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作 者:黄风怡[1] 吴晓丹[1] 郑晓春[1] 陈彦青[1]
出 处:《临床麻醉学杂志》2007年第6期491-493,共3页Journal of Clinical Anesthesiology
基 金:福建省自然科学基金资助项目(编号:C0310031)
摘 要:目的观察肝门阻断再灌注后血流动力学和心肌能量代谢改变。方法大鼠气管切开机械通气。随机分为假手术对照组(A组,n=24):不作肝血流的阻断;肝血流阻断组(B组,n=24):阻断肝十二指肠韧带60min后开放再灌注;门静脉转流下肝血流阻断组(C组,n=24):分别阻断肝左中叶及右叶肝蒂,保留尾叶血供作为门静脉血液回流通道,60min后再灌注。每组各有8只大鼠分别于再灌注前、再灌注后1、6h取材。血气分析研究肝门阻断期间门脉中pH值和电解质变化、ELISA检测脑钠素(BNP)水平以及比色法测定心肌细胞膜Na+-K+ATPase活性。结果与A组比较,B组再灌注前pH值显著降低,K+升高幅超过1倍(P<0.01),再灌注后开始下降,Ca2+也进行性下降;同时再灌注后B组肺动脉压(PAP)显著升高,6h后仍不能恢复;B组BNP再灌注后高于A组(P<0.05),但组内比较差异无统计学意义;再灌注后B组心肌Na+-K+ATPase活性显著降低(P<0.01)。结论肝门阻断后再灌注可引起脑钠素和心肌细胞膜Na+-K+ATPase活性改变。Objective To investigate the change of myocardial cellular membrane Na^+-K^+ ATPase and BNP after reperfusion in the rats after hepatic portal occludion (HPO). Methods Anesthetized SD rats were mechanical ventilated. HPO model was produced by occluding the hepatic portal for I h with a clip and and followed by I h or 6 h reperfusion. The bypass model was produced by occluding the hepatic stem of left middle lobe and right lobe(selecting caudal lobe as the bypass pathway). The animals were randomly divided into 3 groups with 24 animals each:Sham group(A), HPO group(B) and HPO+bypass group(C), were included. The hemodynamics, portal vein blood gas analysis, myocardial cellular membrane Na^+-K^+ ATPase and BNP were measured before reperfusion,at 1 h and 6h after reperfusion. Results Compared with group A,PAP in groups B and C was higher after reperfusion(P〈0.05). The portal vein pH in group B decreased significantly during HPO, but immedially returned after reperfusion. The ATPase was inhibited and BNP increased after reperfusion in group C, which was less than those in group B(P〈 0. 01). Conclusion HPO may impair the myocardial cell energy metabolism and increase BNP.
关 键 词:肝脏 再灌注损伤 脑钠素 Na^+-K^+ATPase
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