Growth hormone induces myocardial expression of creatine transporter and decreases plasma levels of IL-1beta in rats during early postinfarct cardiac remodeling.

Growth hormone has been proposed as a potential new therapeutic agent for treatment of myocardial infarction (MI) and congestive heart failure (CHF). The purpose of this study was to evaluate the effects of GH on: (a) myocardial expression of creatine transporter (CreaT) during early postinfarct remodeling, (b) myocardial levels of total creatine (TCr) and adenine pool (TAN) and (c) plasma levels of inflammatory cytokines interleukin-1beta (IL-1beta), tumor-necrosis-factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in rat model of postinfarct cardiac remodeling. Myocardial infarction (MI) was induced by ligation of the left coronary artery in male Sprague-Dawley rats (200-250 g).

Stress echocardiography using transesophageal atrial pacing in rats.

Background: Echocardiography is increasingly used for noninvasive evaluation of cardiac function and morphology in small animal models of cardiovascular diseases. The aims of this study were to develop a simple method for stress echocardiography in rats and to evaluate left ventricular function of the postinfarct remodeling heart during stress induced by rapid atrial pacing.

Methods: Myocardial infarction (MI) was induced in rats by ligation of left coronary artery.