摘要
在在体猪模型上，于缺血１０分钟静脉推注维生素Ｃ（Ｖｉｔ．Ｃ０．２ｇ／ｋｇ），对缺血１小时和再灌注２小时的血液动力学指标无影响，但能使血清肌酸激酶同功酶再灌注后释放减少，而且用药组的最终心肌梗塞范围小于对照组。在在体兔缺血１小时和再灌注４小时模型上，光镜下可见用药组心肌出血程度较对照组轻，电镜下心肌毛细血管内皮细胞损伤轻于对照组。采用电子自旋共振波谱仪直接测定心肌自由基结果表明：Ｖｉｔ．Ｃ对于缺血１小时再灌注半小时氧自由基升高具有抑制作用，提示Ｖｉｔ．Ｃ的保护作用可能是通过清除氧自由基而发挥作用的。
Abstract To obtain the practical measure for the ischemia-reperfusion injury, we developed an open chest pig model(occlusion for 1 hour and reperfusion for 2 hours). Vitamin C(Vit C 0.2g/ kg)was intravenously given within five minutes to 8 pigs and 12 pigs received only saline as control. The results showed that there were no differences in the hemodynamic parameters, but the release of the creatine kinase isoenzyme after the reperfusion was significantly decreased in the vit C group (P<0.05-0.01), and the ratio of the infarct area and the risk area was 30.2% in the vit C group and 49.2% in controls respectively (P<0.05).Furthermore, the content of myocardial malondiadehyde was significantly decreased in the vit C group. In order to observe the protective effect of vitamin C we also developed an open chest rabbit model. After four-hour reperfusion, vit C group had less severe bleeding and milder damage to the capillary endothelium than that of control group. On the rabbit model,the myocardial free radicals were directly measured with the electron resonance spectrograph after one half hour reperfusion (P<0.05). It was found that the free radical content was significantly elevated in the control group (P < 0.05), vit C could inhibit such elevation (p < 0.01).So it was evident that the protection of vit C was directly related to scavenging the free radicals.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
1994年第1期52-54,共3页
Chinese Journal of Cardiology
