首页> 外文期刊>American Journal of Physiology >Model of nitric oxide diffusion in an arteriole: impact of hemoglobin-based blood substitutes.
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Model of nitric oxide diffusion in an arteriole: impact of hemoglobin-based blood substitutes.

机译:一氧化氮在小动脉中扩散的模型:基于血红蛋白的血液替代品的影响。

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摘要

Administration of hemoglobin-based oxygen carriers (HBOCs) frequently results in vasoconstriction that is primarily attributed to the scavenging of endothelium-derived nitric oxide (NO) by cell-free hemoglobin. The ensuing pressor response could be caused by the high NO reactivity of HBOC in the vascular lumen and/or the extravasation of hemoglobin molecules. There is a need for quantitative understanding of the NO interaction with HBOC in the blood vessels. We developed a detailed mathematical model of NO diffusion and reaction in the presence of an HBOC for an arteriolar-size vessel. The HBOC reactivity with NO and degree of extravasation was studied in the range of 2-58 x 10(6) M(-1) x s(-1) and 0-100%, respectively. The model predictions showed that the addition of HBOC reduced the smooth muscle (SM) NO concentration in the activation range (12-28 nM) for soluble guanylate cyclase, a major determinant of SM contraction. The SM NO concentration was significantly reduced when the extravasation of HBOC molecules was considered. The myoglobin present in the parenchymal cells scavenges NO, which reduces the SM NO concentration.
机译:基于血红蛋白的氧气载体(HBOC)的给药经常导致血管收缩,这主要归因于无细胞血红蛋白清除了内皮衍生的一氧化氮(NO)。随后的升压反应可能是由于血管腔内HBOC的高NO反应性和/或血红蛋白分子外渗引起的。需要定量了解NO与HBOC在血管中的相互作用。我们开发了用于小动脉大小血管的HBOC存在下NO扩散和反应的详细数学模型。 HBOC与NO的反应性和渗入度分别在2-58 x 10(6)M(-1)x s(-1)和0-100%的范围内进行研究。模型预测表明,添加HBOC会降低可溶性鸟苷酸环化酶(SM收缩的主要决定因素)的激活范围(12-28 nM)中的平滑肌(SM)NO浓度。考虑到HBOC分子外渗时,SM NO浓度显着降低。实质细胞中存在的肌红蛋白清除NO,从而降低SM NO浓度。

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