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作 者:曹春梅[1] 姚慧[2] 徐万红[1] 叶治国[1] 陈君柱[3] 夏强[1]
机构地区:[1]浙江大学医学院生理学教研室,浙江杭州310031 [2]杭州师范学院医学院,浙江杭州310012 [3]浙江大学医学院附属第一医院心内科,浙江杭州310003
出 处:《浙江大学学报(医学版)》2003年第3期175-180,共6页Journal of Zhejiang University(Medical Sciences)
基 金:浙江省自然科学基金青年人才专项资金资助(RC990 38)
摘 要:目的 :观察在缺氧 /复氧过程中白细胞介素 - 2 (IL- 2 )对心肌的影响及其可能机制。方法 :采用放射免疫法检测心肌组织中 IL- 2的含量 ;用视频跟踪系统和细胞内双波长钙荧光系统检测心肌细胞收缩和细胞内钙的变化。结果 :在缺血再灌注心肌组织中 IL- 2明显增多 [(14 .34± 5 .99vs2 2 .2 5± 3.6 8) ng/ g心肌组织 ]。在缺氧期间加 IL-2 (2 0 0 U/ ml) ,复氧期间心肌收缩和细胞内钙各参数回复的程度与单纯复氧的细胞相比均降低。IL- 2灌流后心肌线粒体丙二醛的含量在缺氧 /复氧后明显高于对照组 [(7.75± 0 .4 1vs6 .81± 0 .5 3) nmol/ mg蛋白 ]。结论 :IL- 2参与缺氧 /复氧引起的心肌功能损害 ,其机制可能与 IL- 2加重心肌线粒体脂质过氧化有关。Objective: To investigate the effect of interleukin-2 (IL-2) on myocardial impairment during ische-mia/reperfusion or anoxia/reoxygenation.Methods:Chemical anoxia was introduced in the isolated rat ventricular myocytes by Krebs-Henseleit (K-H) solution containing 10 -3 mol/L sodium dithionite.The video-tracking system and spectrofluorometric method were employed to verify the cell contraction and calcium homeostasis of the single myocyte.Radioimmunoassay was used to analyze the IL-2 levels in myocardium.Results:The levels of IL-2 in myocardium subjected to ischemia/reperfusion were elevated [(14.34±5.99 vs 22.25±3.68)ng/g,P<0.01].During anoxia,cell contraction and the amplitude of electrically induced calcium transient were depressed and the parameters did not return to the pre-anoxia level during reoxygenation.IL-2 at 200 U/L administered during anoxia aggravated the effect of reoxygenation on cell contraction and calcium transient.After perfusion with IL-2,the malondialdehyde content of myocardial mitochondria was elevated.Conclusion:Coexistence of IL-2 during anoxia aggravates the effect of reoxygenation on the cell contraction and calcium homeostasis in the isolated rat ventricular myocytes,in which the mitochondrial lipid peroxidation induced by IL-2 is involved.
关 键 词:白细胞介素-2 心肌缺血 再灌注损伤 缺氧/复氧 心肌功能损害 放射免疫法
分 类 号:R541[医药卫生—心血管疾病]
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