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目的 研究batroxobin对狗缺血 /再灌心脏金属硫蛋白含量的影响 ,探讨其对缺血 /再灌损伤的保护机制。方法 结扎狗冠脉左前降支 ,30min后恢复血液灌注 ,造成缺血/再灌模型。于缺血前或缺血后再灌前 15min静脉注射ba troxobin ,分别于缺血前 ,缺血 30min及再灌后 90min ,以生理多道仪测定±dp/dtmax和LVEDP ,并取血测定肌酸磷酸激酶和乳酸脱氢酶浓度 ,测定心肌丙二醛含量及金属硫蛋白含量。结果 缺血 /再灌组动物心肌组织明显损伤 ,死亡率高达 6 5 %。缺血前或再灌前 15min应用batroxobin均显著增加金属硫蛋白含量 ,降低血浆肌酸磷酸激酶和乳酸脱氢酶含量及心肌丙二醛含量 ,增加±dp/dtmax,降低LEVDP ,减轻心肌组织损伤 ,降低动物死亡率。结论 batroxobin可明显增加金属硫蛋白含量 ,拮抗狗心脏缺血 /再灌损伤 ,改善心功能。
Objective To study the effect of batroxobin on the content of metallothionein in dogs with ischemia / reperfusion and the mechanism of its protection on ischemia / reperfusion injury. Methods Ligation of the left anterior descending coronary artery, 30min after the restoration of blood perfusion, resulting in ischemia / reperfusion model. Batroxobin was injected intravenously 15 min before ischemia or after reperfusion, ± dp / dtmax and LVEDP were measured by physiological multi-track before ischemia, 30min after ischemia and 90min after reperfusion. Acid phosphate kinase and lactate dehydrogenase concentration, myocardial MDA content and metallothionein content. Results Myocardial tissue of ischemic / reperfusion animals was obviously damaged with a mortality rate of 65%. Administration of batroxobin before ischemia or 15 min before reperfusion significantly increased the content of metallothionein, decreased plasma creatine phosphokinase and lactate dehydrogenase levels and myocardial MDA levels, increased ± dp / dtmax, decreased LEVDP, and decreased myocardial tissue injury , Reduce animal mortality. Conclusion batroxobin can significantly increase the content of metallothionein, antagonize the dog heart ischemia / reperfusion injury and improve cardiac function.