德菲洛克萨明未能改善心脏缩后的心脏功能
H Nakamura1, P J del Nido, E Jimenez
1Department of Surgery, University of Pittsburgh College of Medicine, Pennsylvania.
Circulation
|November 1, 1990
概括
心肌缩增加了心脏对缺血的脆弱性. 铁化剂德费罗胺在早期的再输液过程中没有保护过度缩小的子心脏免受缺血/再输液损伤.
科学领域:
- 心脏病学 心脏病学
- 生理学 生理学 生理学
- 生物化学 生物化学
背景情况:
- 心肌缩是先天性心脏手术中已知的危险因素.
- 过度缩的心脏表现出对缺血/再输血 (I/R) 损伤的敏感性增加.
研究的目的:
- 为了研究铁化剂和基基吸收剂德菲洛克萨对受过I/R损伤的子心脏的保护作用.
- 在慢性心脏缩的临床前模型中,评估早期再注射期间的德费洛克萨明是否可以减轻I / R损伤.
主要方法:
- 大动脉带带被用于诱导年轻子 (1周大) 的心肌缩.
- 来自6-8周大的子的心脏被分离出来,并接受30分钟的37°C缺血,然后再进行30分钟的再输血.
- 在一个过度缩小的群体中,在重灌的最初10分钟内给出了德菲洛克萨 (50μmol/kg);未经治疗的过度缩小和正常的对照组也被研究.
- 左心室发育的压力在经过缺血复苏后恢复后被用内腔气球测量.
主要成果:
- 与对照组相比,心脏缩显示左心室体重/体重比显著增加 (2.9 ± 0.4 x 10−3对 2.0 ± 0.1 x 10−3).
- 与正常对照组 (102 ± 6%) 相比,未经治疗的过度缩心脏 (75 ± 5%) 中,发育压力的发生病后恢复显著减少.
- 在心脏缩后的病例中,deferoxamine治疗没有显著改善后缺血压的恢复 (71±4%),表明缺乏保护作用.
结论:
- 在生命早期引起的慢性心肌缩导致对缺血和再流损伤的易感性增加.
- 铁化剂deferoxamine在预防这种超大缩心脏模型中的反损伤方面是无效的.
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