地氟醚预处理对中性粒细胞介导心肌细胞凋亡的影响

Effects of Desflurane on Attenuating Neutrophil Mediated Myocardial Apoptosis after Anoxia and Reoxygenation

目的:研究地氟醚预处理心肌细胞对中性粒细胞介导的心肌凋亡的影响及其机制的研究。方法:原代培养的乳鼠心肌细胞,随机分为Ⅰ组缺氧/复氧组、Ⅱ组中性粒细胞介导缺氧/复氧组、Ⅲ组地氟醚预处理组、Ⅳ组地氟醚预处理+中性粒细胞介导缺氧/复氧组四组,每组六复孔,各组实验开始时测定LDH、CK-MB、H2O2,实验结束测定LDH、CK-MB、H2O2和心肌细胞凋亡率。结果:除地氟醚预处理组外,缺氧前和复氧后LDH、CK-MB均有显著差异（P<0.01）,复氧后LDH、CK-MB组间有显著差异（P<0.01）,缺氧/复氧组和地氟醚预处理组H2O2组间元明显差异（P>0.05）,其余组间有显著差异（P<0.01）。复氧后,心肌细胞凋亡率组间有显著差异（P<0.01）。结论:地氟醚减轻中性粒细胞介导心肌细胞凋亡,与LDH、CK-MB酶的释放有相关性,而且与H2O2生成减少有关。

:To assess the role of neutrophils in anoxia-reoxygenation induced damage on primary cultured myocardial cells and the protection of desflurane preconditioning against neutrophil-mediated injury. Methods: Ventricular myocytes, cultured in MEM medium 3 days, were randomly divided into four groups: A/R group receiving 2 hours anoxia and 1 hour reoxygenation, neutrophil -mediated group receiving 1×106 neutrophil during 1 hour reoygenation, desflurane preconditioning group receiving desflurane preconditioning before 2 hours anoxia and neutrophil-mediated with desflurane preconditioning group. The activities of lactic dehydrogenase (LDH), creatine kinase(CK), H2O2, myocardial apoptosis rate were measured before and at end of the experiment. Results: Except desflurane preconditioning group, A/R caused dramatic increase of LDH ,CK(P<0.01). LDH were 26.00±1.09U/L,58.50±7.34 U/L ,22.00±0. 63 U/L ,39. 83±7.25 U/L and CK-MB were 3.95±0.13 U/L ,10.56±0.47 U/L, 3.03±0.16 U/L, 5.66±1.21 U/L in four group after reoxgenation respectively. In A/R group and desflurane preconditioning group, between anoxia and reoxygenation there was no difference of production of H2O2 has (P>0.05), while there was difference among other grousp (P<0.05). After reoxgenation, In A/R group and desflurane preconditioning group, there was no difference of production of H2O2(P>0.05), while there was difference among other groups (P< 0.05). Myocardial apoptosis have the same results. Conclusion: Desflurane preconditioning can attenuate neutrophil-mediated myocardial apoptosis in primary cultured myocytes but not completely and it may relate with the release of H2O2,LDH and CK.