Effect of prostaglandin E1 on myocardial contractility in dogs anesthetized with halothane: load-independent and noninvasive assessment using transesophageal echocardiography.

The presence of an inotropic action of prostaglandin E1 (PGE1) in vivo is controversial, and there are conflicting results obtained by various indices of myocardial contractility. In this study, a direct effect of PGE1 on contractility was investigated in dogs by use of a load-independent contractile index: left ventricular end-systolic wall stress (LVESWS) versus the velocity of circumferential fiber shortening with rate-corrected (Vcfc) relationship using transesophageal echocardiography (TEE). Hemodynamics, arterial blood gas, and TEE data were obtained before PGE1 infusion (control), and with a 10%, 20%, and 30% decrease in mean arterial pressure (MAP) following intravenous PGE1 administration. PGE1 infusion rates were 0.19 +/- 0.03 at 10%, 0.82 +/- 0.17 at 20%, and 2.32 +/- 0.36 micrograms/kg/min at a 30% decrease in MAP. Pulmonary capillary wedge pressure, systemic vascular resistance index, and left ventricular stroke work index significantly decreased, and heart rate, cardiac index, and stroke volume index were not significantly altered. Analysis of the TEE data showed LVESWS (index of afterload) significantly decreased from 92.0 +/- 11.2 g/cm2 to 72.7 +/- 7.8 at 10%, 59.3 +/- 7.8 at 20%, and 44.6 +/- 6.2 at a 30% decrease in MAP, and Vcfc significantly increased from 0.595 +/- 0.065 circ/sec of control value to 0.670 +/- 0.056 at 10%, 0.824 +/- 0.049 at 20%, and 0.939 +/- 0.070 at a 30% decrease in MAP. In the LVESWS versus Vcfc relationship, no significant difference could be detected between the control state and the 10%, 20%, and 30% decrease in MAP, and no inotropic effect was found.(ABSTRACT TRUNCATED AT 250 WORDS)