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目的:探讨灯盏花素联合缺血预适应对家兔心肌缺血再灌注损伤的保护作用和机制。方法:健康新西兰大白兔48只,随机分为:假手术组、缺血再灌注组、缺血预适应组、不同剂量灯盏花素预处理(10 mg/kg,5mg/kg,1 mg/kg)加预适应组,每组8只。于实验前、缺血40 min、再灌注180 min时记录左室收缩压、左室舒张压、左室内压变化的最大速率,并同时采血测定肌酸激酶(CK)、肌酸激酶同工酶(CK-MB);取缺血区心肌组织测定丙二醛(MDA)、超氧化物歧化酶(SOD)、一氧化氮(NO)含量。结果:不同剂量灯盏花素联合预处理组与缺血再灌注组比较能显著改善缺血再灌注损伤心肌心功能,抑制CK、CK-MB释放,增加心肌细胞SOD的活性及NO含量,降低MDA的含量(均P<0.01);中、高剂量灯盏花素组联合预处理组与单纯预适应组相比效果更加显著(P<0.01)。结论:灯盏花素预处理能加强缺血预适应对心肌缺血保护作用,其保护作用机制与增强清除氧自由基,抑制脂质过氧化及增加心肌组织NO含量有关。
Objective: To investigate the protective effect of breviscapine combined with ischemic preconditioning on myocardial ischemia-reperfusion injury in rabbits and its mechanism. METHODS: Forty-eight healthy New Zealand white rabbits were randomly divided into sham operation group, ischemia-reperfusion group, ischemic preconditioning group, and different doses of breviscapine pretreatment (10 mg/kg, 5 mg/kg, 1 mg/kg). ) Plus pre-conditioning group, 8 in each group. Left ventricular systolic blood pressure, left ventricular diastolic pressure, and left ventricular diastolic pressure were recorded before the experiment, 40 min ischemia, and 180 min reperfusion. The creatine kinase (CK) and creatine kinase isoenzymes were also measured at the same time. (CK-MB); myocardial tissue was measured in the ischemic area of malondialdehyde (MDA), superoxide dismutase (SOD), nitric oxide (NO) content. RESULTS: Different doses of breviscapine combined with pretreatment group and ischemia-reperfusion group significantly improved the cardiac function of ischemic reperfusion injury, inhibited the release of CK and CK-MB, increased the activity of SOD and the content of NO, and decreased the content of MDA in cardiomyocytes. The content of Pb (P<0.01) was more significant in the combined pretreatment group of the middle and high doses of breviscapine group than that of the simple preconditioning group (P<0.01). CONCLUSION: Breviscapine pretreatment can enhance the protective effect of ischemic preconditioning on myocardial ischemia, and its protective mechanism is related to enhancing scavenging of oxygen free radicals, inhibiting lipid peroxidation and increasing NO content in myocardial tissue.