■本研究旨在探讨乳化异氟醚减轻心肌缺血再灌注损伤(MIRI)的作用机制。
■将48只健康雄性Sprague-Dawley大鼠随机分为4组(n=12)。假手术组(S组)和缺血再灌注组(I/R组),生理盐水(4ml/kg/h)静脉给药30分钟。在脂质内组(L组)中,静脉内施用脂质(4ml/kg/h)。乳化异氟醚组(EI组),乳化异氟醚(4ml/kg/h)静脉给药.然后在冲洗期间中断输注15分钟。除了S组,缺血是由于左前降支(LADA)闭塞30分钟而产生的。闭塞30分钟后,所有组接受再灌注2小时.
■肌酸激酶MB(CK-MB),心肌肌钙蛋白I(cTnI),肿瘤坏死因子-α(TNF-α),采用酶联免疫吸附试验(ELISA)检测白细胞介素-6(IL-6)。使用氯化三苯基四唑染色测量心肌梗塞的大小。根据结果,乳化异氟醚预处理可降低CK-MB和cTnI浓度(p<0.05)。乳化异氟醚组血清TNF-α、IL-6水平及梗死面积明显下降。与I/R组相比,EI组Toll样受体-4(TLR-4)mRNA的表达明显降低。
■乳化异氟醚预处理对心肌缺血再灌注损伤具有有效的心肌保护作用。其机制可能与TLR-4表达降低和炎症反应降低有关。
UNASSIGNED: This study aimed to investigate the mechanism of emulsified
isoflurane in reducing myocardial ischemia-reperfusion injury (MIRI).
UNASSIGNED: Forty-eight healthy male Sprague-Dawley rats were randomly divided into four groups (n = 12). In the sham group (group S) and ischemia-reperfusion group (group I/R), saline (4 ml/kg/h) was administered intravenously for 30 min. In intralipid group (group L), intralipid (4 ml/kg/h) was administered intravenously. In the emulsified
isoflurane group (group EI), emulsified
isoflurane (4 ml/kg/h) was administered intravenously. The infusion was then discontinued for 15 min during the washout period. Apart from group S, ischemia was produced by occlusion of the left anterior descending artery (LADA) for 30 min. After 30 min of occlusion, all groups received reperfusion for two hours.
UNASSIGNED: Creatine kinase MB (CK-MB), cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were measured by enzyme-linked immunosorbent assay (ELISA). Myocardial infarct size was measured using triphenyl tetrazolium chloride staining. According to the result, pretreatment with emulsified
isoflurane attenuated CK-MB and cTnI concentrations (p < 0.05). And serum TNF-α and IL-6 levels and infarct size in the emulsified
isoflurane group obviously decreased. An obvious decrease in the expression of the toll-like receptor-4 (TLR-4) mRNA in group EI was observed compared with group I/R.
UNASSIGNED: Emulsified
isoflurane precondition had a potent cardioprotective effect against myocardial ischemia-reperfusion injury. The mechanisms involved may be related to the decrease in the expression of TLR-4 and the reduced inflammatory response.