【摘要】：目的探討氫氣對(duì)心肌缺血再灌注(I/R)損傷的保護(hù)作用。方法將48只大鼠隨機(jī)分為實(shí)驗(yàn)組和對(duì)照組各24只。取兩組大鼠心臟,按逆灌注10 min,常溫曠置20 min、再灌注20 min的方法建立心肌缺血再灌注模型。對(duì)照組灌注液用K-R液,實(shí)驗(yàn)組灌注液用K-R液+氫氣飽和生理鹽水。監(jiān)測(cè)兩組大鼠心臟缺血前期、缺血期、再灌注期心肌組織丙二醛(MDA)、超氧化物歧化酶(SOD)水平及左室舒張末期壓力(LVEDP)。結(jié)果對(duì)照組缺血期心肌MDA水平高于缺血前期(P0.05),再灌注期心肌MDA水平低于缺血期(P0.05),但仍高于缺血前期(P0.05)。實(shí)驗(yàn)組各期心肌MDA水平無(wú)統(tǒng)計(jì)學(xué)差異;缺血期、再灌注期心肌MDA水平較對(duì)照組同期下降(P均0.05)。兩組缺血期與缺血前期心肌SOD水平無(wú)統(tǒng)計(jì)學(xué)差異,缺血再灌注期心肌SOD水平低于缺血前期和缺血期(P均0.05)。實(shí)驗(yàn)組缺血期與再灌注期心肌SOD水平較對(duì)照組同期升高(P均0.05)。對(duì)照組再灌注期LVEDP高于缺血前期(P0.05);實(shí)驗(yàn)組再灌注期與缺血前期LVEDP無(wú)統(tǒng)計(jì)學(xué)差異,但與對(duì)照組同期比較下降明顯(P0.05)。結(jié)論氫氣對(duì)大鼠離體心臟心肌I/R損傷有明顯的保護(hù)作用。其機(jī)制可能為抑制心肌組織MDA表達(dá),提高心肌組織SOD水平。
[Abstract]:Objective to investigate the protective effect of hydrogen on myocardial ischemia reperfusion (I / R) injury. Methods 48 rats were randomly divided into experimental group (n = 24) and control group (n = 24). Myocardial ischemia-reperfusion model was established by reverse perfusion for 10 min, at room temperature for 20 min, and reperfusion for 20 min. The control group was perfused with K-R solution, the experimental group with K-R solution hydrogen saturated saline. The levels of malondialdehyde (MDA),) superoxide dismutase (SOD) and left ventricular end-diastolic pressure (LVEDP).) in myocardium of the two groups were monitored in the preischemic, ischemic and reperfusion periods. Results the level of myocardial MDA in the control group was higher than that in the ischemic period (P0.05), and the level of MDA in the reperfusion period was lower than that in the ischemic period (P0.05), but still higher than that in the preischemic period (P0.05). There was no significant difference in myocardial MDA level between the experimental group and the control group, but the level of myocardial MDA in the ischemic and reperfusion period was lower than that in the control group (P < 0. 05). There was no significant difference between the two groups in the level of myocardial SOD during ischemia and pre-ischemia. The level of myocardial SOD in ischemia-reperfusion period was lower than that in preischemic period and ischemic period (P0. 05). The level of myocardial SOD in the experimental group was higher than that in the control group during ischemia and reperfusion (all P 0. 05). The LVEDP of the control group was higher than that of the control group (P0.05), while the LVEDP of the experimental group was not significantly different from that of the control group (P0.05). Conclusion hydrogen has obvious protective effect on myocardial I / R injury in isolated rat heart. The mechanism may be to inhibit the expression of MDA and increase the level of SOD in myocardial tissue.
【作者單位】： 河北大學(xué)附屬醫(yī)院;河北大學(xué)化學(xué)院;河北大學(xué)生理教研室;
【基金】：河北省2013年醫(yī)學(xué)科學(xué)研究重點(diǎn)課題計(jì)劃項(xiàng)目(20130369)
【分類號(hào)】：R965

【相似文獻(xiàn)】

相關(guān)期刊論文 前3條

1 祝忠群,蘇肇伉,陳惠文,胡惠民,陳恩,丁文祥;天門冬氨酸對(duì)缺血期幼兔心肌能量代謝的保護(hù)作用(摘要)[J];中國(guó)循環(huán)雜志;1998年03期

2 王榮娟;;鎂、麻醉和血流動(dòng)力的控制[J];國(guó)外醫(yī)學(xué).麻醉學(xué)與復(fù)蘇分冊(cè);1992年03期

3 ;[J];;年期

，

本文編號(hào)：2304997