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首页> 外文期刊>American Journal of Physiology >Cardioprotection by glucose-insulin-potassium: dependence on KATP channel opening and blood glucose concentration before ischemia.
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Cardioprotection by glucose-insulin-potassium: dependence on KATP channel opening and blood glucose concentration before ischemia.

机译：葡萄糖-胰岛素-钾的心脏保护作用：依赖于缺血前的KATP通道开放和血糖浓度。

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摘要

We tested the hypothesis that glucose-insulin-potassium (GIK)-induced protection against myocardial infarction depends on ATP-dependent K(+) (K(ATP)) channel activation and is abolished by hyperglycemia before the ischemia. Dogs were subjected to a 60-min coronary artery occlusion and 3-h reperfusion in the absence or presence of GIK (25% dextrose; 50 IU insulin/l; 80 mM/l KCl infused at 1.5 ml x kg(-1) x h(-1)) beginning 75 min before coronary artery occlusion or 5 min before reperfusion. The role of K(ATP) channels was evaluated by pretreatment with glyburide (0.1 mg/kg). The efficacy of GIK was investigated with increases in blood glucose (BG) concentrations to 300 or 600 mg/dl or experimental diabetes (alloxan/streptozotocin). Infarct size (IS) was 29 +/- 2% of the area at risk in control experiments. GIK decreased (P < 0.05) IS when administered beginning 5 min before reperfusion. This protective action was independent of BG (13 +/- 2 and 12 +/- 2% of area at risk; BG = 80 or 600 mg/dl, respectively) but was abolished in dogs receiving glyburide (30 +/- 4%), hyperglycemia before ischemia (27 +/- 4%), or diabetes (25 +/- 3%). IS was unchanged by GIK when administered before ischemia independent of BG (31 +/- 3, 27 +/- 2, and 35 +/- 3%; BG = 80, 300, and 600 mg/dl, respectively). The insulin component of GIK promotes cardioprotection by K(ATP) channel activation. However, glucose decreases K(ATP) channel activity, and this effect predominates when hyperglycemia is present before ischemia.
机译：我们测试了这一假设，即葡萄糖-胰岛素-钾（GIK）诱导的针对心肌梗塞的保护依赖于ATP依赖的K（+）（K（ATP））通道激活，并在缺血前被高血糖症所废除。在不存在或存在GIK（25％葡萄糖; 50 IU胰岛素/ l; 80 mM / l KCl以1.5 ml x kg（-1）xh输注）的情况下对狗进行60分钟的冠状动脉闭塞和3小时的再灌注（-1））在冠状动脉闭塞前75分钟或再灌注前5分钟开始。 K（ATP）通道的作用通过用格列本脲（0.1 mg / kg）预处理进行评估。通过将血糖（BG）浓度增加至300或600 mg / dl或实验性糖尿病（四氧嘧啶/链脲佐菌素）来研究GIK的疗效。在对照实验中，梗塞面积（IS）为危险区域的29 +/- 2％。当再灌注前5分钟开始给药时，GIK降低（P <0.05）IS。这种保护作用与BG无关（危险区域的13 +/- 2和12 +/- 2％; BG分别为80或600 mg / dl），但在接受格列本脲的狗中被取消（30 +/- 4％ ），缺血前的高血糖症（27 +/- 4％）或糖尿病（25 +/- 3％）。缺血前给予独立于BG的GIK可使IS不变（分别为31 +/- 3、27 +/- 2和35 +/- 3％; BG分别为80、300和600 mg / dl）。 GIK的胰岛素成分通过K（ATP）通道激活促进心脏保护作用。但是，葡萄糖会降低K（ATP）通道的活性，当缺血前存在高血糖时，这种作用占主导。

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