GROWTH-HORMONE IMPROVES CARDIAC-FUNCTION IN RATS WITH EXPERIMENTAL MYOCARDIAL-INFARCTION

Accumulating evidence suggests from experimental and clinical studies beneficial effects of growth hormone (GH) on contractility, although c oncomitant cardiac hypertrophy, generally considered to be a cardiovas cular risk factor, has also been reported. In the present study, we co mbine a rat model with impaired cardiac performance after myocardial i nfarction (MI) with echocardiographic evaluation of GH effects on card iac structure and function. We have used a rat model with ligation of the left coronary artery in normal, growing male rats resulting in sub sequent impaired cardiac performance. After 6 weeks' recovery, blind t ransthoracic echocardiography was performed to determine infarction si ze, cardiac geometry and performance. Rats with no signs of myocardial infarction were excluded from the study. After randomization, the rat s were treated with daily s.c. injections of saline (n = 8) or recombi nant human growth hormone (rhGH) (n = 6) at a dose of approximately 1 mg kg(-1) body weight for 1 week. A new blind echocardiography examina tion was performed after treatment demonstrating a 13% increase in eje ction fraction (EF) and a 50% increase in cardiac index in GH-treated rats compared with control rats (P < 0.01). Moreover, GH caused a sign ificant decrease in end-systolic volume. There were no significant cha nges in left ventricular (LV) or interventricular wall thickness, LV d imensions, heart rate or diastolic function. No effects were seen on L V weight, cardiac insulinlike growth factor (IGF) I, IGF-I receptor an d GH receptor mRNA content. GH in a physiological dose improves systol ic function in an experimental model of heart failure without signs of hypertrophy, suggesting a potential role as a therapeutic agent in th e treatment of heart failure and merits further investigation.