极化液给予时机对缺血/再灌注犬心脏功能及心肌损伤的影响(PDF)
《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]
- 期数:
- 2005年第5期
- 页码:
- 419-423
- 栏目:
- 基础研究
- 出版日期:
- 2005-10-05
文章信息/Info
- Title:
- Time of administering of glucoseinsulinpotassium cocktail on postischemic cardiac functional recovery and myocardial injury in dogs
- 作者:
- 张航向1; 臧益民1; 黄路3; 霍建华1; 王跃民1; 范谦1; 南 瑛1; 梁少君2; 高峰1
- 第四军医大学：1.生理学教研室，陕西 西安 710032, 2.唐都医院麻醉科，陕西 西安 710038；3. 浙江大学生命科学学院, 浙江 杭州 310012
- Author(s):
- ZHANG Hangxiang1; ZANG Yimin1; HUANG Lu3; HUO Jianhua1; WANG Yuemin1; FAN Qian1; NAN Ying1; LIANG Shaojun2; GAO Feng1
- Fourth Military Medical University: 1. Department of Physiology, Xi’an, Shaanxi 710032, China；2. Department of Anaesthesiology, Tangdu Hospital, Xi’an, Shaanxi 710032, China; 3. College of life sciences, Zhejiang University,Hangzhou,Zhejiang 310012,China
- 分类号:
- R331.31;R542.2
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 目的 探讨不同时间开始给予极化液（葡萄糖胰岛素钾液，GIK）对犬心肌缺血/ 再灌注(MI/R) 后心脏功能及心肌细胞损伤的影响。方法 制备犬MI/ R模型，心肌定量缺血(左前降支血流量降低80%)50 min，再灌注4 h。分别于:①再灌注前30 min（再灌注前）、②再灌注即刻（再灌注时）、③再灌注后1 h（再灌注后）给予GIK。观察对动脉血压、心率、左室压的影响及测定心大静脉血清乳酸脱氢酶(LDH)、肌酸激酶(CK)活性，再灌注结束后检测心肌梗死率或细胞凋亡指数。结果 与再灌注后组相比，再灌注前组和再灌注时组可明显改善再灌注后左室收缩及舒张功能，降低血清CK、LDH活性，减少心肌梗死范围［分别为（5.9±1.1）%和（5.2±0.8）% vs （9.1±1.2）%，均P<0.01］、抑制心肌细胞凋亡的发生［（4.6±0.9）% 和（3.7±1.1 ）% vs （8.9±2.3）%，均P<0.05］。结论 再灌注早期给予GIK可降低MI/R引起的心肌细胞损伤，促进再灌注后心脏功能的恢复，在再灌注后1 h给予GIK对心脏的上述保护作用则明显减弱。
- Abstract:
- AIM To investigate whether glucoseinsulinpotassium (GIK) cocktail given at different occasion will influence the effects of GIK on cardiac myocyte injury and cardiac functional recovery following myocardial ischemia/ reperfusion (MI/R). METHODS The left anterior descending coronary artery was partially occluded (80% reduction in blood flow) in anesthetized openchest dogs, and then dog was subjected to 50 min myocardial ischemia followed by reperfusion for 4 h. GIK (glucose: 250 g/L, insulin: 60 U/L, potassium: 80 mmol/L, infused at 2 ml/kg·h, i.v.) was randomly given began at 30 min before reperfusion (PreR), the beginning of reperfusion (Rep), 1 h after reperfusion (R1 h) and continuing through the 4 h reperfusion. Arterial blood pressure and left ventricular pressure were monitored throughout the experiment. The activities of CK and LDH were assayed spectrophotometrically. Myocardial infarction and cardiac myocyte apoptosis were determined at the end of reperfusion. RESULTS MI/R caused significant cardiac dysfunction and myocardial damage (both necrosis and apoptosis). Compared with the R1 h group, the PreR and Rep groups showed cardiac protection against MI/R as evidenced by the improved recovery of cardiac systolic/ diastolic function, significant decrease of serum creatine kinase(CK) and lactate dehydrogenase(LDH), reduced myocardial infarction［(5.9±1.1)%, (5.2±0.8)% vs (9.1±1.2)% of R-1 h，P<0.05］, decreased apoptosis index［(4.6±0.9)%, (3.7±1.1)% vs (8.9±2.3)% of R1 h，P<0.05］at the end of reperfusion. CONCLUSION GIK exerts by improving cardiac functional recovery and reducing myocardial injury, where as the cardioprotective effect is significantly attenuated when GIK was given 1 h after reperfusion.
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备注/Memo
- 备注/Memo:
- 收稿日期：2004-12-31.
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