Effect of enalaprilat on splanchnic vascular capacitance during acute ischemic heart failure in dogs

This study investigates the effect of angiotensin-converting-enzyme inhibition by intravenous enalaprilat (100 micrograms/kg) on splanchnic vascular capacitance during acute left ventricular failure induced by coronary microembolization in alpha-chloralose/urethan anesthetized dogs. Changes in hepatic and splenic vascular volumes were determined from organ diameters (sonomicrometry) at 15, 30, and 45 min after enalaprilat injection. Changes in vascular capacitance were assessed from organ pressure-diameter curves obtained during transient hepatic outflow occlusion. Thirty minutes after enalaprilat, hepatic volume was increased by 52 +/- 14 ml (P < 0.01), and portal and hepatic vein pressures were decreased from 10.2 +/- 0.9 to 8.7 +/- 0.8 mmHg (P < 0.01) and from 3.9 +/- 1.6 to 3.1 +/- 0.7 mmHg (P < 0.05), respectively. Splenic volume did not change. Enalaprilat shifted the hepatic pressure-diameter curve upward, resulting in a larger hepatic volume at any given pressure. Curve intercept was increased, suggesting an increase in unstressed vascular volume. Curve slope was unchanged. In conclusion, enalaprilat increased hepatic vascular volume during acute left ventricular failure in dogs. The pressure-diameter curve shift suggests a reduction in the smooth muscle tone of hepatic capacitance vessels.

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Systemic and regional effects of vasopressin and angiotensin in acute left ventricular failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.260.2.h499 ◽

1991 ◽

Vol 260 (2) ◽

pp. H499-H506

Author(s):

L. Arnolda ◽

B. P. McGrath ◽

C. I. Johnston

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Diastolic Pressure ◽

Peripheral Resistance ◽

Left Ventricular ◽

Left Ventricular Failure ◽

Angiotensin Converting Enzyme Inhibition ◽

Ventricular Failure ◽

Failure Group ◽

Blood Flows

The systemic and regional hemodynamic effects of arginine vasopressin receptor antagonism (AVPA) and angiotensin-converting enzyme inhibition (ACEi) were examined in rabbits with acute left ventricular failure induced by repetitive direct current (DC) shock. Hemodynamic measurements in 24 rabbits 24 h after DC shock compared with 6 sham-operated controls demonstrated a lowered cardiac output (602 +/- 26 vs. 920 +/- 35 ml/min, P less than 0.01), increased left ventricular end-diastolic pressure (LVEDP, 13.6 +/- 1.3 vs. 1.9 +/- 0.5 mmHg, P less than 0.01) and a raised peripheral resistance (9,734 +/- 495 vs. 6,479 +/- 305 dyn.s.cm-5, P less than 0.01). Cerebral blood flow was not altered in rabbits with acute left ventricular failure but intestinal (29 +/- 2 vs. 53 +/- 9 ml/min, P less than 0.01) and renal (82 +/- 6 vs. 130 +/- 8 ml/min, P less than 0.01) blood flows were significantly reduced. No hemodynamic changes were observed after AVPA alone in the acute heart failure group and ACEi alone reduced LVEDP and increased renal vascular conductance. Treatment with both drugs (i.e., AVPA + ACEi) resulted in a significant increase in cardiac output (21%) and a decrease in blood pressure (19%) and peripheral resistance (34%) and restored renal and intestinal blood flows to near normal levels. Thus both vasopressin and angiotensin contribute to the overall increase in peripheral resistance in this model and to the decrease in intestinal and renal blood flow observed. Presumably blockade of one system produced little hemodynamic change because of compensatory increases in the other system.

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