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Blood pressure (BP) decreases in the first weeks after Roux-and-Y gastric bypass surgery. Yet the pathophysiology of the BP-lowering effects observed after gastric bypass surgery is incompletely understood. We evaluated BP, systemic hemodynamics, and baroreflex sensitivity in 15 obese women[mean age 42 ± 7 standard deviation (SD) yr, body mass index 45 ± 6 kg/m 2 ] 2 wk before and 6 wk following Roux-and-Y gastric bypass surgery. Six weeks after gastric bypass surgery, mean body weight decreased by 13 ± 5 kg (10%, P < 0.001). Office BP decreased from 137 ± 10/86 ± 6 to 128 ± 12/81 ± 9 mmHg (P < 0.001, P < 0.01), while daytime ambulatory BP decreased from 128 ± 14/80 ± 9 to 114 ± 10/73 ± 6 mmHg (P = 0.01, P = 0.05), whereas nighttime BP decreased from 111 ± 13/66 ± 7 to 102 ± 9/62 ± 7 mmHg (P = 0.04, P < 0.01). The decrease in BP was associated with a 1.6 ± 1.2 l/min (20%, P < 0.01) decrease in cardiac output (CO), while systemic vascular resistance increased (153 ± 189 dyn·s·cm -5 , 15%, P < 0.01). The maximal ascending slope in systolic blood pressure decreased (192 mmHg/s, 19%, P = 0.01), suggesting a reduction in left ventricular contractility. Baroreflex sensitivity increased from 9.0 [6.4-14.3] to 13.8 [8.5-19.0] ms/mmHg (median [interquartile range]; P < 0.01) and was inversely correlated with the reductions in heart rate (R = -0.64, P = 0.02) and CO (R = -0.61, P = 0.03). In contrast, changes in body weight were not correlated with changes in either BP or CO. The BP reduction following Roux-and-Y gastric bypass surgery is correlated with a decrease in CO independent of changes in body weight. The contribution of heart rate to the reduction in CO together with enhanced baroreflex sensitivity suggests a shift toward increased parasympathetic cardiovascular control., New & Noteworthy: The reason for the decrease in blood pressure (BP) in the first weeks after gastric bypass surgery remains to be elucidated. We show that the reduction in BP following surgery is caused by a decrease in cardiac output. In addition, the maximal ascending slope in systolic blood pressure decreased suggesting a reduction in left ventricular contractility and cardiac workload. These findings help to understand the physiological changes following gastric bypass surgery and are relevant in light of the increased risk of heart failure in these patients., (Copyright © 2017 the American Physiological Society.)

In the upright position, cerebral blood flow is reduced, maybe because arterial carbon dioxide partial pressure (Pa(CO(2))) decreases. We evaluated the time-dependent influence of a reduction in Pa(CO(2)), as indicated by the end-tidal Pco(2) tension (Pet(CO(2))), on cerebral perfusion during head-up tilt. Mean arterial pressure, cardiac output, middle cerebral artery mean flow velocity (MCA V(mean)), and dynamic cerebral autoregulation at supine rest and 70 degrees head-up tilt were determined during free breathing and with Pet(CO(2)) clamped to the supine level. The postural changes in central hemodynamic variables were equivalent, and the cerebrovascular autoregulatory capacity was not significantly affected by tilt or by clamping Pet(CO(2)). In the first minute of tilt, the decline in MCA V(mean) (10 +/- 4 vs. 3 +/- 4 cm/s; mean +/- SE; P < 0.05) and Pet(CO(2)) (6.8 +/- 4.3 vs. 1.7 +/- 1.6 Torr; P < 0.05) was larger during spontaneous breathing than during isocapnic tilt. However, after 2 min in the head-up position, the reduction in MCA V(mean) was similar (7 +/- 5 vs. 6 +/- 3 cm/s), although the spontaneous decline in Pet(CO(2)) was maintained (P < 0.05 vs. isocapnic tilt). These results suggest that the potential contribution of Pa(CO(2)) to the postural reduction in MCA V(mean) is transient, leaving the mechanisms for the sustained restrain in MCA V(mean) to be identified.

Blood pressure (BP) responses to sodium intake show great variation, discriminating salt-sensitive (SS) from salt-resistant (SR) individuals. The pathophysiology behind salt sensitivity is still not fully elucidated. We aimed to investigate salt-induced effects on body fluid, vascular tone, and autonomic cardiac response with regard to BP change in healthy normotensive individuals. We performed a randomized crossover study in 51 normotensive individuals with normal body mass index and estimated glomerular filtration rate. Subjects followed both a low-Na+ diet (LSD, <50 mmol/day) and a high-Na+ diet (HSD, >200 mmol/day). Cardiac output, systemic vascular resistance (SVR), and cardiac autonomous activity, through heart rate variability and cross-correlation baroreflex sensitivity (xBRS), were assessed with noninvasive continuous finger BP measurements. In a subset, extracellular volume (ECV) was assessed by iohexol measurements. Subjects were characterized as SS if mean arterial pressure (MAP) increased ≥3 mmHg after HSD. After HSD, SS subjects (25%) showed a 6.1-mmHg (SD 1.9) increase in MAP. No differences between SS and SR in body weight, cardiac output, or ECV were found. SVR was positively correlated with Delta BP (r = 0.31, P = 0.03). xBRS and heart rate variability were significantly higher in SS participants compared to SR participants after both HSD and LSD. Sodium loading did not alter heart rate variability within groups. Salt sensitivity in normotensive individuals is associated with an inability to decrease SVR upon high salt intake that is accompanied by alterations in autonomous cardiac regulation, as reflected by decreased xBRS and heart rate variability. No discriminatory changes upon high salt were observed among salt-sensitive individuals in body weight and ECV. NEW & NOTEWORTHY Extracellular fluid expansion in normotensive individuals after salt loading is present in both salt-sensitive and salt-resistant individuals and is not discriminatory to the blood pressure response to sodium loading in a steady-state measurement. In normotensive subjects, the ability to sufficiently vasodilate seems to play a pivotal role in salt sensitivity. In a normotensive cohort, differences in sympathovagal balance are also present in low-salt conditions rather than being affected by salt loading. Whereas treatment and prevention of salt-sensitive blood pressure increase are mostly focused on renal sodium handling and extracellular volume regulation, our study suggests that an inability to adequately vasodilate and altered autonomous cardiac functioning are additional key players in the pathophysiology of salt-sensitive blood pressure increase. [ABSTRACT FROM AUTHOR]

Arterial pulse waves (PWs) such as blood pressure and photoplethysmogram (PPG) signals contain a wealth of information on the cardiovascular (CV) system that can be exploited to assess vascular age and identify individuals at elevated CV risk. We review the possibilities, limitations, complementarity, and differences of reduced-order, biophysical models of arterial PW propagation, as well as theoretical and empirical methods for analyzing PW signals and extracting clinically relevant information for vascular age assessment. We provide detailed mathematical derivations of these models and theoretical methods, showing how they are related to each other. Finally, we outline directions for future research to realize the potential of modeling and analysis of PW signals for accurate assessment of vascular age in both the clinic and in daily life. [ABSTRACT FROM AUTHOR]

The purpose of this study was to assess the effect of vestibular sympathetic activation on estimated measures of central (aortic) hemodynamic load in young adults. Thirty-one participants (n = 14 females and 17 males) underwent cardiovascular measures in the prone position with the head in a neutral position and during 10 min of head-down rotation (HDR), as a means of activating the vestibular sympathetic reflex. Radial pressure waveforms were acquired via applanation tonometry and, with the use of a generalized transfer function, used to synthesize an aortic pressure waveform. Popliteal vascular conductance was derived from diameter and flow velocity measured via Doppler-ultrasound. Subjective orthostatic intolerance was assessed using a 10-item orthostatic hypotension questionnaire. There was a reduction in brachial systolic blood pressure (BP) during HDR (111 ± 10 vs. 109 ± 9 mmHg, P < 0.05), but there was no change in aortic systolic BP (100 ± 9 vs. 99 ± 8 mmHg, P > 0.05). Aortic augmentation index (-5 ± 11 vs. -12 ± 12%, P < 0.05) and reservoir pressure (28 ± 8 vs. 26 ± 8 mmHg, P < 0.05) were reduced with a concomitant reduction in popliteal conductance (5.6 ± 0.7 vs. 4.5 ± 0.7 mL/min·mmHg, P < 0.05). Change in aortic systolic BP was associated with subjective orthostatic intolerance score (r = -0.39, P < 0.05). Activation of the vestibular sympathetic reflex via HDR resulted in slight reductions in brachial BP concomitant with preservation of aortic BP. Despite peripheral vascular constriction during HDR, there was a reduction in pressure from wave reflections and reservoir pressure. Finally, there was an association between change in aortic systolic BP during HDR and orthostatic intolerance score, suggesting that individuals who cannot defend against drops in aortic BP during vestibular sympathetic reflex activation may be more likely to experience higher subjective symptomatology of orthostatic intolerance. [ABSTRACT FROM AUTHOR]

Central aortic pressure waveforms contain valuable prognostic information in addition to central systolic pressure. Using pressure-flow relations, wave separation analysis can be used to decompose aortic pressure waveforms into forward-(Pf) and backward-traveling (Pb) components. Reflection magnitude, the ratio of pressure amplitudes (RM = Pb/Pf), is a predictor of heart failure and all-cause mortality. Aortic flow can be measured via Doppler echocardiography or estimated using a triangular flow waveform; however, the latter may underestimate the flow waveform convexity and overestimate Pb and RM. We sought to determine the accuracy of a personalized synthetic physiologic flow waveform, compared with triangular and measured flow waveforms, for estimating wave reflection indices in 49 healthy young (27 ± 6 yr) and 29 older adults [66 ± 6 yr; 20 healthy, 9 chronic kidney disease (CKD)]. Aortic pressure and measured flow waveforms were acquired via radial tonometry and echocardiography, respectively. Triangular and physiologic flow waveforms were constructed from aortic pressure waveforms. Compared with the measured flow waveform, the triangular waveform underestimated Pf in older, but not young, adults and overestimated Pb and RM in both groups. The physiologic waveform was equivalent to measured flow in deriving all wave reflection indices and yielded smaller mean absolute biases than the triangular waveform in all instances (P < 0.05). Lastly, central pulse pressure was associated with triangular, but not physiologic, mean biases for Pb and RM independent of age or central arterial stiffness (P < 0.05). These findings support the use of personalized physiologic flow waveforms as a more robust alternative to triangular flow waveforms when true flow cannot be measured. [ABSTRACT FROM AUTHOR]

Rapid-onset vasodilation (ROV) in response to a single muscle contraction is attenuated with aging. Moreover, sex-related differences in muscle blood flow and vasodilation during dynamic exercise have been observed in young and older adults. The purpose of the present study was to explore if sex-related differences in ROV exist in young (n =36, 25±1yr)and older (n = 32, 66 ± 1 yr) adults. Subjects performed single forearm contractions at 10%, 20%, and 40% maximal voluntary contraction. Brachial artery blood velocity and diameter were measured with Doppler ultrasound, and forearm vascular conductance (mL·min-1·100mmHg-1) was calculated from blood flow (mL·min-1) and mean arterial pressure (mmHg) and used as a measure of ROV. Peak ROV was attenuated in women across all relative intensities in the younger and older groups (P < 0.05). In a subset of subjects with similar absolute workloads (~5kg and ~11 kg), age-related differences in ROV were observed among both women and men (P < 0.05). However, only older women demonstrated an attenuated peak ROV compared with men (91 ± 6 vs. 121 ± 11 mL·min-1·100mmHg-1, P < 0.05), a difference not observed in the young group (134 ± 8 vs. 154 ± 11 mL·min-1·100mmHg-1, P = 0.15). Additionally, examining the slope of peak ROV across contraction intensities indicated a blunted response in older women compared with their younger counterparts (P < 0.05), with no differences observed between older and young men (P = 0.38). Our data suggest that sex-related differences in the rapid vasodilatory response to single muscle contractions exist in older but not young adults, such that older women have a blunted response compared with older men. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) accounts for a third of all deaths in the United States making it the leading cause of morbidity and mortality. Although CVD affects individuals of all races/ethnicities, the prevalence of CVD is highest in non-Hispanic black (BL) individuals relative to other populations. The mechanism(s) responsible for elevated CVD risk in the BL population remains incompletely understood. However, impaired vascular vasodilator capacity and exaggerated vascular vasoconstrictor responsiveness are likely contributing factors, both of which are present even in young, otherwise healthy BL individuals. Within this review, we highlight some historical and recent data, collected from our laboratories, of impaired vascular function, in terms of reduced vasodilator capacity and heightened vasoconstrictor responsiveness, in the peripheral and cerebral circulations in BL individuals. We provide data that such impairments may be related to elevated oxidative stress and subsequent reduction in nitric oxide bioavailability. In addition, divergent mechanisms of impaired vasodilatory capacity between BL men and women are discussed. Finally, we propose several directions where future research is needed to fill in knowledge gaps, which will allow for better understanding of the mechanisms contributing to impaired vascular function in this population. Ultimately, this information will allow for better lifestyle and therapeutic approaches to be implemented in an effort to minimize the increased CVD burden in the BL population. [ABSTRACT FROM AUTHOR]

Women generally display lower tolerance to acute central hypovolemia than men. The measurement of compensatory reserve (CRM) is a novel metric that provides information about the sum total of all mechanisms that together work to compensate for the relative blood volume deficit. Hemodynamic decompensation occurs with depletion of the CRM (i.e., 0% CRM). In the present study, we hypothesized that the lower tolerance to progressive central hypovolemia reported in women can be explained by a faster reduction rate in CRM compared with men rather than sex differences in absolute integrated compensatory responses. Continuous, noninvasive measures of CRM were collected from 208 healthy volunteers (107 men and 85 women) who underwent progressive stepwise central hypovolemia induced by lower body negative pressure to the point of presyncope. Comparisons revealed shorter (P < 0.01) times in female participants compared with male participants to reach 30% and 0% CRM. Similarly, the lower body negative pressure level, represented by the cumulative stress index, was less at 30% and 0% CRM in women compared with men (P < 0.01). Changes in hemodynamic responses and frequency-domain data (oscillations in cerebral blood flow velocity and mean arterial blood pressure) were similar between men and women at 0% CRM (P > 0.05). We conclude that compensatory responses to central hypovolemia in women were similar to men but were depleted at a faster rate compared with men. The earlier depletion of the compensatory reserve in women appears to be influenced by failure to maintain adequate cerebral oxygen delivery. [ABSTRACT FROM AUTHOR]

Endo-thelial dysfunction is observed in the peripheral vasculature of hypertensive patients, but it is unclear how the cerebral circulation is affected. More specifically, little is known about the impact of human hypertension on vertebral artery (VA) endothelial function. This study evaluated whether the endothelial function of the VA is impaired in hypertensive men. For 13 male hypertensive subjects (46 - 3 yr) and eight age-matched male controls (46 - 4 yr), blood pressure (BP; photoplethysmography), VA, and common carotid (CC) blood flow (duplex ultrasound) were determined at rest and during 30 min of intravenous L-arginine (30 g; a precursor of nitric oxide) or isotonic saline infusion. Controls and hypertensive subjects demonstrated a similar resting CC (601 - 30 vs. controls 570 - 43 ml/min; P - 0.529) and VA blood flow (119 - 11 vs. controls 112 - 9 ml/min; P - -0.878). During administration of L-arginine, CC blood flow increased similarly between groups (hypertensive 12 - 3%, controls 13 - 2%; P - 0.920). In contrast, the increase in VA blood flow was nonexistent in the hypertensive subjects (0.8 -3% vs. controls: 16 - 4%; P -0.015) with no significant change in BP. Both CC and VA flow returned to near-resting values within 30 min after the infusion, and for four hypertensive subjects and three controls, time-control experiments using 0.9% saline did not affect VA or CC blood flow significantly. The results demonstrate endothelial dysfunction in the posterior cerebral circulation of middle-aged hypertensive men. [ABSTRACT FROM AUTHOR]

Cardiac output (CO) assessment as a basic hemodynamic parameter has been of interest in exercise physiology, cardiology, and anesthesiology. Noninvasive techniques available are technically challenging, and thus difficult to use outside of a clinical or laboratory setting. We propose a novel method of noninvasive CO assessment using a single, upper-arm cuff. The method uses the arterial pressure pulse wave signal acquired from the brachial artery during 20-s intervals of suprasystolic occlusion. This method was evaluated in a cohort of 12 healthy individuals (age, 27.7 ± 5.4 yr, 50% men) and compared with an established method for noninvasive CO assessment, the open-circuit acetylene method (OpCirc) at rest, and during low- to moderate-intensity exercise. CO increased from rest to exercise (rest, 7.4 ± 0.8 vs. 7.2 ± 0.8; low, 9.8 ± 1.8 vs. 9.9 ± 2.0; moderate, 14.1 ± 2.8 vs. 14.8 ± 3.2 l/min) as assessed by the cuff-occlusion and OpCirc techniques, respectively. The average error of experimental technique compared with OpCirc was -0.25 ± 1.02 l/min, Pearson's correlation coefficient of 0.96 (rest + exercise), and 0.21 ± 0.42 l/min with Pearson's correlation coefficient of 0.87 (rest only). Bland-Altman analysis demonstrated good agreement between methods (within 95% boundaries); the reproducibility coefficient (RPC) = 0.84 l/min with R2 = 0.75 at rest and RPC = 2 l/min with R2 = 0.92 at rest and during exercise, respectively. In comparison with an established method to quantify CO, the cuff-occlusion method provides similar measures at rest and with light to moderate exercise. Thus, we believe this method has the potential to be used as a new, noninvasive method for assessing CO during exercise. [ABSTRACT FROM AUTHOR]

The hypothesis that cerebrovascular autoregulation was not impaired during head-up tilt (HUT) that followed brief exposures to varying degrees of prior head-down tilt (HDT) was tested in 10 healthy young men and women. Cerebral mean flow velocity (MFV) and cardiovascular responses were measured in transitions to a 60-s period of 75° HUT that followed supine rest (control) or 15 s HDT at -10°, -25°, and -55°. During HDT, heart rate (HR) was reduced for -25° and -55°, and cardiac output was lower at -55° HDT. MFV increased during -10° HDT, but not in the other conditions even though blood pressure at the middle cerebral artery (BPMCA) increased. On the transition to HUT, HR increased only for -55° condition, but stroke volume and cardiac output transiently increased for -25° and -55°. Total peripheral resistance index decreased in proportion to the magnitude of HDT and recovered over the first 20 s of HUT. MFV was significantly less in all HDT conditions compared with the control in the first 5-s period of HUT, but it recovered quickly. An autoregulation correction index derived from MFV recovery relative to BPMCA decline revealed a delay in the first 5 s for prior HDT compared with control but then a rapid increase to briefly exceed control after -55° HDT. This study showed that cerebrovascular autoregulation is modified by but not impaired by brief HDT prior to HUT and that cerebral MFV recovered quickly and more rapidly than arterial blood pressure to protect against cerebral hypoperfusion and potential syncope. [ABSTRACT FROM AUTHOR]

Skeletal muscle deoxygenated hemoglobin and myoglobin concentration ([HHb]), assessed by near-infrared spectroscopy (NIRS), is commonly used as a surrogate of regional O2 extraction (reflecting the O2 delivery-to-consumption ratio, .../...O2). However, [HHb] change Δ[HHb]) is also influenced by capillary-venous heme concentration, and/or small blood vessel volume (reflected in total heme; [THb]). We tested the hypotheses that Δ[HHb] is associated with O2 extraction, and insensitive to [THb], over a wide range of .../...O2 elicited by passive head-up tilt (HUT; 10-min, 15° increments, between -- 10c and 75°). Steady-state common femoral artery blood flow (FBF) was measured by echo-Doppler, and time-resolved NIRS measured [HHb] and [THb] of vastus lateralis (VL) and gastrocnemius (GS) in 13 men. EMG confirmed muscles were inactive. During HUT in VL [HHb] increased linearly (57 ± 10 to 101 ± 16 (µM; P < 0.05 above 15°) and was associated (r² ~ 0.80) with the reduction in FBF (618 ± 75 ml/min at 0° to 268 ± 52 ml/min at 75°; P < 0.05 above 30°) and the increase in [THb] (228 ± 30 vs. 252 ± 32 (µM; P < 0.05 above 15°). GS response was qualitatively similar to VL. However, there was wide variation within and among individuals, such that the overall limits of agreement between Δ [HHb] and AFBF ranged from -- 35 to +19% across both muscles. Neither knowledge of tissue O2 saturation nor vascular compliance could appropriately account for the Δ[HHb]- ΔFBF dissociation. Thus, under passive tilt, [HHb] is influenced by .../...O2, as well as microvascular hematocrit and/or tissue blood vessel volume, complicating its use as a noninvasive surrogate for muscle microvascular O2 extraction. [ABSTRACT FROM AUTHOR]

A cholinergic (muscarinic) contribution to the initial circulatory response to exercise in humans remains controversial. Herein, we posit that this may be due to exercise mode with a cholinergic contribution being important during isometric handgrip exercise, where the hyperemic response of the muscle is relatively small compared with the onset of leg cycling, where a marked increase in muscle blood flow rapidly occurs as a consequence of multiple redundant mechanisms. We recorded blood pressure (BP; brachial artery), stroke volume (pulse contour analysis), cardiac output, and systemic vascular resistance (SVR) in young healthy males, while performing either 20 s of isometric handgrip contraction at 40% maximum voluntary contraction (protocol 1; n = 9) or 20 s of low-intensity leg cycling exercise (protocol 2; n = 8, 42 ± 8 W). Exercise trials were conducted under control (no drug) conditions and following cholinergic blockade (glycopyrrolate). Under control conditions, isometric handgrip elicited an initial increase in BP (+5 ± 2 mmHg at 3 s and +3 ± 1 mmHg at 10 s, P < 0.05), while SVR dropped after 3 s (-27 ± 6% at 20 s; P < 0.05). Cholinergic blockade abolished the isometric handgrip-induced fall in SVR and, thereby, augmented the pressor response (+13 ± 3 mmHg at 10 s; P < 0.05 vs. control). In contrast, cholinergic blockade had a nonsignificant effect on changes in BP and SVR at the onset of leg cycling exercise. These findings suggest that a cholinergic mechanism is important for the BP and SVR responses at the onset of isometric handgrip exercise in humans. [ABSTRACT FROM AUTHOR]

Rapid-onset vasodilation (ROV) following single muscle contractions has been examined in the forearm of humans, but has not yet been characterized in the leg. Given known vascular differences between the arm and leg, we sought to characterize ROV following single muscle contractions in the leg. Sixteen healthy men performed random ordered single contractions at 5, 10, 20, 40, and 60% of their maximum voluntary contraction (MVC) using isometric knee extension made with the leg above and below heart level, and these were compared with single isometric contractions of the forearm (handgrip). Single thigh cuff compressions (300 mmHg) were utilized to estimate the mechanical contribution to leg ROV. Continuous blood flow was determined by duplex-Doppler ultrasound and blood pressure via finger photoplethysmography (Finometer). Single isometric knee extensor contractions produced intensity-dependent increases in peak leg vascular conductance that were significantly greater than the forearm in both the above- and below-heart level positions (e.g., above heart level: leg 20% MVC, +138 ± 28% vs. arm 20% MVC, +89 ± 17%; P < 0.05). Thigh cuff compressions also produced a significant hyperemic response, but these were brief and smaller in magnitude compared with single isometric contractions in the leg. Collectively, these data demonstrate the presence of a rapid and robust vasodilation to single muscle contractions in the leg that is largely independent of mechanical factors, thus establishing the leg as a viable model to study ROV in humans. [ABSTRACT FROM AUTHOR]

In the evaluation of cerebrovascular CO2 reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO2 partial pressure. However, the strong cerebral vasodilatory capacity of CO2 challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO2 on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21–30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, -1 kPa (-7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal PCO2 (PETCO2) above baseline. However, no significant changes in diameter were observed at the -1 kPa (-1.2 ± 2.4%), and +1 kPa 9+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant PETCO2 measurements. In conclusion, the MCA diameter remains constant during small deviations of the PETCO2 from normocapnia, but increases at higher PETCO2 values. [ABSTRACT FROM AUTHOR]

This review summarizes evidence in humans for an association between hyperventilation (HV)-induced hypocapnia and a reduction in cerebral perfusion leading to syncope defined as transient loss of consciousness (TLOC). The cerebral vasculature is sensitive to changes in both the arterial carbon dioxide (Paco2) and oxygen (Paco2) partial pressures so that hypercapnia/hypoxia increases and hypocapnia/hyperoxia reduces global cerebral blood flow. Cerebral hypoperfusion and TLOC have been associated with hypocapnia related to HV. Notwithstanding pronounced cerebrovascular effects of Paco2, the contribution of a low Paco2, to the early postural reduction in middle cerebral artery blood velocity is transient. HV together with postural stress does not reduce cerebral perfusion to such an extent that TLOC develops. However when HV is combined with cardiovascular stressors like cold immersion or reduced cardiac output brain perfusion becomes jeopardized. Whether, in patients with cardiovascular disease and/or defect, cerebral blood flow cerebral control HV-induced hypocapnia elicits cerebral hypoperfusion, leading to TLOC, remains to be established. [ABSTRACT FROM AUTHOR]

The ventricular response to passive heat stress has predominantly been studied in the supine position. It is presently unclear how acute changes in venous return influence ventricular function during heat stress. To address this question, left ventricular (LV) systolic and diastolic function were studied in 17 healthy men (24.3 ± 4.0 yr; mean ± SD), using two-dimensional transthoracic echocardiography with Doppler ultrasound, during tilt-table positioning (supine, 30° head-up tilt, and 30° head-down tilt), under normothermic and passive heat stress (core temperature 0.8 ± 0.1°C above baseline) conditions. The supine heat stress LV volumetric and functional response was consistent with previous reports. Combining head-up tilt with heat stress reduced end-diastolic (25.2 ± 4.1%) and end-systolic (65.4 ± 10.5%) volume from baseline, whereas heart rate (37.7 ± 2.0%), ejection fraction (9.4 ± 2.4%), and LV elastance (37.7 ± 3.6%) increased, and stroke volume (-28.6 ± 9.4%) and early diastolic inflow (-17.5 ± 6.5%) and annular tissue (-35.6 ± 7.0%) velocities were reduced. Combining head-down tilt with heat stress restored end-diastolic volume, whereas LV elastance (16.8 ± 3.2%), ejection fraction (7.2 ± 2.1%), and systolic annular tissue velocities (22.4 ± 5.0%) remained elevated above baseline, and end-systolic volume was reduced (-15.3 ± 3.9%). Stroke volume and the early and late diastolic inflow and annular tissue velocities were unchanged from baseline. This investigation extends previous work by demonstrating increased LV systolic function with heat stress, under varied levels of venous return, and highlights the preload dependency of early diastolic function during passive heat stress. [ABSTRACT FROM AUTHOR]

End-tidal carbon dioxide tension (PETCO2) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on PETCO2 being an accurate surrogate for arterial carbon dioxide tension (PaCO2), the latter being the physiologically relevant variable. This study tested the hypothesis that PETCO2 provides an accurate assessment of PaCO2 during the aforementioned conditions. Comparisons between these measures were made: 1) after two levels of heat stress (N = 11); 2) during combined heat stress and simulated hemorrhage [via lower-body negative pressure (LBNP), N = 8]; and 3) during an end-tidal clamping protocol to attenuate heat stress-induced reductions in PETCO2 (N = 7). PETCO2 and PaCO2 decreased during heat stress (P < 0.001); however, there was no group difference between PaCO2 and PETCO2 (P = 0.36) nor was there a significant interaction between thermal condition and measurement technique (P = 0.06). To verify that this nonsignificant trend for the interaction was not due to a type II error, PETCO2 and PaCO2 at three distinct thermal conditions were also compared using paired t-tests, revealing no difference between PaCO2 and PETCO2 while normothermic (P = 0.14) and following a 1.0 ± 0.2°C (P = 0.21) and 1.4 ± 0.2°C (P = 0.28) increase in internal temperature. During LBNP while heat stressed, measures of PETCO2 and PaCO2 were similar (P = 0.61). Likewise, during the end-tidal carbon dioxide clamping protocol, the increases in PETCO2 (7.5 ± 2.8 mmHg) and PaCO2 (6.6 ± 3.4 mmHg) were similar (P = 0.31). These data indicate that mean PETCO2 reflects mean PaCO2 during the evaluated conditions. [ABSTRACT FROM AUTHOR]

Cerebral autoregulation adjusts cerebrovascular resistance in the face of changing perfusion pressures to maintain relatively constant flow. Results from several studies suggest that cardiac output may also play a role. We tested the hypothesis that cerebral blood flow would autoregulate independent of changes in cardiac output. Transient systemic hypotension was induced by thigh-cuff deflation in 19 healthy volunteers (7 women) in both supine and seated positions. Mean arterial pressure (Finapres), cerebral blood flow (transcranial Doppler) in the anterior (ACA) and middle cerebral artery (MCA), beat-by-beat cardiac output (echocardiography), and end-tidal PCO2 were measured. Autoregulation was assessed using the autoregulatory index (ARI) defined by Tiecks et al. (Tiecks FP, Lam AM, Aaslid R, Newell DW. Stroke 26: 1014-1019, 1995). Cerebral autoregulation was better in the supine position in both the ACA [supine ARI: 5.0 ± 0.21 (mean ± SE), seated ARI: 3.9 ± 0.4, P = 0.01] and MCA (supine ARI: 5.0 ± 0.2, seated ARI: 3.8 ± 0.3, P = 0.004). In contrast, cardiac output responses were not different between positions and did not correlate with cerebral blood flow ARIs. In addition, women had better autoregulation in the ACA (P = 0.046), but not the MCA, despite having the same cardiac output response. These data demonstrate cardiac output does not appear to affect the dynamic cerebral autoregulatory response to sudden hypotension in healthy controls, regardless of posture. These results also highlight the importance of considering sex when studying cerebral autoregulation. [ABSTRACT FROM AUTHOR]

This study sought to test the hypothesis that orthostasis-induced cerebral hypoperfusion would be less severe in physically active elderly humans (ACT group) than in sedentary elderly humans (SED group). The peak O2 uptake of 10 SED (67.1 ± 1.4 yr) and 9 ACT (68.0 ± 1.1 yr) volunteers was determined by a graded cycling exercise test (22.1 ± 1.2 vs 35.8 ± 1.3 ml∙min-1∙kg-1, P <0.01). Baseline mean arterial pressure (MAP; tonometry) and middle cerebral arterial blood flow velocity (yMCA; transcranial Doppler) were similar between the groups (SED vs. ACT group: 91 ± 3 vs. 87 ± 3 mmHg and 54.9 ± 2.3 vs. 57.8 ± 3.2 cmls, respectively), whereas heart rate was higher and stroke volume (bio-impedance) was smaller m the SED group than in the ACT group. Central hypovolemia during graded lower body negative pressure (LBNP) was larger (P < 0.01) in the ACT group than in the SED group. However, the slope of VMCA/LBNP was smaller (P < 0.05) in the ACT group (0.159 ± 0.016 cm/s/Ton) than in the SED group (0.211 ± 0.008 cmls/Torr). During LBNP, the SED group had a greater augmentation of cerebral vasomotor tone (P < 0.05) and hypocapnia (P < 0.001) compared with the ACT group. Baseline MAP variability and VMCA variability were significantly smaller in the SED group than in the ACT group, i.e., 0.49 ± 0.07 vs. 1.04 ± 0.16 (mmHg)2 and 1.06 ± 0.19 vs. 4.24 ± 1.59 (cm/s)2, respectively. However, transfer function gain, coherence, and phase between MAP and VMCA signals (Welch spectral estimator) from 0.08-0.18 Hz were not different between SED (1.41 ± 0.18 cm∙s-1∙mmHg-1, 0.63 ± 0.06 units, and 38.03 ± 6.57°) and ACT (1.65 ± 0.44 cm∙s-1∙mmHg-1, 0.56 ± 0.05 units, and 48.55 ± 11.84°) groups. We conclude that a physically active lifestyle improves the intrinsic mechanism of cerebral autoregulation and helps mitigate cerebral hypoperfusion during central hypovolemia in healthy elderly adults. [ABSTRACT FROM AUTHOR]

The article offers information on methods for estimation of mean systemic filling pressure. Topics discussed include distribution of blood volume that determines cardiac performance, at the level of the filling side of the heart; testing of cardiovascular reserve which involve the manipulation of central blood volume; and mentions hemodynamic management for contemplate both the homeostatic and hemodynamic aspects of blood volume.