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慢性缺氧大鼠模型中青紫心肌的缺血再灌注损伤:青紫心肌抗氧化系统的变化

Ischemic and reperfusion injury of cyanotic myocardium in chronic hypoxic rat model: changes in cyanotic myocardial antioxidant system.

作者信息

Nakanishi K, Inoue M, Sugawara E, Sano S

机构信息

Department of Cardiovascular Surgery, Okayama University Medical School, Japan.

出版信息

J Thorac Cardiovasc Surg. 1997 Dec;114(6):1088-96. doi: 10.1016/S0022-5223(97)70024-2.

Abstract

OBJECTIVE

The objective was to evaluate the effect of left ventricular function on cyanotic myocardium after ischemia-reperfusion and to determine the effect of cyanosis on the myocardial antioxidant system.

METHODS

Cyanotic hearts (cyanotic group) were obtained from rats housed in a hypoxic chamber (10% oxygen) for 2 weeks and control hearts (control group) from rats maintained in ambient air. Isolated, crystalloid perfused working hearts were subjected to 15 minutes of global normothermic ischemia and 20 minutes of reperfusion, and functional recovery was evaluated in the two groups. Myocardial superoxide dismutase, glutathione peroxidase, glutathione reductase activity, and reduced glutathione content were measured separately in the cytoplasm and mitochondria at the end of the preischemic, ischemic, and reperfusion periods.

RESULTS

Mean cardiac output/left ventricular weight was not significantly different between the two groups. Percent recovery of cardiac output was significantly lower in the cyanotic group than in the control group (56.1% +/- 5.7% vs 73.0% +/- 3.1%, p = 0.001). Mitochondrial superoxide dismutase, mitochondrial and cytosolic glutathione reductase activity, and cytosolic reduced glutathione were significantly lower in the cyanotic group than in the control group at end-ischemia (superoxide dismutase, 3.7 +/- 1.3 vs 5.9 +/- 1.5 units/mg protein, p = 0.012; mitochondrial glutathione reductase, 43.7 +/- 14.0 vs 71.0 +/- 30.3 munits/mg protein, p = 0.039; cytosolic glutathione reductase, 13.7 +/- 2.0 vs 23.2 +/- 4.2 munits/mg protein, p < 0.001; and reduced glutathione, 0.69 +/- 0.10 vs 0.91 +/- 0.24 microgram/mg protein, p = 0.037).

CONCLUSIONS

Cyanosis impairs postischemic functional recovery and depresses myocardial antioxidant reserve during ischemia. Reduced antioxidant reserve at end-ischemia may result in impaired postischemic functional recovery of cyanotic myocardium.

摘要

目的

评估左心室功能对缺血再灌注后青紫心肌的影响,并确定青紫对心肌抗氧化系统的影响。

方法

青紫心脏(青紫组)取自置于低氧舱(10%氧气)中饲养2周的大鼠,对照心脏(对照组)取自置于环境空气中的大鼠。分离出的、用晶体液灌注的工作心脏经历15分钟的整体常温缺血和20分钟的再灌注,对两组的功能恢复情况进行评估。在缺血前期、缺血期和再灌注期结束时,分别测量细胞质和线粒体中的心肌超氧化物歧化酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶活性以及还原型谷胱甘肽含量。

结果

两组之间的心输出量/左心室重量均值无显著差异。青紫组的心输出量恢复百分比显著低于对照组(56.1%±5.7%对73.0%±3.1%,p = 0.001)。在缺血末期,青紫组的线粒体超氧化物歧化酶、线粒体和细胞质谷胱甘肽还原酶活性以及细胞质还原型谷胱甘肽显著低于对照组(超氧化物歧化酶,3.7±1.3对5.9±1.5单位/毫克蛋白,p = 0.012;线粒体谷胱甘肽还原酶,43.7±14.0对71.0±30.3毫单位/毫克蛋白,p = 0.039;细胞质谷胱甘肽还原酶,13.7±2.0对23.2±4.2毫单位/毫克蛋白,p<0.001;还原型谷胱甘肽,0.69±0.10对0.91±0.24微克/毫克蛋白,p = 0.037)。

结论

青紫损害缺血后的功能恢复,并在缺血期间降低心肌抗氧化储备。缺血末期抗氧化储备降低可能导致青紫心肌缺血后功能恢复受损。

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