Reduction of heart rate by chronic β1-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart.

摘要: Adequate growth of coronary vasculature in the remaining left ventricular (LV) myocardium after myocardial infarction (post-MI) is a crucial factor for myocyte survival and performance. We previously demonstrated that post-MI angiogenesis can be stimulated by bradycardia induced with ATP-sensitive K(+) channel antagonist alinidine. In this study, we tested hypothesis heart rate reduction beta-blockade may also induce heart. Transmural MI was 12-mo-old male Sprague-Dawley rats occlusion anterior descending artery. Bradycardia administration beta-adrenoceptor blocker atenolol (AT) via drinking water (30 mg/day). Three groups were compared: 1) control/sham (C/SH), 2) MI, 3) + AT. AT rats, consistently reduced 25-28% compared C/SH rats. At 4 wk ligation, infarct size similar (67.1 61.5%, respectively), whereas greater hypertrophy occurred bradycardic as indicated higher weight-to-body weight ratio (3.4 +/- 0.1 vs. 2.8 mg/g rats). Analysis LV function revealed smaller drop ejection fraction than group ( approximately 24 35%). Furthermore, maximal conductance perfusion reserve significantly improved group. The better indexes associated increase arteriolar length density Thus chronic beta-selective blockade promotes arterioles and, thereby, facilitates regional hearts.