在麻醉的心肌中失去原蛋白
R H Charney1, S Takahashi, M Zhao
1Department of Medicine, Albert Einstein College of Medicine, Bronx, N.Y. 10461.
Circulation
|April 1, 1992
概括
心肌麻醉涉及由于激活内源性公原酶而导致原基质降解的原基质降解,导致静脉缩功能障碍和心脏膨胀. 这个过程是理解缺血性心脏病和心肌病的关键.
科学领域:
- 心血管生物学 心血管生物学
- 生物化学 生物化学
- 病理生理学 病理生理学
背景情况:
- 此前已经观察到丧心肌的原基质的超结构性改变.
- 需要生物化学评估来量化这些变化.
研究的目的:
- 生物化学评估和量化超结构性变化震惊心肌的原基质.
- 研究内源蛋白酶在原体降解中的作用.
主要方法:
- 蒙格勒犬接受了冠状动脉封闭和再注射的协议,以诱导心肌麻醉.
- 测量了原蛋白含量 (氧),原酶活性,溶酶酶和原纤维标签.
- 组织中的水含量也被评估.
主要成果:
- 被震惊的心肌表现出缩功能障碍和扩张性心脏尺寸的增加.
- 在心脏中壁和上心脏中观察到不均的原蛋白转移性损失.
- 在激活之前检测到内源性prcollagenase活性增加,完全激活的collagenase没有差异.
- 增加对原纤维的丹西尔标记表明了更大的酶分裂.
结论:
- 内源性公原酶激活有助于细胞外基质降解在麻醉的心肌.
- 这些机制与缺血性心脏扩大和心肌病相关.
- 在90分钟的再输液后,外源蛋白酶来源被排除在外.
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