In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 275, No. 4 ( 1998-10-01), p. H1169-H1177
Abstract:
This study examined reflex vascular responses to large rapid increases and decreases in carotid sinus pressure to determine whether delayed or inappropriate vascular responses might be obtained that, if they occurred in people, could lead to hypotension during exposure to rapidly alternating gravitational forces. In chloralose-anesthetized open-chest dogs, a perfusion circuit controlled carotid sinus and thoracic aortic pressures and blood flows to both the vascularly isolated abdominal circulation and a hindlimb (perfusion pressure changes denoted resistance). When carotid pressure was increased and decreased over the range of 60–180 mmHg, the resulting reflex vasodilatation occurred significantly more rapidly than the vasoconstriction ( P 〈 0.001). In the abdominal vascular bed, time constants for vasodilatation and vasoconstriction were 4.2 ± 0.5 and 7.5 ± 1.0 s, respectively. Decreases in carotid pressure in pulses of 10-s duration or less failed to elicit maximal vasoconstriction, whereas increases in carotid pressure lasting as little as 5 s did elicit maximal vasodilatation. “Square-wave” alternations in carotid pressure with periods of 10 s or less (5 s high, 5 s low) resulted in attenuation of the vasoconstriction, and at a 4-s period, both vascular beds remained almost maximally vasodilated throughout. The failure of vascular resistance to follow carotid pressure changes was not due to a failure of the response of sympathetic efferent activity, since the time constants for the reduction and increase in discharge were much shorter at 0.56 ± 0.13 and 0.43 ± 0.10 s, respectively. These results indicate that rapid changes in carotid pressure could result in inappropriate vasodilatation and hypotension and might, in some circumstances, such as in pilots flying high-performance aircraft, predispose to syncope.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.1998.275.4.H1169
Language:
English
Publisher:
American Physiological Society
Publication Date:
1998
detail.hit.zdb_id:
1477308-9
SSG:
12
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