Deterioration of myocardial injury due to dexmedetomidine administration after myocardial ischaemia
Deterioration of myocardial injury due to dexmedetomidine administration after myocardial ischaemia
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DOI：
10.1016/j.resuscitation.2010.07.021
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发表时间：
2010-12-01
期刊：
影响因子：
6.5
通讯作者：
Sato, Shigehito
中科院分区：
文献类型：
--
作者：
Mimuro, Soichiro;Katoh, Takasumi;Sato, Shigehito
目的：右美托咪定是一种围手术期应用的高选择性α-2肾上腺素能激动剂。右美托咪定对心肌缺血后的心脏保护作用尚不清楚。在本研究中，我们在大鼠离体心缺血后给予右美托咪定，以观察其对心肌缺血再灌注损伤的保护作用。方法：停灌30min后，再灌流120min。在再灌流开始时，分别以0 nM(对照组)、1 nM(地塞米松1组)和10 nM(地塞米松10组)的浓度给药25min。另一组大鼠离体心按上述方法给予育亨宾(α-2肾上腺素能拮抗剂)，1 mU M不加右美托咪定(YOH组)，1 mU M加10 nM右美托咪定(YOH+Dex 10组)。结果：右美托咪定不影响血流动力学和冠脉流量，但增加了心肌梗死面积。由于地塞米松1组和地塞米松10组的梗塞面积几乎相同，因此右旋美托咪定的浓度均不影响梗塞面积。梗塞面积对照组为40.5+/-2.9%，地塞米松1组为60.9+/-5.3%，地塞米松10组为60.9+/-2.8%。育亨宾组心肌梗死面积缩小。心肌梗死面积YOH+Dex 10组为39.2+/-3.3%，YOH组为45.0+/-3.2%。结论：右旋美托咪定不影响血流动力学和心功能，但增加心肌梗死面积。α-2肾上腺素能刺激可能诱导这一机制。(C)2010爱思唯尔爱尔兰有限公司。保留所有权利。
Aim: Dexmedetomidine is a highly selective alpha-2 adrenergic agonist used perioperatively. Dexmedetomidine's cardioprotective effect after myocardial ischaemia remains unknown. In this study, we administered dexmedetomidine after ischaemia to investigate its ability to protect the cardiac muscle from ischaemia-reperfusion injury in isolated rat hearts.Methods: After a 30-min stop of perfusion, isolated rat hearts underwent reperfusion for 120 min. At the initiation of reperfusion, dexmedetomidine was administered for 25 min at concentrations of 0 nM (control group), 1 nM (Dex 1 group), and 10 nM (Dex 10 group). Yohimbine (an alpha-2 adrenergic antagonist) was administered in the manner as above in another group of isolated rat hearts at a concentration of 1 mu M without dexmedetomidine (Yoh group) and at 1 mu M with 10 nM dexmedetomidine (Yoh + Dex 10 group). The area of infarction was measured using 2,3,5-triphenyltetrazolium staining.Results: Dexmedetomidine administration did not influence haemodynamics or the coronary flow (CF), but did increase the myocardial infarct size. Neither concentration of dexmedetomidine affected the infarct size as the Dex 1 and Dex 10 groups had almost the same infarct size. The infarct size was 40.5 +/- 2.9% in the control group, 60.9 +/- 5.3% in the Dex 1 group, and 60.9 +/- 2.8% in the Dex 10 group. The infarct size was reduced in the yohimbine groups. The infarct size was 39.2 +/- 3.3% in the Yoh + Dex 10 group and 45.0 +/- 3.2% in the Yoh group.Conclusion: Dexmedetomidine administration does not influence haemodynamics or CF, but does increase the cardiac infarct size. alpha-2 Adrenergic stimulation may induce this mechanism. (C) 2010 Elsevier Ireland Ltd. All rights reserved.