摘要
目的探讨促血小板生成素对缺血-再灌注损伤心肌的保护作用,初步阐述其作用机制。方法Sprague-Dawley大鼠48只,分为缺血对照组、缺血促血小板生成素治疗组和假手术组。开胸结扎大鼠心脏冠状动脉前降支45min后恢复再灌注,观察再灌注心律失常的情况;术后14d检测血流动力学变化和测量心肌梗死面积;术后3d每组各取4只大鼠行凋亡细胞检测。结果缺血促血小板生成素治疗组大鼠再灌注心律失常的发生明显少于对照组,肌酸激酶和心肌型肌酸激酶活性和心肌梗死面积也较缺血对照组减小,血流动力学情况则有明显的改善,且凋亡细胞数量也显著的减少。结论促血小板生成素能减轻心肌缺血-再灌注损伤,改善心功能,其机制可能与减少细胞凋亡有关。
Objectives To explore the protective effect of thrombopoietin （TPO） on ischemia-reperfusion hearts of rats, and its initial mechanism. Methods Forty-eight SD rats were divided into isehemia group, TPO group and sham-operation group （SHAM）. The left anterior descending coronary artery was tied for 45 rain followed by reperfusion to review the repeffusion arrhythmia; the haemodynamie parameters were detected and the infarct size was measured on day 14. Four rats in each group were elected to count apoptotic myoeytes. Results The incidence of repeffusion arrhythmia was obviously reduced in the TPO group than that in the ischemia-eontrol group, the serum CK and CK-MB and the infarct size were diminished, the haemodynamics were amendmented, apoptotic myocyte count was significantly reduced as seen in TPO group. Conclusions TPO attenuates the myoeardium ischemia-repeffusion injury and improves cardiac functions with a possible mechanism of anti-apoptosis.
出处
《岭南心血管病杂志》
2008年第5期368-372,共5页
South China Journal of Cardiovascular Diseases
基金
2005年广东省科技计划项目资助项目(2005B30601012)
