在急性心肌梗塞期间,高呼吸坦度
Z W Weitz1, A J Birnbaum, P A Sobotka
1Department of Medicine/Rheumatology, University of Illinois, Chicago.
Lancet (London, England)
|April 20, 1991
概括
心脏病发作后的再输液会导致脂质过氧化,通过更高的呼吸水平来表明这一点. 这表明氧基在心肌梗塞期间有助于心脏组织损伤.
科学领域:
- 心脏病学 心脏病学
- 生物化学 生物化学
- 自由激进生物学 自由激进生物学
背景情况:
- 心肌梗塞 (MI) 涉及缺血和再注血.
- 重灌可能会引发氧化应激和细胞损伤.
- 脂质过氧化是氧化损伤的标志物.
研究的目的:
- 调查心肌缺血后的再输是否会导致自由基介导的脂质过氧化.
- 在呼吸样本中测量脂质过氧化的标志物,以测量呼吸样本.
- 评估氧基在心肌梗塞病因发生中的作用.
主要方法:
- 在三个组中测量了呼吸坦水平:健康对照组,怀疑心脏病发作但没有心电图变化的患者 (患者对照组) 和确诊急性心脏病发作的患者.
- 分组根据年龄,性别,潜在疾病和吸烟习惯进行了匹配.
- 从胸部疼痛开始到呼吸收集的时间是标准化的.
主要成果:
- 与患者对照组 (1.96 nmol/l) 和健康对照组 (1.71 nmol/l) 相比,急性MI组 (4.96 nmol/l) 的呼吸坦度显著更高.
- 这一差异具有统计学意义 (p < 0.0001).
- 度较高表明在急性心脏病发作期间脂质过氧化增加.
结论:
- 心肌缺血后的再输液导致脂质过氧化增加.
- 呼吸坦升高表明在急性心脏病发作期间有显著的氧基活性.
- 氧基可能导致心肌组织损伤的发病.
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