Hemodynamic responses to hypoxia and hypercapnia during acute normovolemichemodilution in anesthetized cats

The present study was undertaken to evaluate the effects of hypoxia and hyp ercapnia on circulatory parameters during acute normovolemic hemodilution. Cats anesthetized with a mixture of oi-chloralose and urethane were maintai ned by positive pressure ventilation. Muscles were paralysed by intramuscul ar vecuronium (0.1 mg/kg) to eliminate reflex respiratory movements. Cats w ere exposed to hypoxia (12% O-2 and 7% O-2) and hypercapnia (4% CO2 and 7% CO2) at normal hematocrit (Ht 40.1+/-2.8%) and then at graded levels of nor movolemic hemodilution (Ht 24.0+/-2.0% and Ht 13.0+/-1.5%, respectively). L eft ventricular pressure (LVP), LV dP/dt(max), arterial blood pressure (ABP ), heart rate (HR), and right atrial pressure (RAP) were recorded on a poly graph. Cardiac output (CO) was measured using a cardiac output computer. He modilution per se did not produce any significant change in ABP, RAP or LV dP/dt(max), however, it produced a significant rise in HR and a significant fall in total peripheral resistance (TPR). Exposure to hypoxic gas mixture s caused significant increases in HR and CO at control Ht; but after hemodi lution it caused the reverse effects. Hypercapnia did not produce any signi ficant effect on ABP, LV dP/dt(max) or RAP either at control Ht or after he modilution. Hypercapnia produced a fall in HR, CO and stroke volume (SV) at normal Ht and percent fall in HR response was enhanced following hemodilut ion. The reversal of chronotropic response to hypoxia and enhanced bradycar dia response to hypercapnia, under conditions of acute normovolemic hemodil ution would be deleterious as the tissues would become more hypoxic. Such a response may be attributed to altered control mechanisms under such condit ions of severe stress.