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氧化氘可保护大鼠免受缺血再灌注诱导的心肌损伤。

Deuterium oxide protects against myocardial injury induced by ischemia and reperfusion in rats.

作者信息

Ishikawa Yuko, Kitagawa Hirotoshi, Sawada Tadashi, Seto Tomoyoshi, Takahashi Kan, Yamazaki Toji

机构信息

Department of Anesthesiology, Shiga University of Medical Science, Otsu, Shiga, Japan.

出版信息

Scand Cardiovasc J. 2019 Dec;53(6):329-336. doi: 10.1080/14017431.2019.1657939. Epub 2019 Aug 28.

DOI:10.1080/14017431.2019.1657939
PMID:31455109
Abstract

. Although deuterium oxide (DO) has preservative property on the extracted organ, whether DO also protects the in situ myocardial injury remains unknown. Using cardiac microdialysis, local administration of DO through dialysis probe was applied in situ rat heart. We examined the effect of the DO on the myocardial injury induced ischemia, reperfusion, and chemical hypoxia. . We measured dialysate myoglobin levels during 30 min of coronary occlusion and reperfusion in the absence and presence of DO. Furthermore, to confirm the effect of DO on NaCN induced myocardial injury, we measured the dialysate myoglobin levels with local perfusion of NaCN in the absence and presence of DO. . The dialysate myoglobin levels increased from 177 ± 45 ng/mL at baseline to 3030 ± 1523 ng/mL during 15-30 min of coronary occlusion and further increased to 8588 ± 1684ng/mL at 0-15 min of reperfusion. The dialysate myoglobin levels with 60 min local perfusion of NaCN increased to 1214 ± 279 ng/mL. DO attenuated myocardial myoglobin release during 15-30 min of coronary occlusion and 0-30 min of reperfusion and 15-60 min of local perfusion of NaCN. . DO might have a beneficial effect of myocardium against ischemia, reperfusion and chemical hypoxia.

摘要

尽管重水(DO)对提取的器官具有保存特性,但DO是否也能保护原位心肌损伤仍不清楚。利用心脏微透析技术,通过透析探针将DO局部给药于原位大鼠心脏。我们研究了DO对缺血、再灌注和化学性缺氧诱导的心肌损伤的影响。我们在冠状动脉闭塞和再灌注30分钟期间,在有和没有DO的情况下测量透析液中肌红蛋白水平。此外,为了证实DO对氰化钠诱导的心肌损伤的影响,我们在有和没有DO的情况下,通过局部灌注氰化钠来测量透析液中肌红蛋白水平。透析液中肌红蛋白水平在冠状动脉闭塞15 - 30分钟期间从基线时的177±45 ng/mL增加到3030±1523 ng/mL,并在再灌注0 - 15分钟时进一步增加到8588±1684 ng/mL。局部灌注氰化钠60分钟时,透析液中肌红蛋白水平增加到1214±279 ng/mL。DO在冠状动脉闭塞15 - 30分钟、再灌注0 - 30分钟以及局部灌注氰化钠15 - 60分钟期间减弱了心肌肌红蛋白的释放。DO可能对心肌抵抗缺血、再灌注和化学性缺氧具有有益作用。

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Deuterium oxide protects against myocardial injury induced by ischemia and reperfusion in rats.氧化氘可保护大鼠免受缺血再灌注诱导的心肌损伤。
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