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再灌注早期的高氧并不增加缺血/再灌注损伤。

Hyperoxia during early reperfusion does not increase ischemia/reperfusion injury.

机构信息

Faculty of Medicine, Department of Molecular Biosciences, University of Oslo, and Institute for Experimental Medical Research, Department of Surgery, Oslo University Hospital, Oslo, Norway.

出版信息

Eur J Cardiothorac Surg. 2012 Jan;41(1):149-53. doi: 10.1016/j.ejcts.2011.04.022.

DOI:10.1016/j.ejcts.2011.04.022
PMID:21636285
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3241090/
Abstract

OBJECTIVE

Oxygen is routinely administered to patients undergoing acute myocardial infarction as well as during revascularization procedures and cardiac surgery. Because reactive oxygen species are mediators of ischemia/reperfusion injury, increased oxygen availability might theoretically aggravate myocardial injury during reperfusion. We hypothesized that ventilation with a hyperoxic gas at start of reperfusion might increase ischemia/reperfusion injury.

METHODS

Rats were anesthetized with isoflurane and ventilated with 40% oxygen. The animals were subjected to 40 min of regional myocardial ischemia and 120 min of reperfusion. In the test group, rats (n=11) were ventilated with a normobaric hyperoxic gas (95% O2) during the last 10 min of ischemia and the first 10 min of reperfusion. Control rats (n=14) were ventilated with 40% O2 throughout the experiments. Due to irreversible reperfusion arrhythmias, one animal in the hyperoxia group and six animals in the control group were excluded. Hearts (n=8 in the control group and n=10 in the test group) were harvested for measurement of infarct size.

RESULTS

The incidence of lethal arrhythmias was 1/11 in the test group and 6/14 in the control group (p=0.06). Reperfusion with normobaric hyperoxia did not influence infarct size (20±8% of area at risk) compared with the normoxia group (24±8% and of area at risk), respectively (mean±SD, p>0.2).

CONCLUSION

Normobaric hyperoxia during early reperfusion did not increase ischemia/reperfusion injury.

摘要

目的

在急性心肌梗死以及血运重建术和心脏手术期间,患者通常会接受氧气治疗。由于活性氧是缺血/再灌注损伤的介质,因此理论上增加氧气供应可能会在再灌注期间加重心肌损伤。我们假设在再灌注开始时用高氧气体通气可能会增加缺血/再灌注损伤。

方法

用异氟烷麻醉大鼠,并以 40%氧气通气。动物经历 40 分钟的区域性心肌缺血和 120 分钟的再灌注。在实验组中,大鼠(n=11)在缺血的最后 10 分钟和再灌注的前 10 分钟期间用常压高氧气体(95%O2)通气。对照大鼠(n=14)在整个实验过程中用 40%氧气通气。由于不可逆的再灌注心律失常,高氧组中有一只动物和对照组中有六只动物被排除。收获心脏(对照组 n=8,实验组 n=10)以测量梗死面积。

结果

实验组中致命性心律失常的发生率为 1/11,对照组中为 6/14(p=0.06)。与正常氧组(24±8%和危险区域)相比,常压高氧再灌注对梗死面积没有影响(分别为 20±8%的危险区域)(平均值±SD,p>0.2)。

结论

早期再灌注时的常压高氧并未增加缺血/再灌注损伤。

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The wanderings of a free radical.自由基的游走
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