Effect of ulinastatin on endoplasmic reticulum stress in cardiomyocytes of patients undergoing beat-ing heart mitral valve replacement
10.3760∕cma.j.issn.0254-1416.2017.11.003
- VernacularTitle:乌司他丁对心脏不停跳二尖瓣置换术患者心肌内质网应激的影响
- Author:
Xiongfei RONG
1
;
Zhibin LANG
;
Yali YANG
;
Fanmin MENG
;
Jiaqiang ZHANG
Author Information
1. 450003,河南省人民医院(郑州大学人民医院)麻醉科
- Keywords:
Trypsin inhibitors;
Cardiopulmonary bypass;
Heart valve prosthesis implantation;
Endoplasmic reticulum;
Stress
- From:
Chinese Journal of Anesthesiology
2017;37(11):1291-1295
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of ulinastatin on endoplasmic reticulum stress in car-diomyocytes of patients undergoing beating heart mitral valve replacement(MVR). Methods A total of 80 patients of both sexes with rheumatic heart disease complicated with mitral valve stenosis, aged 38-59 yr, weighing 43-73 kg, with American Society of Anesthesiology physical statusⅡorⅢ, scheduled for elective MVR, were divided into ulinastatin group(UTI group, n=40)and normal saline group(NS group, n=40) using a random number table. Immediately after opening the right atrium(T0), at 30 min of cardiopulmonary bypass(T1)and while suturing the right atrium(T2), blood samples from the radial artery were collected to determine the concentrations of plasma creatine kinase-MB and cardiac troponin T by enzyme-linked immu-nosorbent assay, and the right auricle specimens were collected for determination of the expression of glucose-regulated protein 78, CCAAT∕enhancer-binding protein homologous protein, c-Jun amino-terminal kinase (JNK)protein and mRNA(by real-time polymerase chain reaction or Western blot)and phosphorylated JNK (p-JNK)expression(by Western blot). The apoptosis in cardiomyocytes was detected by TUNEL at T0,2, and the apoptosis rate was calculated. Results Compared with group NS, the concentrations of plasma crea-tine kinase-MB and cardiac troponin T at T1,2and the apoptosis rate of cardiomyocytes were significantly de-creased at T2, and the expression of glucose-regulated protein 78, CCAAT∕enhancer-binding protein homolo-gous protein and JNK protein and mRNA and p-JNK was down-regulated at T1,2in group UTI(P<0.05). Conclusion The mechanism by which ulinastatin reduces myocardial damage is related to inhibiting endo-plasmic reticulum stress in cardiomyocytes of patients undergoing beating heart MVR.
