吸入的氧化可以在没有高血压的情况下进行人工输血
Binglan Yu1, Michael J Raher, Gian Paolo Volpato
1Anesthesia Center for Critical Care Research of the Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Circulation
|April 9, 2008
概括
由基于血红蛋白的氧载体 (HBOCs) 引起的全身血管收缩可以预防. 吸入的氧化 (NO) 在HBOC输注前服用,可以减轻这种副作用,而不会引起甲基红蛋白血症.
科学领域:
- 生物医学工程 生物医学工程
- 药理学 药理学是指药理学的学科.
- 生理学 生理学 生理学
背景情况:
- 基于血红蛋白的氧载体 (HBOCs) 的临床发展受到全身血管收缩的限制.
- 了解HBOC诱导血管收缩的机制对于治疗进步至关重要.
研究的目的:
- 研究HBOCs引起全身血管收缩的机制.
- 评估氧化 (NO) 在预防HBOC诱导的血管收缩方面的疗效.
主要方法:
- 实验对野生型和内皮氧化合成酶 (NOS3) 缺乏的小鼠以及羊羔进行了实验.
- 动物接受了小鼠四度血红蛋白或HBOC-201.的输液.
- 干预措施包括在HBOC输注之前吸入NO或给药酸盐.
主要成果:
- 静脉注射HBOC输液在野生型小鼠中诱导了全身血管收缩,但不是在NOS3缺乏的小鼠中.
- 吸入NO或酸盐的使用在小鼠中预防了HBOC诱导的高血压,而不会引起甲基红蛋白血症.
- 吸入的NO还防止了羊羔的HBOC诱导的高血压.
结论:
- 通过吸收由NOS3.3产生的内皮氧化 (NO),HBOCs会引起全身血管收缩.
- 吸入NO的预处理可以有效地预防多种物种的HBOC诱导的血管收缩.
- 这一策略提供了一种有希望的方法来缓解与HBOC相关的副作用.
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