摘要
据报道,心肌缺血——再灌损伤的机制与活性氧自由基的产生紧切相关,在大鼠心脏产生氧自由基是以黄嘌呤氧化酶(XO)途径为主.心肌中的黄嘌呤脱氢酶(XD)在Ca^(2+)激活水解酶的作用下向XD转化.而此我们设想,协同使用钙拮抗剂与超氧阴离子(O_2~1)清除剂(超氧化物歧化酶,SOD)可能加强对心肌的保护作用.本实验用电子自旋共振波谱仪(ESR)直接检测大鼠缺血——再灌心肌产生的活性氧自由基,从心脏收缩幅度,静息张力,肌酸激酶(CK)释放和心肌组织丙二醛(MDA)为指标,观察钙拮抗剂硫氮(艹卓)酮(DTZ)和SOD的分别作用和联合作用,发现两药合用可明显减少心肌活性氧自由基的产生.
The purpose of this study was to use a direct method-electron spin reso-nance (ESR) spectroscopy to demonstrate the early post-ischemic reperfusion induced enhance of oxygen free radicals. The results showed that the isolated perfused rat heart subjected to 30-minute ischemia followed by 15-second reperfusion revealed a significant increase of oxygen free radicals production in myocardium, compared with 30-minute ischemia group and 30-minutes nor-mal aerobic group. It is featured by a higher ratio of signal 0 (g = 2.026) and signal S (g = 2.004) of ESR spectra (O/S ratio) in reperfusion group (0.47±0.03) than that in ischemia group (0.29 ± 0.04, P<0.01) and normal group(0.34±0.04> P<0.05), respectcAelg SOD(140μ/ml) added to the perfusate 10 minutes prior to ischemia and during reper-fusion significantly decreased the O/S ratio to 0.35±0.04(P<0.05). Combined use of SOD and diltiazem (2.5 × 10-6M) significantly reduced the O/S ratio to 0.26±0.006 (P<0.01). The post-ischemic reperfusion also induced decrease of myocardial contraction and increase of resting tension and creatine kinase release. Diltiazem sig-nifecantly inhibited the rise of resting tension and creatine kinase release.These results indicate that more oxygen free radicals are produced in the early period of reperfusion. The mechanisms of generation of oxygen free radicals are discussed.
出处
《生物物理学报》
CAS
CSCD
北大核心
1990年第3期327-331,共5页
Acta Biophysica Sinica
