【摘要】 目的探讨心肌细胞内三磷酸腺苷酶(ATPase)的变化在钝性胸部创伤(BCT)后心功能障碍发生机制中的意义。方法采用随机数字表法将36只兔分为6组:正常对照组(创伤前),伤后2h、4h、8h、12h和24h组,每组6只。用BIM-Ⅱ型生物撞击机建立BCT模型,经右颈总动脉插管至左心室测左室压力,在创伤后2h、4h、8h、12h和24h各时间点测定血流动力学指标和心肌匀浆组织、线粒体及胞浆内ATPase活性。结果与对照组比较,创伤后2h时2h组左心室收缩期末压(LVESP)、左心室内压最大上升速率(+dp/dtmax)、等容收缩压(IP)、实测心肌最大收缩速度(Vpm)明显下降(P<0.05),在伤后4～12h时4h组、8h组、12h组恢复至创伤前水平(P>0.05);等容舒张期左室内压下降时间常数(T)、左心室舒张期末压(LVEDP)、左室内压最大下降速率(-dp/dtmax)在伤后24h组与对照组比较差异有统计学意义(P<0.05,0.01)。伤后2h组、4h组心肌匀浆组织、线粒体及胞浆ATPase活性下降(P<0.05,0.01),分别至伤后8～12h时分别恢复至创伤前水平(P>0.05)。相关分析表明:LVEDP和-dp/dtmax与心肌匀浆组织Na+-K+-ATPase活性改变呈明显负相关(r=-0.674,-0.691,P<0.05),与Ca2+-ATPase活性改变呈明显负相关(r=-0.613,-0.642,P<0.05);与心肌细胞线粒体Na+-K+-ATPase活性改变呈明显负相关(r=-0.622,-0.616,P<0.05);与心肌细胞胞浆Ca2+-ATPase活性改变呈明显负相关(r=-0.672,-0.658,P<0.05),与心肌细胞胞浆Na+-K+-ATPase活性改变呈明显负相关(r=-0.627,-0.632,P<0.05),与心肌细胞胞浆Mg2+-ATPase活性改变呈明显负相关(r=-0.677,-0.661,P<0.05)。结论BCT后左心室收缩/舒张功能受到损害,尤以舒张功能障碍为主,心肌细胞中ATPase活性下降可能是其原因之一。更多还原

【Abstract】 Objective To investigate the changes and roles of myocardial adenosine triphosphate enzyme(ATPase) in the mechanism of cardiac dysfunction after blunt chest trauma(BCT).Methods Thirty-six rabbits were divided into 6 groups with random number table,control group,2 h group,4 h group,8 h group,12 h group and 24 h group,6 in each group.The models of BCT were established with BIM-Ⅱ biological impact machine,catheterization technique was used through the right jugular artery into the left ventricle measure its pressure.The hemodynamics and the activities of ATPase in myocardial cell plasm,homogenate and mitochondria were measured at pre-injury(control group),2 h,4 h,8 h,12 h and 24 h post-injury.Results Left ventricular end-systolic pressure(LVESP),the maximal ascending rate of left intraventricular pressure(+dp/dtmax),isovolemec pressure(IP) and the maximal physiological velocity(Vpm) decreased significantly at 2 h group after BCT(P<0.05),and recovered to pre-injury level in 4 h,8 h and 12 h group during 4-12 h after BCT;isovolumic relaxation phase left ventricular pressure descending time constant(T).Left ventricular end-diastolic pressure(LVEDP) and the maximal descending rate of left intraventricular pressure(-dp/dtmax) were significantly higher(P<0.05,0.01).The activity of ATPase in homogenate,mitochondria and cell plasm decreased significantly at 2 h group and 4 h group after BCT(P<0.05,0.01,respectively),and 8 h group and 12 h group recovered after BCT.There was negative correlations between LVEDP and-dp/dtmax and the decrease of the activity of Na+-K+-ATPase in homogenate(r=-0.674,-0.691,P<0.05),the Ca2+-ATPase in homogenate(r=-0.613,-0.642,P<0.05),the Na+-K+-ATPase in mitochondria(r=-0.622,-0.616,P<0.05),the Ca2+-ATPase in myocardial cell plasm(r=-0.672,-0.658,P<0.05),the Na+-K+-ATPase in myocardial cell plasm(r=-0.627,-0.632,P<0.05),and the Mg2+-ATPase in myocardial cell plasm(r=-0.677,-0.661,P<0.05).Conclusion The left ventricular function is impaired obviously after BCT,especially in diastolic phase.The decrease of the activity of ATPase in myocardial cells may be one of the reasons of cardiac dysfunction after BCT.更多还原