VASOCONSTRICTOR RESPONSE TO LOWER BODY NEGATIVE PRESSURE DURING AUTONCMIC BLOCKADE

1986 ◽  
Vol 18 (supplement) ◽  
pp. S15
Author(s):  
H. L. Smith ◽  
D. L. Hudson ◽  
H. M. Graitzer ◽  
P. B. Raven
2010 ◽  
Vol 109 (4) ◽  
pp. 996-1001 ◽  
Author(s):  
T. Hachiya ◽  
M. L. Walsh ◽  
M. Saito ◽  
A. P. Blaber

Central blood volume loss to venous pooling in the lower extremities and vasoconstrictor response are commonly viewed as key factors to distinguish between individuals with high and low tolerance to orthostatic stress. In this study, we analyzed calf vasoconstriction as a function of venous pooling during simulated orthostatic stress. We hypothesized that high orthostatic tolerance (OT) would be associated with greater vasoconstrictor responses to venous pooling compared with low OT. Nineteen participants underwent continuous stepped lower body negative pressure at −10, −20, −30, −40, −50, and −60 mmHg each for 5 min or until exhibiting signs of presyncope. Ten participants completed the lower body negative pressure procedure without presyncope and were categorized with high OT; the remaining nine were categorized as having low OT. Near-infrared spectroscopy measurements of vasoconstriction (Hachiya T, Blaber A, Saito M. Acta Physiologica 193: 117–127, 2008) in calf muscles, along with heart rate (HR) responses for each participant, were evaluated in relation to calf blood volume, estimated by plethysmography. The slopes of this relationship between vasoconstriction and blood volume were not different between the high- and low-tolerance groups. However, the onset of vasoconstriction in the high-tolerance group was delayed. Greater HR increments in the low-tolerance group were also observed as a function of lower limb blood pooling. The delayed vasoconstriction and slower HR increments in the high-tolerance group to similar venous pooling in the low group may suggest a greater vascular reserve and possible delayed reduction in venous return.


1994 ◽  
Vol 86 (3) ◽  
pp. 275-283 ◽  
Author(s):  
Tim L. Th. A. Jansen ◽  
Dr Paul Smits ◽  
Jacques W. M. Lenders ◽  
Marie-Cécile G. S. Jacobs ◽  
Jacques Willemsen ◽  
...  

1. Atrial natriuretic factor has been suggested to affect human sympathetic nervous system activity. The interaction between atrial natriuretic factor and the sympathetic nervous system has not been fully elucidated yet, but may occur at different sites. We studied this modulator effect at the level of the forearm vascular bed: the forearm vasoconstrictor response was examined after α-adrenergic sympathetic stimulation in healthy subjects during the loco-regional administration of atrial natriuretic factor, sodium nitroprusside and placebo. As a sympathetic stimulation test, the technique of the lower body negative pressure (–20 mmHg) was used. 2. Lower body negative pressure increased the forearm vascular resistance by +37 ± 8% during concomitant intra-arterial infusion of placebo (n = 10). During a predilator state achieved by infusion of atrial natriuretic factor (10 ng min−1 100 ml−1 forearm volume) into the brachial artery, lower body negative pressure subsequently induced a forearm vasoconstrictor response of +153 ± 22% (P < 0.05 versus placebo), whereas this was +64 ± 14% when predilatation was achieved by infusion of an equipotent vasodilator dose of sodium nitroprusside (P > 0.1 versus placebo; P < 0.05 versus atrial natriuretic factor). The potentiation of the forearm vasoconstrictor response to lower body negative pressure by atrial natriuretic factor only occurred in the experimental and not in the contralateral arm. According to calculations on simultaneously sampled arterial and venous plasma catecholamine concentrations, the augmented forearm vasoconstrictor response seemed not to be caused by an increased release of noradrenaline. 3. In a second experiment (n = 10), we demonstrated that atrial natriuretic factor did not alter the forearm vasoconstrictor response to the intra-arterial administration of exogenous noradrenaline, thereby excluding a postsynaptic modulation by atrial natriuretic factor. In the presence of atrial natriuretic factor, the subsequent infusion of two dosages of noradrenaline (0.1 and 1.0 ng min−1 100 ml−1 forearm volume) increased the forearm vascular resistance by +118 ± 29% and +387 ± 79%, respectively, whereas these numbered +129 ± 18% and + 316 ± 41% when atrial natriuretic factor was replaced by an equipotent dose of sodium nitroprusside. 4. We conclude that atrial natriuretic factor potentiates the forearm vasoconstrictor response to α-adrenergic sympathetic stimulation in man, and that this effect may be located at the level of the forearm vascular bed. This potentiation cannot be explained by an increased vascular α-adrenergic sensitivity. More detailed studies are needed to analyse the effects of atrial natriuretic factor on local noradrenaline kinetics to elucidate influences on sympathetic neurotransmission.


1998 ◽  
Vol 84 (2) ◽  
pp. 454-458 ◽  
Author(s):  
John R. Halliwill ◽  
Lori A. Lawler ◽  
Tamara J. Eickhoff ◽  
Michael J. Joyner ◽  
Sharon L. Mulvagh

Halliwill, John R., Lori A. Lawler, Tamara J. Eickhoff, Michael J. Joyner, and Sharon L. Mulvagh. Reflex responses to regional venous pooling during lower body negative pressure in humans. J. Appl. Physiol. 84(2): 454–458, 1998.—Lower body negative pressure is frequently used to simulate orthostasis. Prior data suggest that venous pooling in abdominal or pelvic regions may have major hemodynamic consequences. Therefore, we developed a simple paradigm for assessing regional contributions to venous pooling during lower body negative pressure. Sixteen healthy men and women underwent graded lower body negative pressure protocols to 60 mmHg while wearing medical antishock trousers to prevent venous pooling under three randomized conditions: 1) no trouser inflation (control), 2) only the trouser legs inflated, and 3) the trouser legs and abdominopelvic region inflated. Without trouser inflation, heart rate increased 28 ± 4 beats/min, mean arterial pressure fell −3 ± 2 mmHg, and forearm vascular resistance increased 51 ± 9 units at 60 mmHg lower body negative pressure. With inflation of either the trouser legs or the trouser legs and abdominopelvic region, heart rate and mean arterial pressure did not change during lower body negative pressure. By contrast, although the forearm vasoconstrictor response to lower body negative pressure was attenuated by inflation of the trouser legs (Δforearm vascular resistance 33 ± 10 units, P < 0.05 vs. control), attenuation was greater with the inflation of the trouser legs and abdominopelvic region (Δforearm vascular resistance 16 ± 5 units, P < 0.05 vs. control and trouser legs-only inflation). Thus the hemodynamic consequences of pooling in the abdominal and pelvic regions during lower body negative pressure appear to be less than in the legs in healthy individuals.


Author(s):  
Akanksha Singh ◽  
Shival Srivastav ◽  
Kavita Yadav ◽  
Dinu S. Chandran ◽  
Ashok Kumar Jaryal ◽  
...  

1990 ◽  
Vol 78 (4) ◽  
pp. 399-401 ◽  
Author(s):  
M. J. Cullen ◽  
J. R. Cockcroft ◽  
D. J. Webb

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.


Sign in / Sign up

Export Citation Format

Share Document