Sodium acetate, an arterial vasodilator: haemodynamic characterisation in normal dogs.

Abstract

Sodium acetate (SA) has been implicated in hypotensive episodes of haemodialysis because of its vasodilatory effects. The haemodynamic correlates of the changes in blood pressure, cardiac output (CO) and total peripheral resistance (TPR) are well known but the site of action of SA (i.e. arteriolar, venular or both) is not yet clarified. We thus studied the changes in CO, TPR and mean arterial pressure (MAP) induced by four graded doses of SA (0.034 to 0.300 mEq/kg/min) in seven normal dogs. To evaluate the site of vasodilation we also measured the changes in cardiopulmonary volume (CPV), mean pulmonary artery pressure (MPAP) and mean transit time (MTT). From control to the highest infusion rate, CO increased from 1.63 +/- 0.20 to 3.59 +/- 0.38L/min (p less than 0.001), TPR decreased from 78.2 +/- 11.3 to 36.4 +/- 4.8A.U. (p less than 0.001). MAP rose significantly from 107.2 +/- 4.0 to 116.5 +/- 8.5 mmHg (p less than 0.05) and stroke volume was maintained (17.2 +/- 2.3 to 19.6 +/- 2.1 ml, NS) in spite of the marked tachycardia observed (heart rate from 106.1 +/- 7.6 to 194.8 +/- 9.1bpm, p less than 0.001). This was associated with increases in MPAP (from 13.3 +/- 0.7 to 19.6 +/- 2.1mmHg, p less than 0.01) and CPV (from 195.0 +/- 21.3 to 224.4 +/- 24.3ml, p less than 0.01) and marked decrease in MTT (from 7.74 +/- 0.73 to 3.78 +/- 0.22 sec, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)