AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 3 619-R627, Copyright © 1994 by American Physiological Society
Cardiovascular responses to hemorrhage during acute and chronic hypoxia
T. C. Resta, R. D. Russ, M. P. Doyle, J. M. Martinez and B. R. Walker
Department of Physiology, University of New Mexico School of Medicine, Albuquerque 87131.
Previous work from our laboratory had demonstrated attenuation of systemic
vasoreactivity to pressor agents in rats after acute or chronic exposure to
hypoxia. Therefore we hypothesized that hemorrhage of acutely hypoxic (12%
O2) or chronically hypoxic (barometric pressure 380 mmHg for 3 wk) rats
would deter the normal increase in total peripheral resistance (TPR) and
thus decrease the ability to maintain blood pressure. Progressive
hemorrhage (2% of blood volume per min) was performed under conditions of
either normoxia or acute hypoxia in conscious rats. In control animals, the
increase in TPR observed during normoxic hemorrhage was absent when
hemorrhage was performed in acute hypoxia. Furthermore, the amount of blood
removal required to achieve hypotension was reduced under conditions of
acute hypoxia. In contrast, chronically hypoxic rats exhibited no
difference in the threshold for hypotension between conditions of acute
normoxia and hypoxia and demonstrated an increased hypotensive threshold
under both normoxic and hypoxic conditions compared with control animals.
We next hypothesized that the prolonged threshold for hypotension observed
in chronically hypoxic rats might be due to hypoxia-induced right
ventricular hypertrophy. Such ventricular hypertrophy may minimize
stimulation of ventricular volume receptors thought to elicit the reflex
fall in heart rate and TPR occurring in extreme underfill conditions.
Therefore we compared the cardiovascular responses to hemorrhage in rats
with right ventricular hypertrophy resulting from administration of
monocrotaline with those from rats treated with vehicle.(ABSTRACT TRUNCATED
AT 250 WORDS)
