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Victoria E. Claydon - One of the best experts on this subject based on the ideXlab platform.
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Evaluation of forearm vascular resistance during Orthostatic Stress: Velocity is proportional to flow and size doesn't matter.
PloS one, 2019Co-Authors: Victoria E. Claydon, Jonathan P. Moore, Ernest R. Greene, Otto Appenzeller, Roger HainsworthAbstract:The upright posture imposes a significant challenge to blood pressure regulation that is compensated through baroreflex-mediated increases in heart rate and vascular resistance. Orthostatic cardiac responses are easily inferred from heart rate, but vascular resistance responses are harder to elucidate. One approach is to determine vascular resistance as arterial pressure/blood flow, where blood flow is inferred from ultrasound-based measurements of brachial blood velocity. This relies on the as yet unvalidated assumption that brachial artery diameter does not change during Orthostatic Stress, and so velocity is proportional to flow. It is also unknown whether the Orthostatic vascular resistance response is related to initial blood vessel diameter. We determined beat-to-beat heart rate (ECG), blood pressure (Portapres) and vascular resistance (Doppler ultrasound) during a combined Orthostatic Stress test (head-upright tilting and lower body negative pressure) continued until presyncope. Participants were 16 men (aged 38.4±2.3 years) who lived permanently at high altitude (4450m). The supine brachial diameter ranged from 2.9-5.6mm. Brachial diameter did not change during Orthostatic Stress (supine: 4.19±0.2mm; tilt: 4.20±0.2mm; -20mmHg lower body negative pressure: 4.19±0.2mm, p = 0.811). There was no significant correlation between supine brachial artery diameter and the maximum vascular resistance response (r = 0.323; p = 0.29). Forearm vascular resistance responses evaluated using brachial arterial flow and velocity were strongly correlated (r = 0.989, p<0.00001) and demonstrated high equivalency with minimal bias (-6.34±24.4%). During severe Orthostatic Stress the diameter of the brachial artery remains constant, supporting use of brachial velocity for accurate continuous non-invasive Orthostatic vascular resistance responses. The magnitude of the Orthostatic forearm vascular resistance response was unrelated to the baseline brachial arterial diameter, suggesting that upstream vessel size does not matter in the ability to mount a vasoconstrictor response to orthostasis.
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evaluation of forearm vascular resistance during Orthostatic Stress velocity is proportional to flow and size doesn t matter
PLOS ONE, 2019Co-Authors: Victoria E. Claydon, Jonathan P. Moore, Ernest R. Greene, Otto Appenzeller, R HainsworthAbstract:Background The upright posture imposes a significant challenge to blood pressure regulation that is compensated through baroreflex-mediated increases in heart rate and vascular resistance. Orthostatic cardiac responses are easily inferred from heart rate, but vascular resistance responses are harder to elucidate. One approach is to determine vascular resistance as arterial pressure/blood flow, where blood flow is inferred from ultrasound-based measurements of brachial blood velocity. This relies on the as yet unvalidated assumption that brachial artery diameter does not change during Orthostatic Stress, and so velocity is proportional to flow. It is also unknown whether the Orthostatic vascular resistance response is related to initial blood vessel diameter. Methods We determined beat-to-beat heart rate (ECG), blood pressure (Portapres) and vascular resistance (Doppler ultrasound) during a combined Orthostatic Stress test (head-upright tilting and lower body negative pressure) continued until presyncope. Participants were 16 men (aged 38.4±2.3 years) who lived permanently at high altitude (4450m). Results The supine brachial diameter ranged from 2.9–5.6mm. Brachial diameter did not change during Orthostatic Stress (supine: 4.19±0.2mm; tilt: 4.20±0.2mm; -20mmHg lower body negative pressure: 4.19±0.2mm, p = 0.811). There was no significant correlation between supine brachial artery diameter and the maximum vascular resistance response (r = 0.323; p = 0.29). Forearm vascular resistance responses evaluated using brachial arterial flow and velocity were strongly correlated (r = 0.989, p<0.00001) and demonstrated high equivalency with minimal bias (-6.34±24.4%). Discussion During severe Orthostatic Stress the diameter of the brachial artery remains constant, supporting use of brachial velocity for accurate continuous non-invasive Orthostatic vascular resistance responses. The magnitude of the Orthostatic forearm vascular resistance response was unrelated to the baseline brachial arterial diameter, suggesting that upstream vessel size does not matter in the ability to mount a vasoconstrictor response to orthostasis.
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the effect of Orthostatic Stress type on cardiovascular control
Blood Pressure Monitoring, 2014Co-Authors: Brett H. Shaw, Thomas M. Loughin, Dawn C. Mackey, Stephen N. Robinovitch, Victoria E. ClaydonAbstract:OBJECTIVES We aimed to compare the cardiovascular responses of a novel Orthostatic Stress test, the passive seated Orthostatic Stress test (PSOST), with those during passive head-up tilt testing (HUTT). We hypothesized that cardiovascular responses during PSOST would be similar to those during HUTT (the 'gold standard'). METHODS We tested 15 healthy volunteers, who underwent both PSOST and HUTT during one session in a random order. We measured beat-to-beat blood pressure, heart rate, peripheral resistance, stroke volume, cardiac output, and middle cerebral artery blood flow velocity during each test. RESULTS Blood pressure responses were not significantly different between PSOST and HUTT, except for a significantly lower delayed nadir and 15-min recovery value in systolic arterial pressure during HUTT. HUTT elicited a significantly larger increase in heart rate during all test intervals in comparison with PSOST, as well as a larger decline in stroke volume during almost all test intervals. Responses for the other hemodynamic variables were not significantly different between the tests at any test interval. Repeated HUTT has large inherent variability, which was also evident from the variability in the mean differences on comparing PSOST and HUTT. There was a significant bias for larger heart rate increases (P<0.01) and a greater delayed systolic arterial pressure decline during HUTT. CONCLUSION We have shown that PSOST and HUTT elicit similar blood pressure and cerebrovascular responses in the early stages of the upright phase. We believe that PSOST is a reasonable surrogate for HUTT in assessing Orthostatic hypotension in population groups that are unable to stand for prolonged periods of time.
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The effect of Orthostatic Stress type on cardiovascular control.
Blood pressure monitoring, 2014Co-Authors: Brett H. Shaw, Thomas M. Loughin, Dawn C. Mackey, Stephen N. Robinovitch, Victoria E. ClaydonAbstract:We aimed to compare the cardiovascular responses of a novel Orthostatic Stress test, the passive seated Orthostatic Stress test (PSOST), with those during passive head-up tilt testing (HUTT). We hypothesized that cardiovascular responses during PSOST would be similar to those during HUTT (the 'gold standard'). We tested 15 healthy volunteers, who underwent both PSOST and HUTT during one session in a random order. We measured beat-to-beat blood pressure, heart rate, peripheral resistance, stroke volume, cardiac output, and middle cerebral artery blood flow velocity during each test. Blood pressure responses were not significantly different between PSOST and HUTT, except for a significantly lower delayed nadir and 15-min recovery value in systolic arterial pressure during HUTT. HUTT elicited a significantly larger increase in heart rate during all test intervals in comparison with PSOST, as well as a larger decline in stroke volume during almost all test intervals. Responses for the other hemodynamic variables were not significantly different between the tests at any test interval. Repeated HUTT has large inherent variability, which was also evident from the variability in the mean differences on comparing PSOST and HUTT. There was a significant bias for larger heart rate increases (P<0.01) and a greater delayed systolic arterial pressure decline during HUTT. We have shown that PSOST and HUTT elicit similar blood pressure and cerebrovascular responses in the early stages of the upright phase. We believe that PSOST is a reasonable surrogate for HUTT in assessing Orthostatic hypotension in population groups that are unable to stand for prolonged periods of time.
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cerebrovascular responses to Orthostatic Stress after spinal cord injury
Journal of Neurotrauma, 2012Co-Authors: Inderjeet S. Sahota, Henrike Rianne J C Ravensbergen, Maureen S Mcgrath, Victoria E. ClaydonAbstract:Abstract Orthostatic hypotension (OH) is a debilitating condition affecting individuals with spinal cord injury (SCI) that may be associated with cerebral hypoperfusion. We studied Orthostatic cerebral control in individuals with SCI with different levels and severities of injury to spinal cardiovascular autonomic pathways. We measured beat-to-beat cardiovascular and cerebrovascular responses to passive Orthostatic Stress in 16 controls and 26 subjects with chronic SCI. Cerebrovascular control was assessed from diastolic cerebral blood flow velocity (CBFVD), and indices of static and dynamic cerebral autoregulation. Severity of autonomic injury was inferred from spectral analyses of systolic arterial pressure, and supine plasma noradrenaline concentrations. Symptoms of OH were evaluated using questionnaires. CBFVD decreased during orthostasis only in individuals with autonomically complete injuries above T6. Orthostatic CBFVD was significantly correlated (p<0.05) with the severity of autonomic injury. Ind...
Benjamin D. Levine - One of the best experts on this subject based on the ideXlab platform.
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Cerebral hemodynamics during Orthostatic Stress assessed by nonlinear modeling.
Journal of applied physiology (Bethesda Md. : 1985), 2006Co-Authors: Georgios D. Mitsis, Rong Zhang, Benjamin D. Levine, Vasilis Z. MarmarelisAbstract:The effects of Orthostatic Stress, induced by lower body negative pressure (LBNP), on cerebral hemodynamics were examined in a nonlinear context. Spontaneous fluctuations of beat-to-beat mean arter...
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Effects of gender and hypovolemia on sympathetic neural responses to Orthostatic Stress.
American journal of physiology. Regulatory integrative and comparative physiology, 2005Co-Authors: Sarah Witkowski, Kazunobu Okazaki, Benjamin D. LevineAbstract:We tested the hypothesis that women have blunted sympathetic neural responses to Orthostatic Stress compared with men, which may be elicited under hypovolemic conditions. Muscle sympathetic nerve a...
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Deterioration of cerebral autoregulation during Orthostatic Stress: insights from the frequency domain
Journal of applied physiology (Bethesda Md. : 1985), 1998Co-Authors: Rong Zhang, Julie H. Zuckerman, Benjamin D. LevineAbstract:To determine whether dynamic cerebral autoregulation is impaired during Orthostatic Stress, cerebral blood flow (CBF) velocity in the middle cerebral artery (transcranial Doppler) and mean arterial...
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effects of head down tilt bed rest on cerebral hemodynamics during Orthostatic Stress
Journal of Applied Physiology, 1997Co-Authors: Rong Zhang, Julie H. Zuckerman, James A Pawelczyk, Benjamin D. LevineAbstract:Zhang, Rong, Julie H. Zuckerman, James A. Pawelczyk, and Benjamin D. Levine. Effects of head-down-tilt bed rest on cerebral hemodynamics during Orthostatic Stress. J. Appl. Physiol. 83(6): 2139–214...
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Effects of head-down-tilt bed rest on cerebral hemodynamics during Orthostatic Stress
Journal of applied physiology (Bethesda Md. : 1985), 1997Co-Authors: Rong Zhang, Julie H. Zuckerman, James A Pawelczyk, Benjamin D. LevineAbstract:Our aim was to determine whether the adaptation to simulated microgravity (microG) impairs regulation of cerebral blood flow (CBF) during Orthostatic Stress and contributes to Orthostatic intolerance. Twelve healthy subjects (aged 24 +/- 5 yr) underwent 2 wk of -6 degrees head-down-tilt (HDT) bed rest to simulate hemodynamic changes that occur when humans are exposed to microG. CBF velocity in the middle cerebral artery (transcranial Doppler), blood pressure, cardiac output (acetylene rebreathing), and forearm blood flow were measured at each level of a ramped protocol of lower body negative pressure (LBNP; -15, -30, and -40 mmHg x 5 min, -50 mmHg x 3 min, then -10 mmHg every 3 min to presyncope) before and after bed rest. Orthostatic tolerance was assessed by using the cumulative Stress index (CSI; mmHg x minutes) for the LBNP protocol. After bed rest, each individual's Orthostatic tolerance was reduced, with the group CSI decreased by 24% associated with greater decreases in cardiac output and greater increases in systemic vascular resistance at each level of LBNP. Before bed rest, mean CBF velocity decreased by 14, 10, and 45% at -40 mmHg, -50 mmHg, and maximal LBNP, respectively. After bed rest, mean velocity decreased by 16% at -30 mmHg and by 21, 35, and 39% at -40 mmHg, -50 mmHg, and maximal LBNP, respectively. Compared with pre-bed rest, post-bed-rest mean velocity was less by 11, 10, and 21% at -30, -40, and -50 mmHg, respectively. However, there was no significant difference at maximal LBNP. We conclude that cerebral autoregulation during Orthostatic Stress is impaired by adaptation to simulated microG as evidenced by an earlier and greater fall in CBF velocity during LBNP. We speculate that impairment of cerebral autoregulation may contribute to the reduced Orthostatic tolerance after bed rest.
Jason R Carter - One of the best experts on this subject based on the ideXlab platform.
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Influence of acute alcohol ingestion on sympathetic neural responses to Orthostatic Stress in humans
American journal of physiology. Endocrinology and metabolism, 2011Co-Authors: Jason R Carter, Sarah F. Stream, John J. Durocher, Robert A. LarsonAbstract:Acute alcohol consumption is reported to decrease mean arterial pressure (MAP) during Orthostatic challenge, a response that may contribute to alcohol-mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during Orthostatic Stress to help maintain MAP, yet the effects of alcohol on MSNA responses during Orthostatic Stress have not been determined. We hypothesized that alcohol ingestion would blunt arterial blood pressure and MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (-5, -10, -15, -20, -30, and -40 mmHg; 3 min/stage) in 30 subjects (age 24 ± 1 yr). After an initial progressive LBNP (pretreatment), subjects consumed either alcohol (0.8 g ethanol/kg body mass; n = 15) or placebo (n = 15), and progressive LBNP was repeated (posttreatment). Alcohol increased resting HR (59 ± 2 to 65 ± 2 beats/min, P < 0.05), MSNA (13 ± 3 to 19 ± 4 bursts/min, P < 0.05), and MSNA burst latency (1,313 ± 16 to 1,350 ± 17 ms, P < 0.05) compared with placebo (group × treatment interactions, P < 0.05). During progressive LBNP, a pronounced decrease in MAP was observed after alcohol but not placebo (group × time × treatment, P < 0.05). In contrast, MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. However, alcohol altered MSNA burst latency response to progressive LBNP. In conclusion, the lack of MSNA adjustment to a larger drop in arterial blood pressure during progressive LBNP, coupled with altered sympathetic burst latency responses, suggests that alcohol blunts MSNA responses to Orthostatic Stress.
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effects of oral contraceptives on sympathetic nerve activity during Orthostatic Stress in young healthy women
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2010Co-Authors: Jason R Carter, Jenna C Klein, Christopher E SchwartzAbstract:Recent studies report that the menstrual cycle alters sympathetic neural responses to Orthostatic Stress in young, eumenorrheic women. The purpose of the present study was to determine whether oral...
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Effects of oral contraceptives on sympathetic nerve activity during Orthostatic Stress in young, healthy women
American journal of physiology. Regulatory integrative and comparative physiology, 2009Co-Authors: Jason R Carter, Jenna C Klein, Christopher E SchwartzAbstract:Recent studies report that the menstrual cycle alters sympathetic neural responses to Orthostatic Stress in young, eumenorrheic women. The purpose of the present study was to determine whether oral contraceptives (OC) influence sympathetic neural activation during an Orthostatic challenge. Based on evidence that sympathetic baroreflex sensitivity (BRS) is increased during the "low hormone" (LH) phase (i.e., placebo pills) in women taking OC, we hypothesized an augmented muscle sympathetic nerve activity (MSNA) response to Orthostatic Stress during the LH phase. MSNA, mean arterial pressure (MAP), and heart rate (HR) were recorded during progressive lower body negative pressure (LBNP; -5, -10, -15, -20, -30, -40 mmHg; 3 min/stage) in 12 healthy women taking OC (age 22 +/- 1 years). Sympathetic BRS was assessed by examining relations between spontaneous fluctuations of diastolic arterial pressure and MSNA. Subjects were examined twice: once during LH phase and once approximately 3 wk after LH during the "high hormone" phase (randomized order). Resting MSNA (10 +/- 2 vs. 13 +/- 2 bursts/min), MAP (85 +/- 3 vs. 84 +/- 3 mmHg), and HR (62 +/- 2 vs. 65 +/- 3 beats/min) were not different between phases. MSNA and HR increased during progressive LBNP (P < 0.001), and these increases were similar between phases. Progressive LBNP did not change MAP during either phase. Sympathetic BRS increased during progressive LBNP, but these responses were not different between LH and high hormone phases. In conclusion, our results demonstrate that OCs do not alter cardiovascular and sympathetic neural responses to an Orthostatic challenge in young, healthy women.
Christopher E Schwartz - One of the best experts on this subject based on the ideXlab platform.
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effects of oral contraceptives on sympathetic nerve activity during Orthostatic Stress in young healthy women
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2010Co-Authors: Jason R Carter, Jenna C Klein, Christopher E SchwartzAbstract:Recent studies report that the menstrual cycle alters sympathetic neural responses to Orthostatic Stress in young, eumenorrheic women. The purpose of the present study was to determine whether oral...
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Effects of oral contraceptives on sympathetic nerve activity during Orthostatic Stress in young, healthy women
American journal of physiology. Regulatory integrative and comparative physiology, 2009Co-Authors: Jason R Carter, Jenna C Klein, Christopher E SchwartzAbstract:Recent studies report that the menstrual cycle alters sympathetic neural responses to Orthostatic Stress in young, eumenorrheic women. The purpose of the present study was to determine whether oral contraceptives (OC) influence sympathetic neural activation during an Orthostatic challenge. Based on evidence that sympathetic baroreflex sensitivity (BRS) is increased during the "low hormone" (LH) phase (i.e., placebo pills) in women taking OC, we hypothesized an augmented muscle sympathetic nerve activity (MSNA) response to Orthostatic Stress during the LH phase. MSNA, mean arterial pressure (MAP), and heart rate (HR) were recorded during progressive lower body negative pressure (LBNP; -5, -10, -15, -20, -30, -40 mmHg; 3 min/stage) in 12 healthy women taking OC (age 22 +/- 1 years). Sympathetic BRS was assessed by examining relations between spontaneous fluctuations of diastolic arterial pressure and MSNA. Subjects were examined twice: once during LH phase and once approximately 3 wk after LH during the "high hormone" phase (randomized order). Resting MSNA (10 +/- 2 vs. 13 +/- 2 bursts/min), MAP (85 +/- 3 vs. 84 +/- 3 mmHg), and HR (62 +/- 2 vs. 65 +/- 3 beats/min) were not different between phases. MSNA and HR increased during progressive LBNP (P < 0.001), and these increases were similar between phases. Progressive LBNP did not change MAP during either phase. Sympathetic BRS increased during progressive LBNP, but these responses were not different between LH and high hormone phases. In conclusion, our results demonstrate that OCs do not alter cardiovascular and sympathetic neural responses to an Orthostatic challenge in young, healthy women.
Roger Hainsworth - One of the best experts on this subject based on the ideXlab platform.
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Evaluation of forearm vascular resistance during Orthostatic Stress: Velocity is proportional to flow and size doesn't matter.
PloS one, 2019Co-Authors: Victoria E. Claydon, Jonathan P. Moore, Ernest R. Greene, Otto Appenzeller, Roger HainsworthAbstract:The upright posture imposes a significant challenge to blood pressure regulation that is compensated through baroreflex-mediated increases in heart rate and vascular resistance. Orthostatic cardiac responses are easily inferred from heart rate, but vascular resistance responses are harder to elucidate. One approach is to determine vascular resistance as arterial pressure/blood flow, where blood flow is inferred from ultrasound-based measurements of brachial blood velocity. This relies on the as yet unvalidated assumption that brachial artery diameter does not change during Orthostatic Stress, and so velocity is proportional to flow. It is also unknown whether the Orthostatic vascular resistance response is related to initial blood vessel diameter. We determined beat-to-beat heart rate (ECG), blood pressure (Portapres) and vascular resistance (Doppler ultrasound) during a combined Orthostatic Stress test (head-upright tilting and lower body negative pressure) continued until presyncope. Participants were 16 men (aged 38.4±2.3 years) who lived permanently at high altitude (4450m). The supine brachial diameter ranged from 2.9-5.6mm. Brachial diameter did not change during Orthostatic Stress (supine: 4.19±0.2mm; tilt: 4.20±0.2mm; -20mmHg lower body negative pressure: 4.19±0.2mm, p = 0.811). There was no significant correlation between supine brachial artery diameter and the maximum vascular resistance response (r = 0.323; p = 0.29). Forearm vascular resistance responses evaluated using brachial arterial flow and velocity were strongly correlated (r = 0.989, p<0.00001) and demonstrated high equivalency with minimal bias (-6.34±24.4%). During severe Orthostatic Stress the diameter of the brachial artery remains constant, supporting use of brachial velocity for accurate continuous non-invasive Orthostatic vascular resistance responses. The magnitude of the Orthostatic forearm vascular resistance response was unrelated to the baseline brachial arterial diameter, suggesting that upstream vessel size does not matter in the ability to mount a vasoconstrictor response to orthostasis.
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Cerebral autoregulation during Orthostatic Stress in healthy controls and in patients with posturally related syncope.
Clinical autonomic research : official journal of the Clinical Autonomic Research Society, 2003Co-Authors: Victoria E. Claydon, Roger HainsworthAbstract:Posturally related syncope (PRS) is a common and diStressing problem, which frequently occurs in people with no apparent clinical disorder and is ultimately caused by a reduction in blood supply to the brain. The aim of this study was to compare cerebrovascular responses to Orthostatic Stress in otherwise healthy patients suffering from PRS, and who were shown to have a poor Orthostatic tolerance (n=28), with those in healthy control subjects with good Orthostatic tolerance (n=11). Responses of heart rate, arterial blood pressure, end tidal carbon dioxide and middle cerebral artery (MCA) blood flow velocity were determined during a progressive Orthostatic Stress test of combined head-up tilting and lower body suction, which was continued until presyncope. We assessed the efficiency of autoregulation of cerebral blood flow from the relationship between values of MCA velocity and pressure obtained over the expected range for autoregulation (> 55mmHg). All patients with PRS had a significant correlation between MCA velocity and pressure, but this was seen in only two of the controls. Furthermore, the values of the correlation coefficients were significantly higher in patients than controls, (p
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Effects of head-up tilting on baroreceptor control in subjects with different tolerances to Orthostatic Stress.
Clinical science (London England : 1979), 2002Co-Authors: V. L. Cooper, Roger HainsworthAbstract:During Orthostatic Stress, an increase in peripheral vascular resistance normally results in arterial blood pressure being well maintained, despite a decrease in cardiac output. The present study was undertaken to determine whether the sensitivity of the carotid baroreceptor reflex was increased during Orthostatic Stress and whether failure to develop this increase was associated with poor Orthostatic tolerance. Three groups of subjects were studied: asymptomatic controls; patients investigated for suspected posturally related syncope but who had normal responses to an Orthostatic Stress test (normal patients); and patients who were shown to have low Orthostatic tolerance (early fainters). We determined responses of R-R interval and forearm vascular resistance (mean arterial pressure/brachial artery velocity by Doppler ultrasonography) to the loading and unloading of carotid baroreceptors by application of pressures of -30 and +30 mmHg to a chamber fitted over the neck. Responses were determined after 20 min of supine rest and after 10 min of head-up tilt at 60 degrees. Responses of cardiac interval were not significantly different between the three groups, and they were not altered by the postural change. Vascular responses also did not differ between the groups during supine rest. However, in healthy volunteers and in normal patients, responses to both neck suction and pressure were significantly enhanced during head-up tilt. In controls, responses to suction were increased by tilt from 0.04+/-0.1 to -1.01+/-0.2%.mmHg(-1) (means+/-S.E.M.; P
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Carotid baroreceptor reflexes in humans during Orthostatic Stress
Experimental physiology, 2001Co-Authors: V. L. Cooper, Roger HainsworthAbstract:Orthostatic Stress, including standing, head-up tilting and lower body suction, results in increases in peripheral vascular resistance but little or no change in mean arterial pressure. This study was undertaken to determine whether the sensitivity of the carotid baroreceptor reflex was enhanced during conditions of decreased venous return. We studied eight healthy subjects and determined responses of pulse interval (ECG) and forearm vascular resistance (mean finger blood pressure divided by Doppler estimate of brachial artery blood velocity) to graded increases and decreases in carotid transmural pressure, effected by a neck suction/pressure device. Responses were determined with and without the application of lower body negative pressure (LBNP) at -40 mmHg. Stimulus-response curves were determined as the responses to graded neck pressure changes and the differential of this provided estimates of reflex sensitivity. Changes in carotid transmural pressure caused graded changes in R-R interval and vascular resistance. The cardiac responses were unaffected by LBNP. Vascular resistance responses, however, were significantly enhanced during LBNP and the peak gain of the reflex was increased from 1.2 +/- 0.3 (mean +/- S.E.M.) to 2.2 +/- 0.3 units (P < 0.05). The increased baroreflex gain may contribute to maintenance of blood pressure during Orthostatic Stress and limit the pressure decreases during prolonged periods of such Stress.
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Vascular responses to Orthostatic Stress in patients with postural tachycardia syndrome (POTS), in patients with low Orthostatic tolerance, and in asymptomatic controls
Clinical Autonomic Research, 2000Co-Authors: Victoria E. Bush, Clive M. Brown, Victoria L. Wight, Roger HainsworthAbstract:Patients with postural tachycardia syndrome (POTS) are characterized by development of symptoms of Orthostatic intolerance during standing that are not because of hypotension but are associated with tachycardia. The goal of this study was to compare the cardiac and vascular responses to Orthostatic Stress for patients with POTS (n=8) with those for patients with low Orthostatic tolerance (n=29) and for healthy control subjects (n=12). Responses of heart rate (ECG), arterial blood pressure, and brachial artery blood velocity (Doppler) were determined during a progressive Orthostatic Stress test of head-up tilt and lower body suction. Changes in forearm vascular resistance (mean arterial pressure/brachial velocity) were less for patients with POTS than for healthy persons, and also less than for most of the patients with low Orthostatic tolerance. However, patients with POTS did not have a low tolerance to Orthostatic Stress (measured as time to discontinuation of the test). For the patients with POTS, the test was discontinued often because of symptoms associated with tachycardia but not hypotension, whereas for the other two groups, the test was discontinued because of hypotension. This study shows that for patients with POTS, abnormal sympathetic responses exist, with an increased sympathetic drive to the heart but deficient peripheral vascular responses, as measured in the forearm. This supports the hypothesis that patients with POTS may have a selective peripheral neuropathy, with small responses in some regions being compensated by overactivity in other regions.