摘要
目的探讨七氟醚是否可以减轻大鼠心脏骤停(CA)后心肌水肿及水通道蛋白1(AQP-1)的作用。方法窒息法建立心脏骤停模型。78只大鼠随机分为假手术组、七氟醚组和对照组,假手术组仅予麻醉及置管,七氟醚组在心肺复苏时予以1MAC七氟醚吸入5min,对照组进行常规心肺复苏。实验一:七氟醚组及对照组大鼠分别于造模前及自主循环恢复(ROSC)6h、12h、18h、24h五个时间点(每个时间点4只)分别处死取材测心肌含水量;实验二:假手术组、七氟醚组、对照组大鼠于造模前、ROSC1h、ROSC24h行心脏超声检查,并于ROSC24h处死(每组6只)测各组大鼠心肌AQP-1蛋白及mRNA表达量。结果ROSC后心肌含水量明显增加,但七氟醚组心肌含水量低于对照组(P〈0.05);ROSC 1h射血分数下降,但七氟醚组高于对照组(P〈0.05);ROSC24h室壁肥厚、左室容量下降,但七氟醚组室壁厚度小于对照组、左室容量高于对照组(P〈0.05);心脏骤停后心肌AQP-1蛋白及mRNA表达均下降,但七氟醚组高于对照组(P〈0.05)。结论七氟醚可以改善复苏后心功能不全,减轻心肌水肿,但APQ-1在缺血后心肌水肿形成与消退中的作用尚不完全明确。
Objective To investigate the effects of sevoflurane on myocardial edema after car- dio-pulmonary resuscitation (CPR) in rats and discuss the function of aquaporin-1 (AQP-1 ) in the formation and regression of myocardial edema. Methods The cardiac arrest model was established by induction of asphyxia. A total of 78 male Wistar rats were assigned to three groups randomly. Rats in the sham group were not induced to cardiac arrest. Rats in the sevo group inhaled 1MAC of sevoflurane during CPR. Rats in the control group operated the standard CPR. At first, the rats in the sevo group and control group were over anesthetic to death at baseline, ROSC 6 h, 12 h, 18 h, 24 h (each n = 4), for measurement of water content in myocardium. Thereafter, at baseline, ROSC 1 h, ROSC 24 h, the rats in these three groups received the echocardiography examination. At ROSC 24 h, the rats were over anesthetic to death, the hearts were removed to detect the expression of AQP- 1. Results After ROSC, the myocardial water content increased, which was lighter in the sevo group (P 〈 0.05). At ROSC 1 h, the EF was decreased, the sevo group had a higher EF than the control group (P 〈 0.05). At ROSC 24 h, the LVPW became thick and the EDV was decreased, the sevo group had a lighter thickness of LVPW and an enhanced EDV than the control group (P 〈 0.05). The expression of myocardial AQP- 1 in protein and mRNA was decreased, the sevo group had a higher expression than the control group (P〈 0.05). Conclusion Sevoflurane can improve myocardial function after ROSC, attenuate the myocardial edema. The role of AQP-1, in the formation and regression of myocardial edema, is not completely clear.
作者
李恒杰
魏红艳
卢远征
杨焰
黎博
毛慧
蔡文伟
廖晓星
Li Heng-jie Wei Hong-yan Lu Yuan-zheng Yang Yah Li Bo Mao Hui Cai Wen-wei Liao Xiao-xing(Zhejiang Province People's Hospital Emergency Department, Hangzhou 310014, China)
出处
《中国急救医学》
CAS
CSCD
北大核心
2017年第1期76-80,共5页
Chinese Journal of Critical Care Medicine
基金
国家自然科学基金(81372023)