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Zhonghua Wei Zhong Bing Ji Jiu Yi Xue · Oct 2014
[The relationship between sarcoplasmic reticulum Ca(2+) modulation proteins and postresuscitation myocardial dysfunction].
- Yu Huang and Qing He.
- 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: 123hq@163.com.
- Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2014 Oct 1;26(10):697-700.
ObjectiveTo investigate the relationship between sarcoplasmic reticulum Ca²⁺ modulation proteins and postresuscitation myocardial dysfunction.MethodsThirty-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.ResultsROSC 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).ConclusionsThe impairment of the p-PLB is closely related to postresuscitation myocardial dysfunction.
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