The effects of dexmedetomidine on left ventricular function during hypoxia and reoxygenation in isolated rat hearts
The effects of dexmedetomidine on left ventricular function during hypoxia and reoxygenation in isolated rat hearts
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DOI：
10.1213/01.ane.0000145065.20816.b5
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发表时间：
2005-03-01
影响因子：
5.7
通讯作者：
Sumikawa, K
中科院分区：
文献类型：
--
作者：
Guo, H;Takahashi, S;Sumikawa, K
睡眠呼吸暂停患者因呼吸暂停引起的缺氧是心脏病的重要因素。本研究旨在确定右美托咪定（DEX）是否对缺氧-复氧诱导的左心室功能障碍具有直接保护作用，而无全身血流动力学和体液效应。将离体大鼠心脏暴露于60分钟缺氧，然后用0、10或100 nM DEX预缺氧给药进行30分钟复氧（每组n = 7）。在第二个实验中（n = 7），缺氧后给予100 nM DEX。在第三个实验中（每组n = 7），给予α 2受体拮抗剂育亨宾，同时给予和不给予100 nM DEX预缺氧. DEX预缺氧而非缺氧后给药显著改善了复氧后左室发展压的恢复（0、10、100 nM DEX缺氧前或100 nM DEX缺氧后值为53 +/- 6、64 +/- 9、78 +/- 13或62 +/- 12 mm Hg [平均SD缺氧]），并被育亨宾逆转，分别为58 +/- 8 mm Hg。结论：DEX对缺氧复氧所致的左室功能障碍有直接的保护作用，主要是通过低氧前和低氧时α 2肾上腺素能的兴奋作用。
Hypoxia resulting from apnea in patients with sleep apnea is an important factor in heart disease. We designed the present study to determine whether dexmedetomidine (DEX) has a direct protective effect against hypoxia-reoxygenation-induced left ventricular dysfunction without systemic hemodynamic and humoral effects. Isolated rat hearts were exposed to 60-min hypoxia followed by 30-min reoxygenation with 0, 10, or 100 nM DEX prehypoxia administration (n = 7 each group). In a second experiment (n = 7), 100 nM DEX was administered posthypoxia. In a third experiment (n = 7 each group), an a 2 antagonist, yohimbine was given with and without 100 nM DEX prehypoxia administration. DEX prehypoxia, but not posthypoxia, administration significantly improved the recovery of left ventricular developed pressure after reoxygenation (0, 10, 100 nM DEX prehypoxia or 100 nM DEX posthypoxia values were 53 +/- 6, 64 +/- 9, 78 +/- 13, or 62 +/- 12 mm Hg [mean SDHypoxia]) and reversed by yohimbine, 58 +/- 8 mm Hg, respectively. We conclude that DEX exerts the direct protective effect on the left ventricular dysfunction caused by hypoxiareoxygenation through mainly alpha 2-adrenergic stimulation before and during the hypoxic period.