肝缺血再灌注损伤后电解质变化对心肌细胞超微结构的影响

Myocardial Morphologic Change after Hepatic Portal Occludion Ischema-Reperfusion Injury in the Rats

目的观察大鼠肝门阻断后缺血再灌注(IR)损伤对心肌细胞超微结构的影响。方法大鼠气管切开机械通气,监测肺动脉压(PAP)。72只大鼠随机分为对照组(A组)、肝血流阻断组(B组)及门静脉转流下肝血流阻断组(C组)。于IR前和IR后1,6 h取左心室前壁心肌组织数块。血气分析肝门阻断期间门脉血pH和电解质;光、电镜下观察心肌细胞形态学改变。结果与A组比较,B,C组IR后PAP显著升高(P<0.05),但C组较B组更快恢复至阻断前水平。肝门阻断期间,B组pH降低显著(P<0.05,);K+较IR前升幅超过1倍(P<0.01),IR后下降,但6 h时仍处于较高水平(P<0.05);Ca2+呈进行性下降。C组变化与A组比较差别无统计意义(P>0.05)。电镜观察,A组心肌细胞超微结构正常;B组心肌细胞6 h可见线粒体水肿,心肌肌丝断裂,细胞间隙增大,部分心肌细胞可见坏死区域,结构崩解;C组IR后部分心肌肌丝模糊,线粒体肿胀,心肌细胞局灶性坏死。结论肝门阻断后门脉内酸性物质和高钾血症直接抑制心肌收缩力,减少心排,肠道IR损伤是引起心肌细胞超微结构损害的主要因素。

Objective To investigate the myocardial morphologic changes after hepatic portal occlusion（HPO） ischema-reperfusion injury. Methods Rats were mechanical ventilated. The animals were randomly divided into 3 groups. （1）control group was sham-operated; （2）HPO group, the animals were subjected to reperfusion after 60 min hepatic portal occlusion;（3）bypass group, HPO 60 min while bypassed by caudal lobe. The animals in each group were killed before reperfusion and the end of reperfusion 60 or 360 min. The hemodynamics and portal vein blood gas analysis were measured, the myocardial cell morphology were studied by optics and electron microscopy. Results Hemodynamics data in both B,C groups showed low cardiac output during HPO phase, and pulmonary artery pressure（PAP） was higher than group A after reperfusion（P〈0.05）, but in group C the PAP return to baseline was faster than group B（P〈0.05）. Compared with groups A and C, the portal vein pH in group B decreased significantly during HPO but immedially return after reperfusion, simultaneously the K^＋ remarkablely increased and lasted to 6 h; the Ca^2＋ decreased gradually（P〈0.05）. The electron microscopy showed the myocardial morphology in group A was normal, group C appeared myofilament broken ,mitochondrium swelling, and some cell focus necrosis. Group B was serious than group C, such as mitochondrium edema, there were myofilament and muscle rod broken, cell spaces increasing, and local necrosis or disintegration. Conclusion The ischemia-reperfusion injury afer HPO may affected myocardial cell and inhibit cardiac contractibility. The interruption of bowel blood stream and reperfusion of intestinal metabolites may be the principal cause of myocardium damage.