风湿性心脏病心肌细胞线粒体膜磷脂损伤与换瓣术后低心排血量的关系

Study on the relationship between myocytic mitochondrial membrane phospholipid injure of rheumatic heart disease and low cardiac output following cardiac valve replacement

目的 探讨风湿性心脏病心肌细胞线粒体膜磷脂损伤与换瓣术后低心排血量的关系。方法 将 2 0例风湿性二尖瓣替换患者按术后有无严重低心排血量分为正常心排血量组 (n =1 4)和低心排血量组 (n =6) ,另 8例健康意外脑死亡者心肌为正常对照组。应用电镜细胞化学法测定术前右房心肌细胞线粒体膜磷脂超微结构定位改变 ,同时测定术中再灌注 3～ 5min时全心肌氧摄取率 ,并定量分析上述指标变化与术后低心排血量的关系。结果 风湿性心脏病心肌细胞线粒体膜磷脂结构定位呈现不同程度的脱失改变。其中低心排血量组与正常心排血量组比较 ,心肌细胞线粒体膜磷脂结构小部分脱失 (7 5%± 2 6%vs 4 9%± 1 6% )和大部分脱失(4 5%± 2 0 %vs 2 6%± 1 7% )比率均明显增高 ,且再灌注 3～ 5min时全心肌氧摄取率 [(2 .30± 0 50 )Vol%vs(3.42± 0 .60 )Vol% ]明显降低 (P均 <0 0 5)。结论 风湿性心脏病心肌细胞线粒体膜磷脂结构定位脱失程度与换瓣术后低心排血量的发生密切相关 ,可能是参与术后低心排血量形成、发展的细胞基础之一。

Objective To explore the relationship between myocytic mitochondrial membrane phospholipid(mtMPL) injure of rheumatic heart disease and low cardiac output following cardiac valve replacement.Methods The myocytic mtMPL localization of right atrial muscles in 20 patients underwent rheumatic mitral valve replacement were quantitatively detected by modified Demers tricomplex flocculation,and oxygen extraction of global myocardium in 3～5 min reperfusion were measured by blood gas analysis.The extent of above mentioned parameters were analyzed by comparing normal cardiac output group and low cardiac output group.Results mtMPL localization of rheumatic heart disease presented diverse loss.In comparing low cardiac output group( n =6) and normal cardiac output group( n =14):mtMPL localization with partial loss(7.5±2.6)% vs (4.9±1.6)% and with most loss (4.5±2.0)% vs (2.6±1.7)% were markedly increased respectively( P <0.05),and oxygen extraction of global myocardium[(2.30±0.50)Vol% vs(3.42±0.60)Vol%, P <0.05] were significantly decreased in 3～5 min reperfusion.Conclusion The extent of myocytic mtMPL localization injure of rheumatic heart disease is closely associated with low cardiac output,and is probable cellular basis involving in the formation and development of low cardiac output following cardiac valve replacement.