川芎嗪和参麦注射液对老龄大鼠脑缺血再灌注心肌损伤的保护作用

目的：从多巴胺（DA）、去甲肾上腺素（NE）、肾上腺素（E）和神经肽Y（NPY）的变化研究川芎嗪和参麦注射液及其配伍对老龄大鼠脑缺血再灌注心肌损伤防护作用的机制。方法：老龄大鼠分为模型组和对照组、尼莫通组、川芎嗪组、参麦注射液组（参麦组）、川芎参麦组（川参组）,观察大鼠全脑缺血再灌注后心肌组织形态和乳酸脱氢酶（LDH）、肌酸磷激酶（CPK）活性及NE、DA、E、NPY含量的变化。结果：与老龄对照组比较，老龄模型组心肌组织出现明显的病理改变和单胺类神经递质紊乱，血清中CPK和LDH活性及脑组织NPY含量增高，参麦组和川参组心肌病理改变和脑组织NPY含量明显改善，川参组、川芎嗪组血清CPK水平和参麦组、川芎嗪组血清中LDH水平显著降低，川参组、参麦组、川芎嗪组单胺类神经递质紊乱改善明显。结论：老龄大鼠脑缺血再灌注心肌损伤与交感－肾上腺系统兴奋增强有关。川芎嗪和参麦注射液及其配伍调节单胺类神经递质紊乱作用和降低NPY含量可能是防治脑缺血再灌注心肌损伤的机制之一。

Effect of ligustrazine and shenmai injection on myocardial injury in the aged rats with brain ischemia reperfusion

Objective To study the protective mechanism of Ligustrazine(LT),Shenmai Injection (SI),combination of Ligustrazine and Shenmai injection (LSI) to myocardial injury after brain ischemia reperfusion in aged rats from the changes of Dopamine(DA), Noradrenalin(NE) ,Epinephrine(E),Neuropeptide Y.Methods Aged rats (more than 20 months) were divided into model group(AMG) ,control group(ACG),nimotop group(NG),LT group, SI group and LSI group. The contents of NE, DA, E, NPY, the activity of lactic dehydrogenate (LDH) and creative phosphokinase(CPK) were measured in the rats with brain ischemia. Results Comparing with the ACG' s, the obvious pathological change of myocardium was found in the AMG;the activity of sern CPK and LDH and the content of brain NPY increased,the serum NE and hypothalamus DA content was higher,the hypothalamus NE content was lower. The pathological improved change of myocardium was obvious and the level of brain NPY was lower in the SI's and the LSI's; serum CPK activity in the LT's and the LSI's and serum LDH activity in the LT's and the SI's decreased;the changes in hypothalamus DA content decrease and in hypothalamus NE content increase in the LT's, the SI's, the LSI's were obvious,than the AMG's. Conclusions The myocardial injury induced by ischemia reperfusion in aged rats was correlated with the enhanced excitability of sympathetic - adrenal system, the effect of LT, SI and LSI regulating the abnormal of NE, DA in the central nervous and improving NPY change might be one of mechanismes of preventing and curing myocardial injury.