CARDIOVASCULAR-RESPONSES TO HEMORRHAGE DURING ACUTE AND CHRONIC HYPOXIA

Previous work from our laboratory has demonstrated attenuation of syst emic vasoreactivity to presser agents in rats after acute or chronic e xposure to hypoxia. Therefore we hypothesized that hemorrhage of acute ly hypoxic (12% O-2) or chronically hypoxic (barometric pressure 380 m mHg for 3 wk) rats would deter the normal increase in total peripheral resistance (TPR) and thus decrease the ability to maintain blood pres sure. Progressive hemorrhage (2% of blood volume per min) was performe d under conditions of either normoxia or acute hypoxia in conscious ra ts. In control animals, the increase in TPR observed during normoxic h emorrhage was absent when hemorrhage was performed in acute hypoxia. F urthermore, the amount of blood removal required to achieve hypotensio n was reduced under conditions of acute hypoxia. In contrast, chronica lly hypoxic rats exhibited no difference in the threshold for hypotens ion between conditions of acute normoxia and hypoxia and demonstrated an increased hypotensive threshold under both normoxic and hypoxic con ditions compared with control animals. We next hypothesized that the p rolonged threshold for hypotension observed in chronically hypoxic rat s 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 occ urring in extreme underfill conditions. Therefore we compared the card iovascular responses to hemorrhage in rats with right ventricular hype rtrophy resulting from administration of monocrotaline with those from rats treated with vehicle. The hypotensive threshold during hemorrhag e in either normoxic or hypoxic conditions was not different between m onocrotaline- and vehicle-treated animals. These data suggest that the altered reflex responses to hemorrhage in chronically hypoxic rats ar e not due to right ventricular hypertrophy.