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作 者:郑惠珍[1,2] 唐朝枢[1,2] 苏加林 吴涛[1,2]
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:《生理学报》1999年第1期25-30,共6页Acta Physiologica Sinica
摘 要:为探讨大鼠心脏缺血再灌注损伤(IRI)期间一氧化氮(NO)生成增加的环节和过程。本实验用离体灌流大鼠心脏,预灌流15min,停灌45min,取30mlKH液循环灌流15min,观察冠脉流出液中细胞胞浆酶(LDH)、蛋白质、肌红蛋白漏出量和NO-2含量、心肌组织NOS活性、L精氨酸(LArg)转运的改变。结果显示,心脏IRI后,冠脉流出液中LDH活性、蛋白质和肌红蛋白量较对照组分别增加41,54和1倍(均P<001)。NO-2含量增加12倍(P<001)。心肌组织tNOS活性、iNOS活性和cNOS活性分别增加482%、432%和521%(均P<001)。NO-2含量与心肌组织iNOS活性呈正相关,(r=07942,P<001)。心肌组织LArg转运呈现高、低亲和两种方式。IRI组心肌LArg转运能力增强,最大转运速率(Vmax)较对照组升高48%(低亲和,P<005)和2倍(高亲和,P<001);低亲和Km值降低474%(P<005),高亲和Km值改变无统计学意义。LArg转运高、低亲和转运载体的Vmax与iNOS活性、NO-2含量均呈高度正相关关系。结果提示:心脏?Ischemia reperfusion injury(IRI) model of rat heart was prepared by preperfusion for 15 min, then a suspension for 45 min and recycling reperfusion for 15 min with 30 ml KH buffer. The leakage of lactate dehydrogenase(LDH), protein, myoglobine and nitrite (NO - 2) in the circular perfusion fluid were measured. Myocardial nitric oxide synthase(NOS) activity and L arginine transport were observed. In the IR group,the leakage of LDH, protein, myoglobine and NO - 2 were increased respectively by 4 1, 5 4, 1 and 1 2 times( P <0 01) and NOS(tNOS, iNOS, cNOS) activity by 48 2%, 43 2%and 52 1%, ( P <0 01, respectively) as compared with the control group. L arginine transport might be mediated by either high or low affinity transport system in cardiac tissue. In the IR group, L arginine transport increased significantly with the V max being increased by 48% and 2 times respectively for the low affinity and the high affinity transport as compared with control. Michaelis constant (km) was decreased by 47 4% for low affinity transport ( P <0 05), but not significantly changed for the high affinity transport. These results suggest that the increase of nitric oxide generation might result from the increased myocardial NOS activity and L arginine transport during IRI.
分 类 号:R331.3[医药卫生—人体生理学]
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