Reflex Responses of Venous Capacitance Vessels in Patients with Hypertrophic Cardiomyopathy

1998 ◽  
Vol 94 (4) ◽  
pp. 339-346 ◽  
Author(s):  
Helen L. Thomson ◽  
Jayne Morris-Thurgood ◽  
John Atherton ◽  
William J McKenna ◽  
Michael P. Frenneaux
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Percentage Reduction ◽  
Lower Body ◽  
Venous Capacitance ◽  
History Of ◽  
Venous Volume ◽  
Exercise Induced ◽  
Blood Pressure Responses

1. The aim of this study was to determine if there is impaired reflex venoconstriction in patients with hypertrophic cardiomyopathy and whether this is related to a history of syncope or exercise hypotension. 2. Thirty percent of patients with hypertrophic cardiomyopathy have exercise-induced hypotension associated with a failure of arteriolar constriction. Impaired venoconstriction could exacerbate this situation. 3. We evaluated 43 patients with hypertrophic cardiomyopathy and 24 controls. Nuclear venous plethysmography was used to measure forearm venous capacitance during lower body negative pressure, splenic venous volume changes during bicycle exercise and blood pressure responses to treadmill exercise. We assessed any association between abnormal reflex venous control and a history of syncope and exercise hypotension. 4. The percentage reduction in unstressed forearm venous volume during lower body negative pressure was similar in patients and controls (8.9 ± 7.1% versus 9.7 ± 5.9%, P not significant). Patients with a history of syncope demonstrated a less marked percentage reduction in volume than those without (−2.1 ± 6.9% versus −10.6 ± 6.0%, P = 0.001). In three patients with a history of syncope there was a paradoxical increase in forearm venous volume during lower body negative pressure. During exercise there was a substantially smaller decrease in splenic venous volume in patients compared with controls (−20.1 ± 14.0% and −42.6 ± 12.6% respectively, P = 0.0001). Furthermore, there was an association between attenuated splenic venoconstriction or venodilation and exercise hypotension in patients (P = 0.005). 5. Abnormal reflex control of venous capacitance beds in patients with hypertrophic cardiomyopathy was associated with both syncope and exercise hypotension.

Effect of temperature and baroreceptor stimulation on reflex venomotor responses

1984 ◽  
Vol 57 (5) ◽  
pp. 1384-1392 ◽  
Author(s):  
A. Tripathi ◽  
X. Shi ◽  
C. B. Wenger ◽  
E. R. Nadel
Keyword(s):  
Heart Rate ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Effect Of Temperature ◽  
Lower Body ◽  
Venous Capacitance ◽  
Ambient Temperatures ◽  
Wide Range ◽  
Baroreceptor Stimulation ◽  
Venous Volume

To investigate the interaction of thermal reflexes and baroreflexes in the control of the peripheral veins, we studied in supine humans the effects of lower body negative pressure (LBNP) and neck suction (NS) on forearm veins at ambient temperatures (Ta) of 18, 28, and 37 degrees C. Forearm venous volume (FVV)-venous pressure (FVP) relations (forearm venous capacitance) on six subjects showed an increase from 18 through 28 to 37 degrees C (P less than 0.001). Heart rate increased (P less than 0.001) and forearm venous capacitance decreased (P less than 0.001) in proportion to the level of LBNP applied from 20 to 50 Torr at all Ta. At 50 Torr LBNP, FVV at 30 cmH2O, FVP decreased from control values of 2.5, 3.8, and 4.4 to 1.6, 2.7, and 3.4 ml/100 ml at 18, 28, and 37 degrees C, respectively. We also studied venomotor responses using the occluded limb technique. Although LBNP caused venoconstriction, NS applied either alone or during LBNP produced no change in venomotor tone. Therefore we concluded that carotid baroreceptors play little role in reflex venomotor adjustments. Since changes in mean arterial and pulse pressures during LBNP did not account for the observed venomotor responses, we concluded that low-pressure baroreceptors initiate significant venoconstrictor reflexes over a wide range of Ta.

scholarly journals Impact of environmental stressors on tolerance to hemorrhage in humans

2019 ◽  
Vol 316 (2) ◽  
pp. R88-R100 ◽  
Author(s):  
Craig G. Crandall ◽  
Caroline A. Rickards ◽  
Blair D. Johnson
Keyword(s):  
Heat Stress ◽  
Blood Loss ◽  
Cause Of Death ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Environmental Stressors ◽  
Lower Body ◽  
Physiological Conditions ◽  
Exercise Induced ◽  
The Impact

Hemorrhage is a leading cause of death in military and civilian settings, and ~85% of potentially survivable battlefield deaths are hemorrhage-related. Soldiers and civilians are exposed to a number of environmental and physiological conditions that have the potential to alter tolerance to a hemorrhagic insult. The objective of this review is to summarize the known impact of commonly encountered environmental and physiological conditions on tolerance to hemorrhagic insult, primarily in humans. The majority of the studies used lower body negative pressure (LBNP) to simulate a hemorrhagic insult, although some studies employed incremental blood withdrawal. This review addresses, first, the use of LBNP as a model of hemorrhage-induced central hypovolemia and, then, the effects of the following conditions on tolerance to LBNP: passive and exercise-induced heat stress with and without hypohydration/dehydration, exposure to hypothermia, and exposure to altitude/hypoxia. An understanding of the effects of these environmental and physiological conditions on responses to a hemorrhagic challenge, including tolerance, can enable development and implementation of targeted strategies and interventions to reduce the impact of such conditions on tolerance to a hemorrhagic insult and, ultimately, improve survival from blood loss injuries.

Cardiovascular Responses to Maximal Graded and Acute Lower Body Negative Pressure

2010 ◽  
Vol 18 (1) ◽  
pp. 27-42 ◽  
Author(s):  
Juliane P. Hernandez ◽  
Kristin Roever ◽  
Tonya Seed
Keyword(s):  
Heart Rate ◽  
Negative Pressure ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Responses ◽  
Tolerance Index ◽  
Lower Body ◽  
Age Related ◽  
Per Se ◽  
Blood Pressure Responses

This investigation attempted to determine whether heart-rate and blood pressure responses to maximal acute lower body negative pressure (LBNP) are exacerbated compared with maximal graded LBNP in active older (n= 9, 70 ± 7 yr) and endurance-trained younger (n= 10, 23 ± 3 yr) individuals. Heart rate increased earlier during graded LBNP in the younger group (−40 mm Hg vs. tolerance) and was significantly higher than that of the older adults at the point of tolerance. Mean arterial pressure (MAP) decreased more in the older than the younger individuals during graded LBNP. LBNP-tolerance index was significantly greater in the younger group (309 ± 52 vs. 255.6 ± 48 mm Hg/min). Acute doses of LBNP elicited slower heart-rate responses in the older group. Despite these age-related differences, MAP responses were not different between groups with acute LBNP, so age per se does not appear to predispose individuals to orthostatic intolerance.

Neurohormonal responses to oscillatory lower body negative pressure in healthy subjects

2021 ◽  
Author(s):  
Akanksha Singh ◽  
Shival Srivastav ◽  
Kavita Yadav ◽  
Dinu S. Chandran ◽  
Ashok Kumar Jaryal ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Lower Body

Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

1990 ◽  
Vol 78 (4) ◽  
pp. 399-401 ◽  
Author(s):  
M. J. Cullen ◽  
J. R. Cockcroft ◽  
D. J. Webb
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Negative Pressure ◽  
Enzyme Inhibitor ◽  
Lower Body Negative Pressure ◽  
Acute Effect ◽  
Acute Administration ◽  
Lower Body ◽  
Resistance Vessels ◽  
Sympathetic Responses

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

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