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|本期目录/Table of Contents|

卡托普利对再灌注损伤心肌细胞LDH 和MDA 的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2003年第6期
页码:
498-500
栏目:
实验研究
出版日期:
2003-11-01

文章信息/Info

Title:
Effects of Captopril to reperfusion injury of rat ventricular myocytes lactate dehydrogenase and malondialdehyde
作者:
陈江斌; 李庚山; 李建军; 黄从新; 唐其柱; 王晶
武汉大学人民医院心内科, 湖北 武汉 430060
Author(s):
CHEN Jian-bin;  LI Geng-shan;  LI Jian-jun;  HUANG Cong-xin;  TANG Qi-zhu;  WANG Jing
Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan, Hubei 430060, China
关键词:
卡托普利; 缺氧-复氧损伤; 心肌细胞; 乳酸脱氢酶; 丙二醛
Keywords:
Captopril;  anoxia-reoxygenation injury;  myocyte;  lactate dehydrogenase;  malondialdehyde
分类号:
R542.2　
DOI:
-
文献标识码:
A
摘要:
目的:观察卡托普利对大鼠心室肌细胞缺氧-复氧损伤的影响。方法: 酶解法分离心肌细胞, 将实验分为9 组:不缺氧组、单纯缺氧组、缺氧-复氧组、卡托普利0.05、0.1、0.2、0.4、0.8 和116 Lmo l?L 灌流组。观察杆形心肌细胞百分比、测定乳酸脱氢酶(LDH) 活性、LDH 活性百分比和丙二醛(MDA ) 含量。结果: 不缺氧组心肌细胞的生存率、释放LDH 活性百分比、MDA 含量无明显变化。单纯缺氧组心肌细胞的生存率下降, 释放LDH 活性百分比明显增加,MDA 的含量亦增加; 复氧组较缺氧组心肌细胞造成更严重的损伤(P <0.01); 卡托普利0.05, 0.1 Lmo l?L 对缺氧-复氧造成的损伤无明显作用(P>0.05) , 但0.2, 0.4, 0.8 和116 Lmo l?L 能明显提高心肌细胞缺氧-复氧过程中的生存率、减少脂质过氧化产物的生成, 且呈剂量依赖性。结论: 卡托普利对缺氧2复氧损伤的心肌细胞具有剂量依赖性保护作用。
Abstract:
AIM: To observe the effect of Captopril on the injury induced by anoxia-reoxygenation.METHODS: Myocytes were obtained by enzymatic dissociation technique and were divided into 9 groups: normal condition, anoxia, anoxia-reoxygenation, and 0.05, 0.1, 0.2, 0.4, 0.8 and 1.6 Lmol?L Captopril reperfusion groups. viability of myocytes, lactate dehydrogenase (LDH) activity, LDH activity percentage and malondialdehyde (MDA) were measured. RESULTS: There was no change in myocyte viability, LDH releasing activity percentage and MDA in the normal condition group (P>0.05). In the anoxia group cell viability decreased, and LDH releasing activity percentage and MDA increased. And in the anoxia-reoxygenation group, the damage was more serious than that of the anoxia group (P<0.01). There was no statistically significant difference between the anoxia-reoxygenation group and 0.05, 0.1 Lmol?L Captopril reperfusion groups. Captopril inhibited the myocytes contracture, increase the cell viability, reduced formation of lipids perxidation products of 0.2, 0.4, 0.8 and 1.6 Lmol?L Captopril reperfusion groups. And the higher the dose of Captopril, the better the salutary effects. CONCLUSION: Captopril could protect rat ventricular myocytes the anoxia-reoxygenation injury of in a dose-dependent manner, and the myocytes treated with Captopril were significantly resistant to the anoxia-reoxygenation injury.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2002-10-18.
更新日期/Last Update: 2003-11-01