Myocardial protective effect of propofol postconditioning in renal hypertensive rats

税春玲; 杨建平; 唐佩灵; 江伟; 杨柳

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Myocardial protective effect of propofol postconditioning in renal hypertensive rats

更新时间：2026-01-09

- Myocardial protective effect of propofol postconditioning in renal hypertensive rats
- Journal of Army Medical University Vol. 38, Issue 6, Pages: 609-613(2016)
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  CLC： R322.11;R544.1;R971.2
- Published：2016
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税春玲,杨建平,唐佩灵,江伟,杨柳.丙泊酚后处理对肾性高血压大鼠心肌的保护作用[J].陆军军医大学学报(原第三军医大学学报),2016,38(06):609-613.

　Shui Chunling,Yang Jianping,Tang Peiling,Jian Wei,Yang Liu.Myocardial protective effect of propofol postconditioning in renal hypertensive rats[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(06):609-613.
税春玲,杨建平,唐佩灵,江伟,杨柳.丙泊酚后处理对肾性高血压大鼠心肌的保护作用[J].陆军军医大学学报(原第三军医大学学报),2016,38(06):609-613. DOI：

　Shui Chunling,Yang Jianping,Tang Peiling,Jian Wei,Yang Liu.Myocardial protective effect of propofol postconditioning in renal hypertensive rats[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(06):609-613. DOI：

摘要

目的探讨丙泊酚后处理对肾性高血压大鼠（renal hypertensive rats，RHR）的心肌保护作用，并探讨其可能的机制。方法健康成年雄性SD大鼠采用“两肾一夹”法制备肾性高血压大鼠模型，在此模型基础上制备结扎RHR左冠状动脉前降支30 min、再灌注60 min的急性心肌缺血再灌注损伤模型。将24只RHR按照随机数字表法分为3组（n=8）：缺血再灌注组（I/R组）、丙泊酚组（P组）、丙泊酚+苍术苷（ATR）组（PA组）。3组分别于再灌注同时通过尾静脉缓慢注入生理盐水1.5 mL（I/R组）或丙泊酚（2 mg/kg）（P组）或丙泊酚（2 mg/kg）+ 苍术苷（Atractyloside，ATR）（5 mg/kg ）（PA组），然后再灌注至60 min。记录左冠状动脉结扎前（T0）、结扎后15 min（T1）、结扎后30 min（T2）、再灌注15 min（T3）、再灌注30 mim（T4）、再灌注60 min（T5）时收缩压（SBP）、舒张压（DBP）和心率（HR）。电子显微镜下观察再灌注60 min时的心肌细胞超微结构的改变情况，TUNEL法检测细胞凋亡。结果再灌注15 min和30 min时P组的SBP和DBP较I/R组和PA组高（P0.05）。电子显微镜观察再灌注60 min后的心肌细胞超微结构，P组心肌细胞线粒体膜轻度水肿，而I/R组和PA组心肌细胞线粒体肿胀明显，数量减少。P组的心肌细胞凋亡指数（apoptosis index，AI）[(16±4) %]低于I/R组[(48±5)%]和 PA组[(38±8)%]，差异有统计学意义（P0.05）。结论丙泊酚后处理对RHR大鼠心肌缺血再灌组损伤具有保护作用，其机制可能与抑制线粒体通透性转换有关。

Abstract

Objective To investigate the protective effect of propofol postconditioning on myocardial ischemia-reperfusion (I/R) injury in renal hypertensive rats (RHR) and possible mechanism. Methods Renal hypertensive model was induced in adult male Sprague-Dawley (SD) rats with two-kidney one-clip method

and cardiac I/R injury was established by ligaturing left anterior descending (LAD) coronary artery for 30 min and then reperfusing for 60 min. Twenty-four RHR were randomly divided into 3 groups (n=8): I/R group

propofol group (P group) and propofol+atractyloside group (PA group). Normal saline 1.5 mL (I/R group)

propofol 2 mg/kg (P group)

and propofol 2 mg/kg and atractyloside 5 mg/kg (PA group) were intravenously infused at the beginning of reperfusion (propofol and atractyloside diluted to 1.5 mL with normal saline equally). Systolic blood pressure (SBP)

diastolic blood pressure (DBP) and heart rate (HR) were recorded before ligaturing LAD coronary artery (T0)

at 15 min (T1) and 30 min (T2) after ligaturing LAD coronary artery

and at 15 min (T3)

30 min (T4) and 60 min (T5) of reperfusion

respectively. Morphologic change of myocardial cells was observed with an electron microscope at 60 min of reperfusion. Apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay at 60 min of reperfusion. Results SBP and DBP of the P group were higher than those of the PA group and I/R group (P0.05) at T3 and T4. Microscopic observation showed the majority of myocardial cells were intact and mitochondria were moderately swollen at 60 min of reperfusion in the P group. The I/R group and PA group showed obvious mitochondrial swelling

disorganized cristae

and vacuolation at 60 min of reperfusion. The apoptosis index [(16±4)%] of myocardial cells in the P group was decreased compared with that [(48±5)%] of the I/R group and that [(38±8)%] of the PA group (P0.05). Conclusion Propofol postconditioning effectively protects the RHR against I/R injury by inhibition of mitochondrial permeability transition pore during the early reperfusion.

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