Ethanol enhances the functional recovery of stunned myocardium independent of K(ATP) channels in dogs.

Ethanol enhances the functional recovery of stunned myocardium independent of K(ATP) channels in dogs.
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乙醇可增强犬心肌顿抑功能的恢复,与 K(ATP) 通道无关。

DOI:
10.1097/00000539-200102000-00003
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发表时间:
2001
影响因子:
5.7
通讯作者:
Pagel,PS
Pagel,PS
中科院分区:
医学2区
文献类型:
--
作者:
Gross,ER;Gare,M;Toller,WG;Kersten,JR;Warltier,DC;Pagel,PS

文献摘要

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长期、间歇性接触少量乙醇可减少体内心肌梗塞的面积。我们测试了这样的假设:急性给予乙醇可增强受损心肌的功能恢复,并且三磷酸腺苷依赖性钾 (K ATP) 通道介导这种有益作用。用巴比妥麻醉的狗用仪器测量主动脉和左心室压力、+ dP/dt max 和心内膜下节段缩短 (% SS),并进行 5 个 5 分钟的冠状动脉闭塞期,每个期间隔 5 分钟的再灌注,然后是 3 小时的最终再灌注。在四组中(每组 n = 7 只),狗在闭塞和再灌注之前以随机方式接受 0.9% 盐水或乙醇(0.25、0.5 或 1.0 g/kg,持续 30 分钟)。在其他组(每组 n = 7)中,狗在施用盐水或乙醇(0.25 g/kg)之前 30 分钟接受 K ATP 通道拮抗剂格列本脲(0.3 mg/kg,IV)。单独接受盐水或格列本脲的狗在再灌注期间表现出收缩功能恢复不良(3小时时%SS分别= 0.9%±2.0%和1.6%±1.2%)。接受 0.25 克/千克和 0.5 克/千克剂量乙醇的狗(3 小时分别为 10.0%±1.8% 和 8.6%±2.2%)的%SS 恢复得到增强,与血流动力学或冠状动脉侧支血流(放射性微球)的变化无关。格列本脲不影响乙醇产生的休克心肌恢复的改善(3小时11.8%±2.2%)。结果表明,乙醇在体内增强了不依赖于 K ATP 通道的顿顿心肌的功能恢复。 意义:少量乙醇可改善巴比妥麻醉犬缺血后再灌注心肌的功能恢复。这些有益作用与三磷酸腺苷依赖性钾通道无关。
Chronic, intermittent exposure to small amounts of ethanol reduces myocardial infarct size in vivo. We tested the hypothesis that acute administration of ethanol enhances the functional recovery of stunned myocardium and that adenosine triphosphate-dependent potassium (K ATP) channels mediate this beneficial effect. Barbiturate-anesthetized dogs were instrumented for measurement of aortic and left ventricular pressure,+ dP/dt max, and subendocardial segment shortening (% SS) and were subjected to five 5-min periods of coronary artery occlusion, each separated by 5 min of reperfusion followed by a 3-h final reperfusion. In four groups (n= 7 each), dogs received 0.9% saline or ethanol (0.25, 0.5, or 1.0 g/kg over 30 min) in a random manner before occlusions and reperfusions. In other groups (n= 7 each), dogs received the K ATP channel antagonist glyburide (0.3 mg/kg, IV) 30 min before saline or ethanol (0.25 g/kg) was administered. Dogs receiving saline or glyburide alone demonstrated poor recovery of contractile function during reperfusion (% SS= 0.9%±2.0% and 1.6%±1.2% at 3 h, respectively). Recovery of% SS was enhanced in dogs receiving the 0.25-and 0.5-g/kg doses of ethanol (10.0%±1.8% and 8.6%±2.2% at 3 h, respectively) independent of alterations in hemodynamics or coronary collateral blood flow (radioactive microspheres). Glyburide did not affect improvement of recovery of stunned myocardium produced by ethanol (11.8%±2.2% at 3 h). The results indicate that ethanol enhances the functional recovery of stunned myocardium independent of K ATP channels in vivo.ImplicationsSmall amounts of ethanol improve the functional recovery of postischemic, reperfused myocardium in barbiturate-anesthetized dogs. These beneficial effects are not related to adenosine triphosphate-dependent potassium channels.