle. Vascular responses to acetylcholine were impaired in the early stage of CHF (at 2 weeks), whereas the reaction to bradykinin was preserved. NG-monomethyl-L-arginine (L-NMMA) inhibited the responses of acetylcholine; however, L-NMMA only partially inhibited the responses to bradykinin. Vascular reactivity to A23187 was preserved in the early stage and was impaired in the late stage of CHF (at 8 weeks). These reactions were inhibited by L-NMMA. The response to sodium nitroprusside remained constant in both stages of CHF. The responses were similar in the coronary resistance and peripheral resistance vessels. This suggests that acetylcholine transmission is impaired in the early stages of CHF but that with CHF of longer duration there is progressive impairment of nitric oxide production and release in both coronary and peripheral resistance vessels.

Background: Peripheral resistance (R) is measured by flow (Q) and a pressure difference (P1-P2), where R equals (P1-P2)/Q. The pulsatility index (PI) has been used to assess peripheral vascular resistance by measuring flow velocities. Alternatively, PI can be expressed by the ratio of the flow volume amplitude and mean flow volume which both are quantified by a flowmeter. While reflected flow due to a distally located stenosis will considerably influence PI, this parameter theoretically could provide a good estimation of resistance. The appropriateness of this presumption has not been evaluated in this setting though, why the correlation of PI in flow recordings was examined by comparing PI with the true R using the stenosis of the internal carotid artery (ICA) as a clinical model. Methods: The volume flow in the ICA was measured by a transit-time flowmeter in 400 patients undergoing carotid endarteriectomy. The pressure in the common carotid artery (CCA) proximal to and in the ICA distal to the stenosis was determined by direct puncture allowing the calculation of a pressure gradient (PG) and R in analogy to Ohm’s law. R and PI were then correlated using Spearman’s correlation. Results: The blood flow in the ICA ranged from 2 to 478 ml/min with a median value of 165. The median PG was 14 mm Hg (0 to 88). Median R was 0.08 mm Hg × min / ml (0–26.5). PI varied between 0.8 and 114.1 with a mean of 1.9. Since a concentration of R and PI values in the lower ranges was observed, a logarithmic transformation was performed. Log PI showed only weak correlation to log R (r = 0.426, p < 0.0001). Conclusions: Log PI was intermediately correlated to log R in carotid artery stenosis, with a low discriminating power in the lower ranges due to the close distribution of measurements. Further studies are required to clarify the role of PI in hemodynamic questions and its general usefulness in other fields of vascular surgery like in peripheral bypass surgery.