Sickle cell disease and nitric oxide: A paradigm shift?
Sickle cell disease and nitric oxide: A paradigm shift?
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DOI：
10.1016/j.biocel.2006.01.010
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发表时间：
2006-01-01
影响因子：
4
通讯作者：
Kato, Gregory J.
中科院分区：
文献类型：
--
作者：
Mack, A. Kyle;Kato, Gregory J.
传统上，镰状细胞病的病理生理学被认为是由于在缺氧条件下红细胞中血红蛋白S的聚合，导致血管闭塞。细胞粘附于小静脉内皮似乎也起作用。最近的研究还表明，除了红细胞中血红蛋白S的聚合之外，内源性血管扩张剂一氧化氮的缺乏也可能参与其中。由于溶血而释放的血红蛋白迅速消耗一氧化氮，导致抑制血液流动的整个事件程序。旨在减少一氧化氮破坏、增加一氧化氮产生或放大一氧化氮反应的治疗可能是有益的。爱思唯尔有限公司出版
Traditionally the pathophysiology of sickle cell disease is thought to result from the polymerization of hemoglobin S in red cells, under hypoxic conditions, resulting in the occlusion of blood vessels. Adhesion of cells to the venular endothelium also appears to play a role. Recent studies have also suggested that in addition to the polymerization of hemoglobin S in the red blood cell, a deficiency of the endogenous vasodilator, nitric oxide may be involved. Hemoglobin released as a result of hemolysis rapidly consumes nitric oxide resulting in a whole program of events that inhibit blood flow. Therapies directed at decreasing the destruction of nitric oxide, increasing the production of nitric oxide, or amplifying the nitric oxide response may prove beneficial. Published by Elsevier Ltd.