HEMODILUTION-INDUCED INHIBITION OF CARDIOVASCULAR-RESPONSES TO SOME VASOACTIVE AGENTS IN ANESTHETIZED CATS

Cardiovascular responses to adrenaline and acetylcholine (ACh) were in vestigated in anesthetized, artificially ventilated cats in control an d after induction of acute normovolemic hemodilution. Progressive repl acement of blood by high molecular weight dextran was performed in thr ee steps of 20% each of the total estimated blood volume. Hemodynamic responses were recorded at four stages: the control stage and after th e 1st, 2nd, and 3rd exchanges of blood for dextran. With the fall in h ematocrit (Ht) there was a corresponding significant (p < 0.05) increa se in heart rate (HR), cardiac output (CO), and stroke volume (SV), an d a decrease in systemic vascular resistance (TPR). However, left vent ricular systolic pressure (LVSP), left ventricular contractility (LVdP /dt(max)), mean arterial pressure (MAP), and right atrial pressure (RA P) did not show any significant (p > 0.05) change due to hemodilution. The cardiovascular responses of intravenously administered adrenaline and ACh were significantly (p < 0.05) attenuated. Responses to sodium nitroprusside (SNP), a potent vasodilator and an exogenous source of nitric oxide, were also attenuated after hemodilution. The increase in SV and HR seem to be the contributing factors to the CO response. Our results indicate that the cardiovascular responsiveness to adrenaline , ACh and SNP is reduced during acute hemodilution which could be due to inadequate myocardial and vascular O-2 supply. The possibility of a modulatory role of an endothelium-dependent mechanism and reflex regu latory responses by arterial baroreceptors during hemodilution also ex ists.