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选择性生长激素缺乏大鼠心脏缺血损伤的加重

Worsening of ischemic damage in hearts from rats with selective growth hormone deficiency.

作者信息

De Gennaro Colonna V, Rossoni G, Bonacci D, Ciceri S, Cattaneo L, Müller E, Berti F

机构信息

Department of Pharmacology, Chemoterapy and Toxicology, University of Milano, Italy.

出版信息

Eur J Pharmacol. 1996 Oct 31;314(3):333-8. doi: 10.1016/s0014-2999(96)00585-7.

DOI:10.1016/s0014-2999(96)00585-7
PMID:8957255
Abstract

The effects of growth hormone (GH) deficiency on cardiac function were studied in young male rats administered an anti-GH-releasing hormone (GHRH) serum from postnatal day 20 to 40. Dependence of heart abnormalities on GH deficiency was ascertained by giving a group of anti-GHRH serum-treated rats GH replacement therapy. Heart preparations from anti-GHRH serum-treated rats, undergoing low-flow ischemia, showed a progressive increase in left ventricular end-diastolic pressure with poor recovery of mechanical activity and increased coronary perfusion pressure upon reperfusion. Hearts from anti-GHRH serum + GH-treated rats, undergoing global reduction to the flow, showed only a minimal increase of left ventricular end-diastolic pressure and, upon reperfusion, cardiac mechanical activity recovered almost completely. Similar findings were also observed in heart preparations from control (normal rabbit serum-treated) rats. Infusion of acetylcholine (10(-6) M) into heart preparations in the preischemic period increased coronary perfusion pressure values more markedly in hearts from normal rabbit serum- and anti-GHRH serum + GH-treated rats than in those from anti-GHRH serum-treated rats. These results indicate that selective GH deficiency in young male rats renders the heart more sensitive to ischemic damage and leads to an impairment of cardiac muscarinic receptor function.

摘要

在出生后第20天至40天给予抗生长激素释放激素(GHRH)血清的年轻雄性大鼠中,研究了生长激素(GH)缺乏对心脏功能的影响。通过对一组接受抗GHRH血清治疗的大鼠进行GH替代疗法,确定了心脏异常对GH缺乏的依赖性。接受低流量缺血的抗GHRH血清治疗大鼠的心脏制剂显示,左心室舒张末期压力逐渐升高,机械活动恢复不良,再灌注时冠状动脉灌注压力增加。接受整体流量减少的抗GHRH血清+GH治疗大鼠的心脏,左心室舒张末期压力仅略有增加,再灌注时心脏机械活动几乎完全恢复。在对照(正常兔血清治疗)大鼠的心脏制剂中也观察到了类似的结果。在缺血前期向心脏制剂中注入乙酰胆碱(10^(-6) M),正常兔血清和抗GHRH血清+GH治疗大鼠心脏的冠状动脉灌注压力值增加比抗GHRH血清治疗大鼠的更明显。这些结果表明,年轻雄性大鼠的选择性GH缺乏使心脏对缺血损伤更敏感,并导致心脏毒蕈碱受体功能受损。

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