Growth hormone, cardiomyocyte contractile reserve, and heart failure.

In this issue of Circulation, Tajima et al 1 report that recombinant human growth hormone (GH) (3.5 mg z kg z d) given for 2 weeks, while not affecting baseline function, restored myocardial contractile reserve in cardiomyocytes isolated from rats 4 to 6 weeks after myocardial infarction (MI) compared with vehicle-treated post-MI rats. In addition, the peak of the Ca transient, which was normal at baseline in both GHand vehicle-treated rats, was depressed in response to increased external Ca (3.5 mm/L) in vehicle-treated rats, whereas in the GH-treated group, increased Ca restored the peak at the Ca transient, as well as cardiomyocyte contractile function. Also, in the GH-treated post-MI hearts, mRNA and protein levels of sarcoplasmic reticulum Ca ATPase 2 (SERCA-2) were increased,1 which lends support to the proposed mechanism for restoration of contractile reserve, because only a small increase in the expression of SERCA-2 protein was reported to enhance myocardial contractility in transgenic mice.2 The authors indicate that cardiomyocytes were used to obviate effects of altered loading on the heart by the vasodilator actions of GH, and the dose of GH used was said to be sufficiently low to avoid myocardial hypertrophy. This study is the first to analyze the effects of GH in cardiomyocytes from postinfarction rats and provides convincing data concerning a beneficial effect of GH on contractile reserve. It also begins to shed light on mechanisms involved in the effects of GH on myocardial function. However, some of the findings in this study raise questions about GH effects under differing study conditions.