Hemodynamic responses to hypoxia and hypercapnia during acute normovolemic hemodilution in anesthetized cats

The present study was undertaken to evaluate the effects of hypoxia and hypercapnia on circulatory parameters during acute normovolemic hemodilution. Cats anesthetized with a mixture of alpha-chloralose and urethane were maintained by positive pressure ventilation. Muscles were paralysed by intramuscular vecuronium (0.1 mg/kg) to eliminate reflex respiratory movements. Cats were exposed to hypoxia (12% O(2) and 7% O(2)) and hypercapnia (4% CO(2) and 7% CO(2)) at normal hematocrit (Ht 40.1 +/- 2.8%) and then at graded levels of normovolemic hemodilution (Ht 24.0 +/- 2.0% and Ht 13.0 +/- 1.5%, respectively). Left ventricular pressure (LVP), LV dP/dt(max), arterial blood pressure (ABP), heart rate (HR), and right atrial pressure (RAP) were recorded on a polygraph. Cardiac output (CO) was measured using a cardiac output computer. Hemodilution 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 mixtures caused significant increases in HR and CO at control Ht; but after hemodilution it caused the reverse effects. Hypercapnia did not produce any significant effect on ABP, LV dP/dt(max) or RAP either at control Ht or after hemodilution. Hypercapnia produced a fall in HR, CO and stroke volume (SV) at normal Ht and percent fall in HR response was enhanced following hemodilution. The reversal of chronotropic response to hypoxia and enhanced bradycardia response to hypercapnia, under conditions of acute normovolemic hemodilution would be deleterious as the tissues would become more hypoxic. Such a response may be attributed to altered control mechanisms under such conditions of severe stress.