心肺复苏后大鼠肾脏损伤的实验研究

目的 观察心肺复苏（CPR）后大鼠肾小管上皮细胞损伤情况并研究其可能机制。方法 采用窒息（琥珀酰胆碱）并冰氧化钾停跳液致大鼠心跳骤停，5min后开始CPR的动物模型．健康Sprague Dawley雄性大鼠48只，随机分为6组：对照组（假手术组）及复苏后3,6、12、24、48h组，每组8只。采用酶法测定对照组及复苏后3、6、12、24、48h大鼠血清中BUN、Cr的浓度；采用透射电镜观察肾小管上皮细胞的损伤情况；采用比色法测定肾脏组织丙二醛（MDA）含量及超氧化物歧化酶（SOD）、Na^＋-K^＋-ATP酶活力。结果 复苏后3h血清中BUN、Cr浓度开始升高，随后持续升高，至24h达峰值。复苏后各组肾脏组织中MDA含量较对照组显著升高（P〈0.01），同时，SOD及Na^＋-K^＋-ATP酶活力显著降低（P〈0．01）；透射电镜下可见复苏后大鼠肾小管上皮细胞损伤表现。结论 心跳骤停及CPR后大鼠存在急性肾小管上皮细胞损伤；氧自由基（OFR）介导的脂质过氧化损伤、细胞能量代谢障碍在复苏后肾小管上皮细胞损伤中起着重要作用，肾小管上皮细胞损伤是CPR后大鼠急性肾功能衰竭的重要机制之一。

Experimental study on mechanism of kidney injury after cardiopulmonary resuscitation in rats

Objective To investigate the mechanism of renal tubule epithelium injury after cardiopulmonary resuscitation(CPR) in rats using the Sprague Dawley rat model of cardial arrest(CA) and CPR induced by asphyxiation combined with iced KCl.Methods CA was induced by asphyxiation(succinylcholine) and ice-cold 0.5 mol/L KCl in rats and resuscitation began five minutes later.In this experiment,48 male SD rats were randomized into six groups: control group(sham),postresuscitation 3,6,12,24,48 h groups(n=8,per group).Except control group,rats were allowed to reperfuse spontaneously for 3 hours,6 hours,12 hours,24 hours,48 hours after CPR.Blood urea nitrogen(BUN) and creatinine(Cr) were quantitized of each groups respectively.And using the chromametery,the quantity of maleic dialdehyde(MDA) and enzyme activity of superoxide dismutase(SOD) and Na~+-K~+-ATPase in renal tissues were analyzed of the control group and postresuscitation groups.Result Three hours after resuscitation,the serum concentration of BUN,Cr began to increase and remain in higher level,leading to peak elevations 24 h post-ischemia.Under TEM,injury of renal tubule epithelium could be observed in post-resuscitation rats.After CPR,quantity of MDA increased greatly(P<0.05),meanwhile,enzyme activity of SOD and Na~+-K~+-ATPase in kidney declined significantly compared to the control group(P<0.05).Conclusions Acute renal tubule epithelium injury happened in rats after CPR.OFR-triggered lipid peroxidation,cellular energy metabolism disturbance and apoptosis may be principal manifestation of renal tubule epithelium injury in post-resuscitation rats.renal tubule epithelium injury could also be a important factor of acute renal failure after resuscitation.