心脏瓣膜病患者心肌组织脂联素抵抗及其相关机制探讨

摘要

Objective To investigate the effect of adiponectin resistance on heart valve disease and the related resist -ance mechanism .Methods Thirty-six patients undergoing cardiopulmonary bypass ( CPB) heart valve replacement surger-y ( the treatment group ) and 22 cases of heart transplant donors who needed heart surgery ( the control group ) were select-ed.The myocardial tissues which were cut off in the cardiac operation under CPB were collected .The adiponectin expres-sion in the myocardial tissue samples was detected by RT-PCR.The adiponectin important molecular pathways downstream AMP-activated protein kinase ( AMPK) activity was detected by Western blotting .The cardiac pathology was detected by HE staining method.Results Compared with the control group , adiponectin mRNA was significantly higher , and the level of downstream pathways AMPK phosphorylation was significantly lower in the treatment group (all P<0.01).Histopathol-ogy results complied with the appropriate cardiac function of myocardial performance .Conclusion The adiponectin levels in the tissues of patients with heart valve disease are significantly increased , but adiponectin receptor AMP-activated protein kinase ( AMPK) phosphorylation levels are decreased , thus adiponectin can not play the protective effect , and myocardial tissues of patients show adiponectin resistance .%目的：探讨心脏瓣膜病患者心肌组织脂联素抵抗及其相关机制。方法选择行体外循环下瓣膜置换手术的心脏瓣膜病患者36例为观察组，心脏移植捐献者及心脏外伤需手术患者22例为对照组。两组均手术中体外循环建立时剪除心肌组织，用RT-PCR法检测脂联素表达，Western Blot法检测脂联素下游通路重要分子腺苷酸活化蛋白激酶（ AMPK）活性，HE染色观察心肌组织病理情况。结果与对照组相比，观察组心肌组织脂联素mRNA表达显著升高，AMPK活性显著降低，P均＜0．05。心肌组织病理改变与相应心功能特点相符。结论心脏瓣膜病患者心肌组织脂联素水平显著升高，脂联素受体后AMPK磷酸化水平降低导致脂联素无法发挥正常的心肌保护效应，心脏瓣膜病患者的心肌组织出现脂联素抵抗。