摘要
目的 探讨肝素化剂量肝素对在体家兔短暂缺血 -再灌注顿抑心肌的功能的影响。方法 2 3只雄性家兔 ,分为实验 (A)组和对照 (B)组 ,建立在体心肌短暂缺血 (15min) -再灌注 (6 0min)损伤模型。A组于前降支阻断前 2 0min给予肝素 (70 0U/kg)。分别于给药前、缺血前、再灌注期间 ,检测 2组NO、ET 1、MDA、SOD水平 ,测定血流动力学指标变化 ,对心肌超微结构做定性观察。结果 A组在给药后 2 0min ,NO含量即较给药前明显升高 (P <0 0 5 ) ,且在整个再灌注期较B组有显著性差别 (P <0 0 5 ) ,心功能、超微结构明显改善。结论 肝素参与短暂缺血 -再灌注顿抑心肌功能的保护 ,机制可能是通过药物性预适应 ,增强内皮源性NO的产生 ,从而减轻心肌缺血 -再灌注损伤。
Objective: To investigate the role of heparin in modulating coronary endothelial function and stunning myocardium after brief ischemic-reperfusion (IR) injury, with an emphasis on defining the role of the nitrite oxide (NO). Methods: Twenty-three male rabbits were randomly divided into two groups. Group A (n=10), received heparin (700 U/kg), 20 minutes before ischemia. Group B (n=10), received physiological sodium chloride solution. The Hemodynamics index, NO, endothelin-1 (ET-1), superoxide dismutase (SOD), Malondialdehyde (MDA) and myocardial ultrastructure were measured after 15 minutes of regional ischemia of the left anterior descending artery (LAD) following by 60 minutes of reperfusion. Results: Cardial function and myocardial ultrastructure in group A were significantly better than those in group B, the lever of NO and SOD were higher, and ET-1 and MDA were lower in group A than that in group B during 60 minute reperfusion. Conclusions: These results suggest that heparin preserve the function of myocardium after brief IR injury, the mechanism in part by promoting the production of NO, preserving the endothelium function.
出处
《中华胸心血管外科杂志》
CSCD
北大核心
2002年第6期362-364,共3页
Chinese Journal of Thoracic and Cardiovascular Surgery
