Acute effects of ethanol on cardiac output and its derivatives in spontaneously hypertensive and normotensive rats.

This study investigated the influence of small to moderate doses of ethanol on arterial pressure (MAP), heart rate, cardiac index (CI), stroke volume (SV) and total peripheral resistance (TPR) of anesthetized spontaneously hypertensive rats (SHRs) and two age-matched normotensive strains, Wistar Kyoto (WKY) and Sprague-Dawley (SD) rats. Compared with WKY values, the significantly higher MAP of SHRs (175 +/- 4 vs. 118 +/- 4 mm Hg) was the result of a significantly elevated TPR (6.1 +/- 0.3 vs. 3.1 +/- 0.2 mm Hg/ml/min/100 g; P < .05), because Cl was significantly lower (31 +/- 1.6 vs. 41 +/- 2.5 ml/min/100 g; P < .05). A lower SV (261 +/- 13 vs. 394 +/- 20 microliters/min; P < .05) accounted for the reduced Cl in SHRs, because HR was similar (318 +/- 4 vs. 328 +/- 11 beats/min). In spite of similar MAP (114 +/- 3.9 vs. 118 +/- 4 mm Hg) of SD and WKY rats, Cl was significantly higher (33 +/- 2 vs. 41 +/- 2.5 ml/min/100 g; P < .05) due to a higher SV (339 +/- 19 vs. 394 +/- 20 microliters/min; P < .05) and TPR was significantly lower (3.7 +/- 0.2 vs. 3.1 +/- 0.2 mm Hg/ml/min/100 g; P < .05) in the latter strain. Low dose ethanol (0.1-0.25 g/kg) had no effect, whereas a moderate dose of 0.5 g/kg elicited strain-dependent hemodynamic responses which comprised significant increases in Cl and SV in normotensive rats, but not in SHRs. However, because of a reduction in TPR, MAP did not change.(ABSTRACT TRUNCATED AT 250 WORDS)