DIRECT PROTECTIVE EFFECTS OF DEXMEDETOMIDINE AGAINST MYOCARDIAL ISCHEMIA-REPERFUSION INJURY IN ANESTHETIZED PIGS
DIRECT PROTECTIVE EFFECTS OF DEXMEDETOMIDINE AGAINST MYOCARDIAL ISCHEMIA-REPERFUSION INJURY IN ANESTHETIZED PIGS
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DOI：
10.1097/shk.0b013e318254d3fb
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发表时间：
2012-07-01
期刊：
影响因子：
3.1
通讯作者：
Sumikawa, Koji
中科院分区：
文献类型：
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作者：
Yoshitomi, Osamu;Cho, Sungsam;Sumikawa, Koji
全身给予α(2)-肾上腺素能激动剂已被证明可以保护缺血心肌，但对缺血再灌注心肌的直接影响尚未阐明。本研究旨在确定冠状动脉内右美托咪定（DEX）对麻醉猪心肌缺血再灌注损伤的影响。在开胸猪中，左冠状动脉前降支通过来自颈动脉的体外回路进行灌注。他们接受 DEX 冠状动脉内输注，剂量为 1 ng。 mL(-1)（LD 组，n = 9），10 ng。 mL(-1)（MD 组，n = 9）或 100 ng。缺血前 30 分钟的冠状动脉血流或载体（C 组，n = 12）mL(-1)（HD 组，n = 9）。左冠状动脉前降支灌注区缺血 12 分钟，再灌注 90 分钟，产生心肌顿抑。使用再灌注后室性心动过速或颤动的发生率来评估对再灌注引起的心律失常的影响。通过节段缩短（%SS）来评估区域心肌收缩力。右美托咪定显着降低再灌注引起的室性心律失常的发生率。右美托咪定显着改善再灌注后 90 分钟节段缩短百分比的恢复（C 组为 32.6% +/- 3.1%，LD 组为 58.2% +/- 2.1%，MD 组为 61.1% +/- 1.8%，HD 组为 72.0% +/- 2.0%）。右美托咪定抑制再灌注后血浆去甲肾上腺素浓度的增加。结果表明，DEX通过直接作用于心肌发挥对缺血再灌注损伤的保护作用，而不是通过中枢神经系统介导。
Systemic administration of alpha(2)-adrenergic agonists has been shown to protect ischemic myocardium, but the direct effects on ischemia-reperfused myocardium have not yet been clarified. This study was carried out to determine the effects of intracoronary dexmedetomidine (DEX) on the myocardial ischemia-reperfusion injury in anesthetized pigs. In open-chest pigs, the left anterior descending coronary artery was perfused through an extracorporeal circuit from the carotid artery. They received intracoronary infusion of DEX at a rate of 1 ng . mL(-1) (group LD, n = 9), 10 ng . mL(-1) (group MD, n = 9), or 100 ng . mL(-1) (group HD, n = 9) of coronary blood flow or vehicle (group C, n = 12) for 30 min before ischemia. Myocardial stunning was produced by 12-min ischemia of the perfused area of left anterior descending coronary artery and 90-min reperfusion. The effect on reperfusion-induced arrhythmias was evaluated using the incidence of ventricular tachycardia or fibrillation after reperfusion. Regional myocardial contractility was evaluated with segment shortening (%SS). Dexmedetomidine significantly reduced the incidence of reperfusion-induced ventricular arrhythmias. Dexmedetomidine significantly improved the recovery of percentage segment shortening at 90 min after reperfusion (32.6% +/- 3.1% in group C, 58.2% +/- 2.1% in group LD, 61.1% +/- 1.8% in group MD, and 72.0% +/- 2.0% in group HD). Dexmedetomidine suppressed the increase in plasma norepinephrine concentration after reperfusion. The results indicate that DEX would exert the protective effect against ischemia-reperfusion injury by the direct action on the myocardium, which is not mediated through the central nervous system.