摘要目的探讨心肌内质网Ca2＋调控蛋白表达与心肺复苏（CPR）后心功能障碍的关系。方法38只SPF级雄性SD大鼠按随机数字表法分为对照组（12只）和心搏骤停组（26只）。静脉弹丸式注射氯化钾40μg/g诱导心搏骤停，8 min后进行CPR；对照组大鼠仅麻醉后置管并监测指标，不诱导心搏骤停。在复苏后进行有创血流动力学监测1 h，采用超声心动图测定心功能。分别于自主循环恢复（ROSC）后5 min和60 min时采集心肌标本，采用蛋白质免疫印迹试验（Western Blot）检测内质网Ca2＋ATP酶（SERCA2a）、磷酸化受磷蛋白（p-PLB）和兰尼定受体（RyR）水平。结果心搏骤停组ROSC率为92.3%（24/26），平均复苏时间为（68±39）s。心搏骤停组复苏后1 h心功能明显下降，与对照组相比，射血分数、短轴缩短率（FS）、左室内压上升或下降最大速率（±dp/dt max）明显降低〔射血分数：0.548±0.060比0.809±0.043，F＝71.692，P＝0.000；FS：（34.4±4.4）%比（46.0±3.5）%，F＝55.443，P＝0.000；+dp/dt max （mmHg/s）：4718±743比7098±394，P＜0.01；-dp/dt max （mmHg/s）：-3824±612比-6187±473，P＜0.01〕。与对照组相比，心搏骤停组ROSC后5 min及60 min PLB磷酸化水平（灰度值）均显著降低（5 min：0.64±0.15比1.29±0.13，P＜0.01；60 min：0.95±0.08比1.30±0.09，P＜0.05），而内质网SERCA2a活性（灰度值）和RyR水平（灰度值）差异均无统计学意义（SERCA2a 5 min：1.01±0.18比1.24±0.07，60 min：1.03±0.14比1.25±0.06；RyR 5 min：0.96±0.13比0.97±0.13，60 min：0.88±0.14比0.99±0.11，均P＞0.05）。结论内质网PLB磷酸化水平异常与CPR后心功能障碍密切相关。

abstractsObjective To investigate the relationship between sarcoplasmic reticulum Ca2+modulation proteins and postresuscitation myocardial dysfunction. Methods Thirty-eight SPF male Sprague-Dawley (SD) rats were randomly divided into control group(n=12)and cardiac arrest(CA)group(n=26). CA was induced by intravenous bolus of potassium chloride(40μg/g),and cardiopulmonary resuscitation(CPR)was conducted 8 minutes later. No CA was induced in control group except catheter placement for monitoring cardiopulmonary parameters after anesthesia. Invasive hemodynamic parameters were monitored for 1 hour after CPR. Echocardiogram was performed to evaluate cardiac function. Myocardial samples were harvested 5 minutes and 1 hour after restoration of spontaneous circulation (ROSC),and sarcoplasmic reticulum Ca2+ ATPase (SERCA2a),phosphorylated phospholamban (p-PLB) and rynodine receptor(RyR)were determined by Western Blot. Results ROSC rate of CA group was 92.3%(24/26),and mean recovery time was (68 ±39)seconds. Cardiac function was significantly impaired in CA group at 1 hour after resuscitation, and ejection fraction, fraction shortening (FS), the maximal rate of left ventricular pressure increase/decline (±dp/dt max)were significantly decreased compared with those in control group 〔ejection fraction:0.548±0.060 vs. 0.809±0.043,F=71.692,P=0.000;FS:(34.4±4.4)%vs. (46.0±3.5)%,F=55.443,P=0.000;+dp/dt max(mmHg/s):4 718±743 vs. 7 098±394,P<0.01;-dp/dt max(mmHg/s):-3 824±612 vs.-6 187±473,P<0.01〕. Compared with control group,the expression levels of p-PLB (gray value)was significantly decreased at 5 minutes and 60 minutes(5 minutes:0.64±0.15 vs. 1.29±0.13,P<0.01;60 minutes:0.95±0.08 vs. 1.30±0.09,P<0.05)after resuscitation in CA group,while the level of sarcoplasmic SERCA2a(gray value)and RyR (gray value)showed no significant differences(SERCA2a 5 minutes:1.01±0.18 vs. 1.24±0.07,60 minutes:1.03± 0.14 vs. 1.25 ±0.06;RyR 5 minutes:0.96 ±0.13 vs. 0.97 ±0.13,60 minutes:0.88 ±0.14 vs. 0.99 ±0.11,all P>0.05). Conclusions The impairment of the p-PLB is closely related to postresuscitation myocardial dysfunction.