Hemodilution-induced inhibition of cardiovascular responses to some vasoactive agents in anesthetized cats.

Cardiovascular responses to adrenaline and acetylcholine (ACh) were investigated in anesthetized, artificially ventilated cats in control and after induction of acute normovolemic hemodilution. Progressive replacement of blood by high molecular weight dextran was performed in three steps of 20% each of the total estimated blood volume. Hemodynamic responses were recorded at four stages: the control stage and after the 1st, 2nd, and 3rd exchanges of blood for dextran. With the fall in hematocrit (Ht) there was a corresponding significant (p < 0.05) increase in heart rate (HR), cardiac output (CO), and stroke volume (SV), and a decrease in systemic vascular resistance (TPR). However, left ventricular systolic pressure (LVSP), left ventricular contractility (LV dP/dtmax), mean arterial pressure (MAP), and right atrial pressure (RAP) 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 O2 supply. The possibility of a modulatory role of an endothelium-dependent mechanism and reflex regulatory responses by arterial baroreceptors during hemodilution also exists.