[肌浆网钙离子调节蛋白与复苏后心肌功能障碍的关系]
[The relationship between sarcoplasmic reticulum Ca(2+) modulation proteins and postresuscitation myocardial dysfunction].
作者信息
Huang Yu, He Qing
机构信息
Department of Critical Care Medicine, the Third People's Hospital of Chengdu/Second Affiliated Hospital of Chengdu, Chongqing Medical University, Chengdu 610031, Sichuan, China, Corresponding author: He Qing, Email:
出版信息
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2014 Oct;26(10):697-700. doi: 10.3760/cma.j.issn.2095-4352.2014.10.003.
OBJECTIVE
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 (40 μg/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 ± 43 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.
目的
探讨肌浆网Ca²⁺调节蛋白与复苏后心肌功能障碍之间的关系。
方法
将38只SPF级雄性Sprague-Dawley（SD）大鼠随机分为对照组（n = 12）和心脏骤停（CA）组（n = 26）。通过静脉推注氯化钾（40 μg/g）诱导心脏骤停，8分钟后进行心肺复苏（CPR）。对照组除在麻醉后放置导管监测心肺参数外，未诱导心脏骤停。心肺复苏后监测有创血流动力学参数1小时。进行超声心动图评估心脏功能。在自主循环恢复（ROSC）后5分钟和1小时采集心肌样本，通过蛋白质免疫印迹法测定肌浆网Ca²⁺ATP酶（SERCA2a）、磷酸化受磷蛋白（p-PLB）和兰尼碱受体（RyR）。
结果
CA组自主循环恢复率为92.3%（24/26），平均恢复时间为（68±39）秒。复苏后1小时，CA组心脏功能明显受损，与对照组相比，射血分数、缩短分数（FS）、左心室压力上升/下降最大速率（±dp/dt max）明显降低[射血分数：0.548±0.060对0.809±0.043，F = 71.692，P = 0.000；FS：（34.4±4.4）%对（46.0±3.5）%，F = 55.443，P = 0.000；+dp/dt max（mmHg/s）：4 718±43对7 098±394，P<0.01；-dp/dt max（mmHg/s）：-3 824±612对-6 187±473，P<0.01]。与对照组相比，CA组复苏后5分钟和60分钟时p-PLB的表达水平（灰度值）明显降低（5分钟：0.64±0.15对1.29±0.13，P<0.01；60分钟：0.95±0.08对1.30±0.09，P<0.05），而肌浆网SERCA2a（灰度值）和RyR（灰度值）水平无明显差异（SERCA2a 5分钟：1.01±0.18对1.24±0.07，60分钟：1.03±0.14对1.25±0.06；RyR 5分钟：0.96±0.13对0.97±0.13，60分钟：0.88±0.14对0.99±0.11，均P>0.05）。
结论
p-PLB的损伤与复苏后心肌功能障碍密切相关。
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