GROWTH-HORMONE IMPROVES CARDIAC-PERFORMANCE IN EXPERIMENTAL HEART-FAILURE

Background Growth hormone has been shown to increase maximum isometric active force of the left ventricular papillary muscle of rats in vitr o. Administration of growth hormone causes an increase in myocardial c ontractility in normal humans. Our preliminary study suggests that tre atment with growth hormone results in increased ventricular contractil ity in rats with left ventricular dysfunction. In the present study, t he effects of growth hormone on cardiac function, including cardiac ou tput, stroke volume, and peripheral vascular resistance, were determin ed in a rat model of heart failure. Methods and Results Ligation of th e left coronary artery or sham operation was performed; 4 weeks after surgery, recombinant human growth hormone (2 mg/kg per day SC) or vehi cle then was administered for 15 days. The animals were catheterized a fter 13 days of the treatment. Cardiac output, measured by a thermodil ution method, and other hemodynamic parameters were measured in the co nscious animals 2 days after catheterization. The infarct sizes induce d by left coronary ligation were comparable between growth hormone-tre ated vehicle-treated rats. Six weeks after ligation, rats treated with vehicle exhibited significant decreases in cardiac index, stroke volu me index, and left ventricular maximum dP/dt and increases in left ven tricular end-diastolic pressure compared with sham rats. In the ligate d rats, treatment with growth hormone increased cardiac index, stroke volume index, and left ventricular maximum dP/dt (P<.05) and reduced l eft ventricular end-diastolic pressure and systemic vascular resistanc e (P<.05). In sham rats, growth hormone slightly reduced arterial pres sure but did not significantly alter cardiac performance. There was no significant difference in heart rate between the experimental groups. Conclusions These results suggest that growth hormone treatment may i mprove cardiac function by both increased myocardial contractility and decreased peripheral vascular resistance in heart failure.