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作 者:郑惠珍[1] 王述恒[2] 符明桂 姜志胜[2] 唐朝枢[2] 刘乃奎[2]
机构地区:[1]广东医学院生理学教研室 [2]北京医科大学心血管基础研究所
出 处:《中国病理生理杂志》1998年第6期664-668,共5页Chinese Journal of Pathophysiology
摘 要:目的:观察一氧化氮(NO)对心肌细胞缺氧-复氧损伤(HRI)的作用。方法:培养的大鼠心肌细胞,培养液中分别预先加入NO前体L-精氨酸(L-Arg)、NO供体SIN-1或硝普钠(SNP)、NOS抑制剂L-NNA或NOS诱导剂脂多糖(LPS),经缺氧120min,复氧60min处理后,检测细胞存活率,乳酸脱氢酶(LDH)漏出量,亚硝酸盐(NO2)含量及细胞诱导型NO合酶(iNOS)活性等指标的改变。结果:①与常氧组比较,缺氧-复氧HR降低细胞存活率(23%,P<0.01),增加LDH漏出(62倍,P<0.01),iNOS活性(77%,P<0.01),NO2含量(617%,P<0.01)。②HR前预先加入SIN-1、SNP或L-Arg,均引起LDH漏出进一步增高(P<0.01),细胞存活率进一步降低(P<0.01或P<0.05)。③L-NNA2mmol/L,单独应用对细胞损伤的影响无统计学意义,与L-Arg联合应用,则减弱L-Arg的细胞损伤作用。④LPS1μg/mL,增加iNOS活性(26倍,P<0.01)和LDH漏出(56%,P<0.01)。结论:NO加重心肌细胞HRI。Abstract AIM:To investigate the effect of nitric oxide (NO) on hypoxia and reoxygenation injury(HRI) of cardiomyocytes. METHODS:With cardiomyocytes cultured in newborn rats subjected to hypoxia 120 min and reoxygenation 60 min in the presence of either NO precursor L-arginine(L-Arg), or NO donors 3-morpholino sydnonimine-hydrochloride (SIN-1), or sodium nitroprusside (SNP), or NOS inhibitor N ω-nitro-L-arginine (L-NNA), or lipopolysaccharide (LPS), changes of cell viability, leakage of lactate dehydrogenase (LDH), inducible nitric oxide synthase (iNOS) activity and nitrite (NO 2) content were observed. RESULTS:①Hypoxia and reoxygenation reduced cell viability (23%, P <0.01),increased leakage of LDH (6.2 times, P <0.01), iNOS activity (77%, P <0.01) and NO 2 content (61.7%, P <0.01) vs 21% O 2 control group.②With SIN-1 or SNP or L-Arg pretreated, the leakage of LDH was further increased ( P <0.01) and cell viability was further reduced ( P <0.01 or P <0.05) compared with HR group. ③L-NNA (2mmol/L) had no significant effects on cell injury, but it attenuated the cell injury effects of L-arginine. ④ LPS increased iNOS activity (2.6 times, P <0.01) and the leakage of LDH (56%, P <0.01).CONCLUSION: NO can exacerbate cardiomyocytes HRI. It is a injury factor to cardiomycytes HRI. MeSH Nitric oxide; Cardiomyocyte; Reperfusion injury; Rat
分 类 号:R542.202[医药卫生—心血管疾病]
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