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葡萄糖胰岛素钾液对缺血/再灌注心肌的保护作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2005年第4期
页码:
345-348,352
栏目:
基础研究
出版日期:
2005-09-05

文章信息/Info

Title:
Protective effects of glucoseinsulinpotassium on ischemicreperfused canine heart
作者:
霍建华1; 张航向2; 苏慧2; 张海锋1; 梁少君3; 王跃民1; 高峰1; 4
1. 第四军医大学生理学教研室，陕西 西安 710032；2. 第四军医大学西京医院老年病科；3. 第四军医大学唐都医院麻醉科；4. 北京大学分子医学研究所，北京 100871
Author(s):
HUO Jianhua1;  ZHANG Hangxiang2; SU Hui2;  ZHANG Haifeng1;  LIANG Shaojun3;  WANG Yuemin1;  GAO Feng1;  4
1. Department of Physiology ; 2. Department of Gerontology, Xijing Hospital; 3. Department of Anesthesiology, Tangdu Hospital, Fourth Military Medical University， Xi′an，Shaanxi 710032，China; 4. Molecular Medical Institute of Peking University, Beijing, 1
关键词:
胰岛素; 缺血/再灌注; 心肌梗塞; 冠脉血流量; 犬
Keywords:
insulin;  ischemia/reperfusion;  myocardial infarction;  coronary blood flow;  dogs
分类号:
Q463；R331
DOI:
-
文献标识码:
A
摘要:
目的 观察极化液(葡萄糖胰岛素钾液，GIK)对急性心肌缺血/再灌注(MI/R) 犬心脏功能、冠脉血流量及心肌损伤的影响，分析胰岛素在GIK上述效应中的作用。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。24只杂种犬随机分为GIK、葡萄糖钾液（GK）和盐水对照组（n=8/组），再灌注前5 min输注GIK、GK、生理盐水。观察冠脉血流量及血流动力学指标；检测不同时间血清乳酸脱氢酶(LDH)、肌酸激酶(CK)活性；再灌注4 h后测量并计算心肌梗死范围。结果 与盐水对照组相比，GIK明显增加左前降支冠脉血流量（CBFLAD），改善再灌注后左室收缩及舒张功能，降低血清CK、LDH，减少心肌梗死范围，而GK无上述作用。结论 再灌注时输注GIK可促进再灌注心脏功能恢复及减轻心肌损伤，该作用可能与GIK增加冠脉血流量有关；胰岛素是GIK上述作用的关键成分。
Abstract:
AIM To study the effects of glucoseinsulinpotassium (GIK) on coronary blood flow (CBF), cardiac functional recovery and myocardial injury following acute myocardial ischemia/reperfusion (MI/R), and analyze the role of insulin in the cardioprotective effects of GIK. METHODS In anesthetized openchest dogs, the left anterior descending coronary artery (LAD) was partially occluded (80% reduction in its blood flow) for 50 min and reperfused for 4 h. Dogs were randomly divided into three groups: GIK, GK and Saline. All treatments were given beginning at 5 min before the reperfusion (infused at 2 ml·kg-1·h-1, i.v.) and continuing during the 4 h reperfusion. Arterial blood pressure, ECG, CBF and left ventricular pressure were monitored. The activities of CK and LDH were assayed spectrophotometrically. Myocardial infarction was determined by Evans blueTTC double staining at the end of the reperfusion. RESULTS During the reperfusion, compared with the saline group, GIK increased the CBFLAD of the dogs treated at the end of the reperfusion, P<0.05, improved recovery of LVSP and ±LVdp/dtmax. In addition, GIKtreated dogs showed protection against MI/R as evidenced by significant decreases in serum CK and LDH, and reduced myocardial infarction, while GK failed to show any significant cardioprotection against MI/R injury. CONCLUSION GIK exerts cardioprotective effects by improving cardiac functional recovery and reducing myocardial injury during reperfusion, which may be partly attributable to the increased coronary blood flow elicited by GIK infusion. Insulin plays a leading role in the aforementioned actions of GIK.

参考文献/References

［1］ Diaz R, Paolasso EA, Piegas LS, et al. Metabolic modulation of acute myocardial infarction: the ECLA glucoseinsulinpotassium pilot trial［J］. Circulation, 1998, 98: 2227-2234.

［2］ Gao F, Gao E, Yue TL, et al. Nitric oxide mediates the antiapoptotic effect of insulin in myocardial ischemia/reperfusion: the roles of PI3kinase, Akt, and endothelial nitric oxide synthase phosphorylation［J］. Circulation, 2002, 105: 1497-1502.

［3］ 许俊堂, 胡大一. 对急性冠状动脉综合征分型的看法［J］. 中华心血管病杂志, 2001, 29: 566568.

［4］ Scarabelli T, Stephanou A, Rayment N, et al. Apoptosis of endothelial cells precedes myocyte cell apoptosis in ischemia/reperfusion injury［J］. Circulation, 2001, 104: 253-256.

［5］ Gao F, Ma H, Huo JH, et al. Insulin preserves endothelialdependent coronary function in a canine mode of myocardial ischemia and reperfusion (Abstract)［J］. J Mol Cell Cardiol, 2004, 37: 283.

［6］ Taegtmeyer H, Goodwin GW, Doenst T, et al. Substrate metabolism as a determinant for postischemic functional recovery of the heart［J］. Am J Cardiol, 1997, 80: 3A-10A.

［7］ Kragelund C, Snorgaard O, Kober L, et al. Hyperinsulinaemia is associated with increased longterm mortality following acute myocardial infarction in nondiabetic patients［J］. Eur Heart J, 2004, 21:1891-1897.

［8］ Gao F, Tao L, Yan W, et al. Early antiapoptosis treatment reduces myocardial infarct size after a prolonged reperfusion［J］. Apoptosis, 2004, 9: 553-559.

备注/Memo

备注/Memo:
收稿日期：2005-03-17.基金项目：国家自然科学基金资助项目（No.30370525，No.30471923）
更新日期/Last Update: 2010-01-05