What determines systemic blood flow in vertebrates?

In the 1950s, Arthur C. Guyton removed the heart from its pedestal in cardiovascular physiology by arguing that cardiac output is primarily regulated by the peripheral vasculature. This is counterintuitive, as modulating heart rate would appear to be the most obvious means of regulating cardiac output. In this Review, we visit recent and classic advances in comparative physiology in light of this concept. Although most vertebrates increase heart rate when oxygen demands rise (e.g. during activity or warming), experimental evidence suggests that this tachycardia is neither necessary nor sufficient to drive a change in cardiac output (i.e. systemic blood flow, Q̇sys) under most circumstances. Instead, Q̇sys is determined by the interplay between vascular conductance (resistance) and capacitance (which is mainly determined by the venous circulation), with a limited and variable contribution from heart function (myocardial inotropy). This pattern prevails across vertebrates; however, we also highlight the unique adaptations that have evolved in certain vertebrate groups to regulate venous return during diving bradycardia (i.e. inferior caval sphincters in diving mammals and atrial smooth muscle in turtles). Going forward, future investigation of cardiovascular responses to altered metabolic rate should pay equal consideration to the factors influencing venous return and cardiac filling as to the factors dictating cardiac function and heart rate.

Pulmonary arterial compliance is a useful predictor of pulmonary vascular disease in congenital heart disease.

Histopathological assessment of the pulmonary arteries is crucial to determine the surgical indications in patients with congenital heart disease (CHD) and intractable pulmonary vascular disease (PVD). We aimed to clarify whether pulmonary hemodynamic parameters can predict PVD in patients with CHD and pulmonary arterial hypertension (PAH) We performed histopathological evaluations of lung specimens and cardiac catheterizations in 27 patients with CHD-PAH. We divided these patients into the patients with and without PVD, and compared pulmonary hemodynamic parameters including pulmonary arterial compliance (Cp) between two groups. Age at lung biopsy was 4 (2-7) months. There were 16 patients with trisomy 21. Cardiac diagnosis included ventricular septal defect in 16, atrial septal defect in 5, atrioventricular septal defect in 4, and others in 2. There were 11 patients with histopathologically proven PVD (Heath-Edwards classification grade ≥ 3 in 5; the index of PVD ≥ 1.1 in 3; extremely thickened media in 6; hypoplasia of the pulmonary arteries in 3). Cp in the patients with PVD was significantly lower than that in patients without PVD (0.99 [0.74-1.42] vs 1.56 [1.45-1.88], p = 0.0047), although there was no significant difference in the ratio of systemic to pulmonary blood flow, pulmonary arterial pressure, and resistance between two groups. A Cp cutoff value of < 1.22 ml/mmHg m2 as a predictor of PVD yielded a sensitivity and a specificity of 93% and 64%, respectively. Pulmonary arterial compliance can be a predictor of PVD among patients with CHD-PAH.

Ethnic differences in stratum corneum functions between Chinese and Thai infants residing in Bangkok, Thailand.

BACKGROUND/OBJECTIVES: Ethnic and racial differences in infant skin have not been well characterized. The purpose of this study was to establish whether there are ethnic differences and similarities in the stratum corneum (SC) functions of Thai and Chinese infants. METHODS: Healthy infants 6 to 24 months of age (N = 60; 30 Thai, 30 Chinese) who resided in Bangkok, Thailand, were enrolled. Transepidermal water loss (TEWL) and SC hydration (capacitance) on the thigh, buttock, and upper arm were measured. Ceramide content was determined in the SC on the upper arm. RESULTS: SC hydration was not remarkably different between the two ethnicities at any site measured, but TEWL was significantly higher in Chinese infants than in Thai infants at all sites. Hydration of the SC was not significantly correlated with age in either ethnicity. TEWL had significant but weak correlations with age on the thigh and upper arm in Thai infants. Ceramide content was significantly higher in Chinese SC than in Thai SC. No relationship between ceramide content and TEWL or hydration was observed in either ethnicity. CONCLUSION: The significant differences in TEWL and ceramide contents between Chinese and Thai infant skin could prove useful in designing skin care and diapering products that are best suited for each ethnicity.

Altered cardiovascular function is related to reduced BDNF in Parkinson's disease.

Brain-derived neurotrophic factor (BDNF) has been linked to cardiovascular health and function, however, the exact role is yet to be understood. The current study examined the relationship of circulatory BDNF with vascular function in Parkinson's disease (PD). ELISA was used to determine plasma BDNF in PD patients and healthy control (CT). Additionally, forearm resting blood flow (RBf), vascular resistance (RVr), venous capacitance (RVc), and venous outflow (RVo) as well as post occlusion blood flow (OcBf), vascular resistance (OcVr), venous capacitance (OcVc), and venous outflow (OcVo) were obtained using strain-gauge plethysmography. Simple linear regression showed that being PD patient can predict (p < 0.05) 12.9% of BDNF, 16.8% of RVc, 15.0% of OcVc, and 13.6% of OcVo. Subsequent stepwise regression included BDNF, RVc, OcVc, and OcVo, showed that being PD patient predicted (p < 0.05) 58.0% of BDNF, 47.7% of OcVo, and 15.1% of OcVc. Another simple linear regression demonstrated that BDNF predicted (p < 0.05) 18.5% of OcBf, 22.0% of OcVr, and 24.1% of OcVc in PD. In a subsequent stepwise linear regression, BDNF explained 26% ofOcVr (p = 0.008) and 42% of OcVc (p = 0.002) in PD. The study showed that BDNF is reduced and related to altered vascular function in PD. The results suggest that BDNF might contribute to preserving and maybe improving vascular function in PD.

Abdominal Aortic Hemodynamics in Intermittent Claudication Patients at Rest and during Dynamic Pedaling Exercise.

BACKGROUND: Lower-extremity exercise has been shown to eliminate adverse hemodynamics conditions, such as low and oscillating blood flow and wall shear stress, in the abdominal aortas of healthy young and older adults. METHODS: We use cine phase-contrast magnetic resonance imaging and a custom MRI-compatible exercise cycle to quantify hemodynamic changes because of pedaling exercise in patients diagnosed with intermittent claudication. RESULTS: With only an average heart increase of 35 ± 18% and exercise workload of 36 ± 16 watts, the patients experienced approximately 3- and 6-fold increases in blood flow, and 4- and 16-fold increases in wall shear stress at the supraceliac and infrarenal aortic locations, respectively. Also, all oscillations in flow and shear stress at rest were eliminated with exercise. CONCLUSIONS: Claudication patients experience 3- to 4-fold lower oscillations in flow and shear stress at rest as compared with healthy age-matched controls, likely because of reduced distal arterial compliance as a result of distal atherosclerosis. The magnitude of flow and shear oscillatory indices may be good indicators of distal arterial compliance and health, and may provide predictive power for the efficacy of focal interventions.

Exercise ventilatory parameters for the diagnosis of reactive pulmonary hypertension in patients with heart failure.

BACKGROUND: Reactive pulmonary hypertension (PH) in left heart disease is associated with poor prognosis. This study aimed to evaluate the diagnostic utility of exercise ventilatory parameters on cardiopulmonary exercise testing for the diagnosis of reactive PH in patients with heart failure (HF) and reduced ejection fraction. METHODS: This was a single-center, retrospective analysis of a prospectively collected database of 131 patients with HF who underwent in-hospital assessment for heart transplantation. Pulmonary hemodynamics was assessed by direct cardiac catheterization. Minute ventilation/carbon dioxide production (VE/VCO2) slope, partial pressure of end-tidal carbon dioxide (ETCO2) changes on exercise, oxygen pulse, and exercise oscillatory ventilation were determined from cardiopulmonary exercise testing. RESULTS: Sixty-one of 131 consecutive patients had reactive PH. VE/VCO2 slope (>41), change in ETCO2 on exercise (<1.2 mm Hg) and exercise oscillatory ventilation were independently associated with reactive PH. These 3 parameters in combination produced 3 possible diagnostic scenarios: (1) if all 3 criteria ("if all") were present, (2) if any 2 of the 3 criteria ("2 of 3") were present, and (3) if any of the criteria ("if any") were present. The corresponding positive/negative likelihood ratios for reactive PH if all 3 criteria were present were 3.73/0.83, if 2 of the 3 criteria were present were 2.19/0.45, and if any of the 3 criteria were present were 1.75/0.11. The posttest probability increased from 46% to 76% ("if all" present) and reduced to 9% (if none of the criteria was present). CONCLUSION: Ventilatory parameters on cardiopulmonary exercise test are associated with reactive PH in patients with HF. The absence of abnormalities in these 3 ventilatory parameters can effectively exclude reactive PH in patients with HF and poor ejection fraction.

Chemohypersensitivity and autonomic modulation of venous capacitance in the pathophysiology of acute decompensated heart failure.

Heart failure is increasing in prevalence around the world, with hospitalization and re-hospitalization as a result of acute decompensated heart failure (ADHF) presenting a huge social and economic burden. The mechanism for this decompensation is not clear. Whilst in some cases it is due to volume expansion, over half of patients with an acute admission for ADHF did not experience an increase in total body weight. This calls into question the current treatment strategy of targeting salt and water retention in ADHF. An alternative hypothesis proposed by Fallick et al. is that an endogenous fluid shift from the splanchnic bed is implicated in ADHF, rather than an exogenous fluid gain. The hypothesis states further that this shift is triggered by an increase in sympathetic tone causing vasoconstriction in the splanchnic bed, a mechanism that can translocate blood rapidly into the effective circulating volume, generating the raised venous pressure and congestion seen in ADHF. This hypothesis encourages a new clinical paradigm which focuses on the underlying mechanisms of congestion, and highlights the importance of fluid redistribution and neurohormonal activation in its pathophysiology. In this article, we consider the concept that ADHF is attributable to episodic sympathetic hyperactivity, resulting in fluid shifts from the splanchnic bed. Chemosensitivity is a pathologic autonomic mechanism associated with mortality in patients with systolic heart failure. Tonic and episodic activity of the peripheral chemoreceptors may underlie the syndrome of acute decompensation without total body salt and water expansion. We suggest in this manuscript that chemosensitivity in response to intermittent hypoxia, such as experienced in sleep disordered breathing, may explain the intermittent sympathetic hyperactivity underlying renal sodium retention and acute volume redistribution from venous storage sites. This hypothesis provides an alternative structure to guide novel diagnostic and treatment strategies for ADHF.

The α2 isoform of the Na,K-pump is important for intercellular communication, agonist-induced contraction, and EDHF-like response in rat mesenteric arteries.

The specific role of different isoforms of the Na,K-pump in the vascular wall is still under debate. We have previously suggested that the α(2) isoform of the Na,K-pump (α(2)), Na(+), Ca(2+)-exchange (NCX), and connexin43 form a regulatory microdomain in smooth muscle cells (SMCs), which controls intercellular communication and contractile properties of the vascular wall. We have tested this hypothesis by downregulating α(2) in cultured SMCs and in small arteries with siRNA in vivo. Intercellular communication was assessed by using membrane capacitance measurements. Arteries transfected in vivo were tested for isometric and isobaric force development in vitro; [Ca(2+)](i) was measured simultaneously. Cultured rat SMCs were well-coupled electrically, but 10 µM ouabain uncoupled them. Downregulation of α(2) reduced electrical coupling between SMCs and made them insensitive to ouabain. Downregulation of α(2) in small arteries was accompanied with significant reduction in NCX expression. Acetylcholine-induced relaxation was not different between the groups, but the endothelium-dependent hyperpolarizing factor-like component of the response was significantly diminished in α(2)-downregulated arteries. Micromolar ouabain reduced in a concentration-dependent manner the amplitude of norepinephrine (NE)-induced vasomotion. Sixty percent of the α(2)-downregulated arteries did not have vasomotion, and vasomotion in the remaining 40% was ouabain insensitive. Although ouabain increased the sensitivity to NE in the control arteries, it had no effect on α(2)-downregulated arteries. In the presence of a low NE concentration the α(2)-downregulated arteries had higher [Ca(2+)](i) and tone. However, the NE EC50 was reduced under isometric conditions, and maximal contraction was reduced under isometric and isobaric conditions. The latter was caused by a reduced Ca(2+)-sensitivity. The α(2)-downregulated arteries also had reduced contraction to vasopressin, whereas the contractile response to high K(+) was not affected. Our results demonstrate the importance of α(2) for intercellular coupling in the vascular wall and its involvement in the regulation of vascular tone.

Congestive renal failure: the pathophysiology and treatment of renal venous hypertension.

Longstanding experimental evidence supports the role of renal venous hypertension in causing kidney dysfunction and "congestive renal failure." A focus has been heart failure, in which the cardiorenal syndrome may partly be due to high venous pressure, rather than traditional mechanisms involving low cardiac output. Analogous diseases are intra-abdominal hypertension and renal vein thrombosis. Proposed pathophysiologic mechanisms include reduced transglomerular pressure, elevated renal interstitial pressure, myogenic and neural reflexes, baroreceptor stimulation, activation of sympathetic nervous and renin angiotensin aldosterone systems, and enhanced proinflammatory pathways. Most clinical trials have addressed the underlying condition rather than venous hypertension per se. Interpreting the effects of therapeutic interventions on renal venous congestion are therefore problematic because of such confounders as changes in left ventricular function, cardiac output, and blood pressure. Nevertheless, there is preliminary evidence from small studies of intense medical therapy or extracorporeal ultrafiltration for heart failure that there can be changes to central venous pressure that correlate inversely with renal function, independently from the cardiac index. Larger more rigorous trials are needed to definitively establish under what circumstances conventional pharmacologic or ultrafiltration goals might best be directed toward central venous pressures rather than left ventricular or cardiac output parameters.

Using dynamic analysis of Laser-Doppler blood flowmetry to measure nasal mucosa bloody flow in postural changes.

BACKGROUND: The regulation of nasal mucosa blood flow (NMBF) is affected by multiple factors, such as the autonomic nervous system, medications, temperature, humidity, endocrine, even emotional stress and vision. The effects of postural changes on NMBF have been described in numerous studies. However, the results are far from consistent due to different experimental designs. OBJECTIVE: Dynamic analysis of Laser-Doppler blood flowmetry (LDBF) is employed to recognize the effect of postural changes on NMBF. METHODS: NMBF was continuously measured by LDBF in 14 participants with changing postures (sitting and supine). NMBF was measured in Blood Perfusion Unit (BPU), equivalent to the number of red blood cells multiplied by their mean velocity in a measured volume. RESULTS: NMBF increases significantly in a supine posture compared with that in a sitting posture. CONCLUSION: Our study demonstrates that NMBF is significantly influenced after initial postural change, suggesting that changes in posture may be regarded as an important factor regulating NMBF.

Prognostic Importance of Pulmonary Arterial Capacitance in Acute Decompensated Heart Failure With Preserved Ejection Fraction.

Background Although the prognostic importance of pulmonary arterial capacitance (PAC; stroke volume/pulmonary arterial pulse pressure) has been elucidated in heart failure with reduced ejection fraction, whether its significance in patients suffering from heart failure with preserved ejection fraction is not known. We aimed to examine the association of PAC with outcomes in inpatients with heart failure with preserved ejection fraction. Methods and Results We prospectively studied 705 patients (median age, 83 years; 55% women) registered in PURSUIT-HFpEF (Prospective Multicenter Observational Study of Patients With Heart Failure With Preserved Ejection Fraction). We investigated the association of echocardiographic PAC at discharge with the primary end point of all-cause death or heart failure rehospitalization with a mean follow-up of 384 days. We further tested the acceptability of the prognostic significance of PAC in a subgroup of patients (167/705 patients; median age, 81 years; 53% women) in whom PAC was assessed by right heart catheterization. The median echocardiographic PAC was 2.52 mL/mm Hg, with a quartile range of 1.78 to 3.32 mL/mm Hg. Univariable and multivariable Cox regression testing revealed that echocardiographic PAC was associated with the primary end point (unadjusted hazard ratio, 0.82; 95% CI, 0.72-0.92; P=0.001; adjusted hazard ratio, 0.86; 95% CI, 0.74-0.99; P=0.035, respectively). Univariable Cox regression testing revealed that PAC assessed by right heart catheterization (median calculated PAC, 2.82 mL/mm Hg) was also associated with the primary end point (unadjusted HR, 0.70; 95% CI, 0.52-0.91; P=0.005). Conclusions A prospective cohort study revealed that impaired PAC diagnosed with both echocardiography and right heart catheterization was associated with adverse outcomes in inpatients with heart failure with preserved ejection fraction. Registration URL: https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000024414. Unique identifier: UMIN000021831.

Cardiovascular disintegration: A conceptual, model-based approach to heart failure hemodynamics.

OBJECTIVE: The current understanding of heart failure (HF) largely centers round left ventricular (LV) function; however, disorders in serial integration of cardiovascular system may cause a hemodynamic picture similar to left-sided HF. Therefore, focusing only on LV function may be a limited and misleading approach. We hypothesized that cardiovascular system has four major integration points, and disintegration in any of these points may produce the hemodynamic picture of HF. METHODS: We used a computational model in which mechanical properties of each chamber were characterized using time-varying elastance, and vascular beds were modeled by series of capacitances and resistances. The required percent changes in stressed volume (Vstressed) was presented as a measure of congestion susceptibility. RESULTS: As mean systemic pressure is closely correlated with pulmonary capillary wedge pressure (PCWP), arteriovenous disintegration can create a diastolic dysfunction pattern, even without any change in diastolic function. For 10%, 20%, 30%, 40%, and 50% interventricular disintegration, required Vstressed for reaching a PCWP over 20 mmHg was decreased by 42.0%, 31.2%, 22.5%, 15%, and 8.3%, respectively. Systolodiastolic disintegration, namely combined changes in the end-diastolic and systolic pressure-volume curves and ventriculoarterial disintegration significantly decreases the required percent change in Vstressed for generating congestion. CONCLUSION: Four disintegration points can produce the hemodynamic picture of HF, which indicates that combination of even seemingly mild abnormalities is more important than an isolated abnormality in a single function of a single chamber. Our findings suggest that a "cardiovascular disintegration" perspective may provide a different approach for assessing the HF syndrome.

Extracardiac Abnormalities of Preload Reserve: Mechanisms Underlying Exercise Limitation in Heart Failure with Preserved Ejection Fraction, Autonomic Dysfunction, and Liver Disease.

While many of the cardiac limitations to exercise performance are now well-characterized, extracardiac limitations to exercise performance have been less well recognized but are nevertheless important. We propose that abnormalities of cardiac preload reserve represents an under-recognized but common cause of exercise limitations. We further propose that mechanistic links exist between conditions as seemingly disparate as heart failure with preserved ejection fraction, nonalcoholic fatty liver disease, and pelvic venous compression/obstruction syndromes (eg, May-Thurner). We conclude that extracardiac abnormalities of preload reserve serve as a major pathophysiologic mechanism underlying these and other disease states.

Retinal vascular caliber and brachial flow-mediated dilation: the Multi-Ethnic Study of Atherosclerosis.

BACKGROUND AND PURPOSE: Retinal vascular caliber changes have been shown to predict stroke, but the underlying mechanism of this association is unknown. We examined the relationship between retinal vascular caliber with brachial flow-mediated dilation (FMD), a measure of systemic endothelial function. METHODS: The Multi-Ethnic Study of Atherosclerosis (MESA) is a population-based study of persons 45 to 84 years of age residing in 6 US communities free of clinical cardiovascular disease at baseline. Brachial FMD data were collected at baseline (July 2000 to June 2002), and retinal vascular caliber was measured from digital retinal photographs at the second examination, immediately after the first (August 2002 to January 2004). Data were available for 2851 participants for analysis. RESULTS: The mean brachial FMD was 4.39+/-2.79%. After adjusting for age and gender, brachial FMD was reduced in persons with wider retinal venular caliber (changes in FMD -0.25, 95% CI, -0.36, - 0.13; P<0.001, per SD increase in venular caliber). This relationship persists after adjusting for systolic blood pressure, serum total cholesterol, use of lipid-lowering and antihypertensive medication, body mass index, current smoking status, and hemoglobinA(1C) (-0.18; 95% CI -0.30, - 0.06; P=0.004, per SD increase in venular caliber). Brachial FMD was not associated with retinal arteriolar caliber. CONCLUSIONS: Persons with wider retinal venules have reduced brachial FMD, independent of other vascular risk factors. This suggests that retinal venular caliber, previously shown to predict stroke, may be a marker of underlying systemic endothelial dysfunction.

WISE-2005: tibial and gastrocnemius vein and calf tissue response to LBNP after a 60-day bed rest with and without countermeasures.

The objective of this study was to quantify by echography the changes in the intramuscular [gastrocnemius (Gast)] and nonintramuscular [posterior tibial (Tib)] calf veins cross-sectional area (CSA) and the superficial tissue thickness (STth) in response to lower body negative pressure (LBNP) after 60-day head-down bed rest (HDBR). Twenty-four healthy women (25-40 yr) were divided into three groups: control (Con), treadmill-LBNP and flywheel (Ex-Lb), nutrition (Nut; protein supplement). All underwent a LBNP (0 and -45 mmHg) before and on day 55 of HDBR. Subjects were identified as finisher (F) or nonfinisher (NF) of a 10-min tilt test after 60 days of HDBR. There were no differences in resting CSA of the Tib and Gast veins on HDBR day 55 compared with pre-HDBR for the Ex-Lb, Con and Nut, or the F groups; however, for NF both the Tib and Gast vein CSA at rest were significantly smaller after HDBR. At -45 mmHg LBNP, Tib and Gast CSAs were not significantly different from before HDBR in all groups (Ex-Lb, Con, Nut, F, NF). However, percent change in CSA of both veins from rest to -45 mmHg LBNP was significantly greater in the Con and Nut groups compared with Ex-Lb, and also NF compared with F. Similarly, the percent increase in STth on going from rest to -45 mmHg was higher after HDBR in the Con and Nut groups compared with Ex-Lb, as well as NF compared with F. These results showed that the Ex-Lb countermeasure minimized the bed rest effect on leg vein capacitance (CSA percent change) and STth increase during LBNP, whereas Nut had no effect and that higher leg vein and superficial tissue capacitance were associated with reduced orthostatic tolerance.

Venous function and central venous pressure: a physiologic story.

The veins contain approximately 70% of total blood volume and are 30 times more compliant than arteries; therefore, changes in blood volume within the veins are associated with relatively small changes in venous pressure. The terms venous capacity, compliance, and stressed and unstressed volumes are defined. Decreases in flow into a vein are associated with decreases in intravenous pressure and volume, and vice versa. Changes in resistance in the small arteries and arterioles may affect venous return in opposite directions; this is explained by a two-compartment model: compliant (mainly splanchnic veins) and noncompliant (nonsplanchnic veins). Effects of intrathoracic and intraabdominal pressures on venous return and central venous pressure as well as the value of central venous pressure as a diagnostic variable are discussed.

Effect of 4 weeks of aerobic or resistance exercise training on arterial stiffness, blood flow and blood pressure in pre- and stage-1 hypertensives.

The benefits of aerobic exercise (AE) training on blood pressure (BP) and arterial stiffness are well established, but the effects of resistance training are less well delineated. The purpose of this study was to determine the impact of resistance vs aerobic training on haemodynamics and arterial stiffness. Thirty pre- or stage-1 essential hypertensives (20 men and 10 women), not on any medications, were recruited (age: 48.2 +/- 1.3 years) and randomly assigned to 4 weeks of either resistance (RE) or AE training. Before and after training, BP, arterial stiffness (pulse wave velocity (PWV)) and vasodilatory capacity (VC) were measured. Resting systolic BP (SBP) decreased following both training modes (SBP: RE, pre 136 +/- 2.9 vs. post 132 +/- 3.4; AE, pre 141 +/- 3.8 vs. post 136 +/- 3.4 mm Hg, P = 0.005; diastolic BP: RE, pre 78 +/- 1.3 vs post 74 +/- 1.6; AE, pre 80 +/- 1.6 vs. post 77 +/- 1.7 mm Hg, P = 0.001). Central PWV increased (P = 0.0001) following RE (11 +/- 0.9-12.7 +/- 0.9 ms(-1)) but decreased after AE (12.1 +/- 0.8-11.1 +/- 0.8 m s(-1). Peripheral PWV also increased (P = 0.013) following RE (RE, pre 11.5 +/- 0.8 vs. post 12.5 +/- 0.7 ms(-1)) and decreased after AE (AE, pre 12.6 +/- 0.8 vs post 11.6 +/- 0.7 m s(-1)). The VC area under the curve (VC(AUC)) increased more with RE than that with AE (RE, pre 76 +/- 8.0 vs. post 131.1 +/- 11.6; AE, pre 82.7 +/- 8.0 vs. post 110.1 +/- 11.6 ml per min per s per 100 ml, P = 0.001). Further, peak VC (VCpeak) increased more following resistance training compared to aerobic training (RE, pre 17 +/- 1.9 vs. post 25.8 +/- 2.1; AE, pre 19.2 +/- 8.4 vs post 22.9 +/- 8.4 ml per min per s per 100 ml, P = 0.005). Although both RE and AE training decreased BP, the change in pressure may be due to different mechanisms.

Physiological sleep-dependent changes in arterial blood pressure: central autonomic commands and baroreflex control.

Sleep is a heterogeneous behaviour. As a first approximation, it is subdivided objectively into two states: non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS). The mean value and variability of arterial blood pressure (ABP) decrease physiologically from wakefulness to NREMS. In REMS, there may be a further decrease or increase in mean ABP as well as phasic hypertensive events, which enhance the variability of ABP. The reduced mean ABP during NREMS results from a decrease in either heart rate or sympathetic vasoconstrictor tone. During REMS, sympathetic activity to the different cardiovascular effectors undergoes a substantial repatterning. Thus, the mean ABP in REMS reflects a balance between changes in cardiac output and constriction or dilatation of different vascular beds. In both sleep states, the phasic changes in ABP are driven by bursts of vasoconstriction, which may be accompanied by surges of heart rate. The available evidence supports the hypothesis that the sleep-dependent changes in ABP, either tonic or phasic, result from the integration between cardiovascular reflexes and central autonomic commands that are specific to each sleep state.

Evaluating middle cerebral artery collateral blood flow reserve using acetazolamide transcranial Doppler ultrasound in patients with carotid occlusive disease.

BACKGROUND: The objective of this study is to examine the utility of acetazolamide TCD ultrasound in the evaluation of MCA collateral blood flow reserve in patients with carotid occlusive disease. METHODS: Acetazolamide TCD and cerebral angiography were performed for 28 carotid territories in 14 patients with carotid occlusive disease. The percentage change in mean blood flow velocity and PI in the MCA was measured before and after 1 g of acetazolamide was administered. The carotid territories were divided into groups according their angiographic findings: (1) mild/moderate (<70%) vs severe (> or =70%) extracranial carotid artery stenosis, and (2) active collateral blood flow to the MCA territory vs no collateral blood flow to the MCA. RESULTS: After acetazolamide injection, the percentage increase in mean MCA velocity for mild/moderate vs severe carotid artery stenosis was 43% +/- 10% and 19% +/- 6%, respectively, indicating less collateral blood flow reserve in patients with severe stenosis (P = .04). The percentage decrease in the PI for MCA territories with vs without angiographic evidence of collateral blood flow was 4.6% +/- 4% and 16% +/- 3%, respectively (P = .04), indicating an exhausted vascular reserve in patients with evidence of active collateral blood flow on angiography. CONCLUSIONS: A decrease in the PI after acetazolamide administration represents a safe and noninvasive indicator of limited collateral blood flow reserve to the MCA territory ipsilateral to an extracranial carotid stenosis. Further study into the role acetazolamide TCD has in the preoperative evaluation of these patients, including threshold values, is warranted.

Relationship between parameters of air plethysmography and types of superficial venous reflux in patients with primary varicose veins.

AIM: We investigated whether parameters of air plethysmography (APG) were correlated with types of superficial venous reflux as categorized by ascending venography in patients with primary varicose veins. METHODS: Two hundred and eight limbs with primary varicose veins in 135 patients were evaluated by both APG and ascending venography. Venous hemodynamics was assessed with APG. The location of incompetent vein segments was determined based on the results of ascending venography. RESULTS: Seventy-seven limbs had incompetence of the greater saphenous vein (GSV, G group), 36 had incompetence of the lesser saphenous vein (LSV, L group), and 77 had incompetence of the GSV and LSV (GL group). Twenty-five limbs did not have incompetence of the GSV or LSV (N group). The venous filling index (VFI) differed significantly between the N and the G and GL groups, the L group and the G and GL groups, and the G and GL groups. No significant difference was found between the N and L groups. The venous volume, ejection fraction, and residual volume fraction did not differ significantly among all four groups. CONCLUSION: The VFI as measured by APG discriminates well between limbs with incompetence of the GSV and those without incompetence of the GSV or LSV, and between limbs with incompetence of the GSV and those with the LSV in patients with primary varicose veins, suggesting that the hemodynamic severity of superficial venous reflux progresses with involvement from the LSV to the GSV to both saphenous veins.