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首页> 外文期刊>American Journal of Physiology >Inhibition of sickle red cell adhesion and vasoocclusion in the microcirculation by antioxidants.
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Inhibition of sickle red cell adhesion and vasoocclusion in the microcirculation by antioxidants.

机译：抗氧化剂抑制镰状红细胞粘附和微循环中的血管闭塞。

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摘要

In sickle cell anemia (SCA), inflammatory (i.e., intravascular sickling and transient vasoocclusive) events result in chronic endothelial activation. In addition to sickling behavior, sickle (SS) red blood cells exhibit abnormal interaction with the vascular endothelium, which is considered to have an important role in initiation of vasoocclusion. Upregulation of endothelial adhesion molecules caused by oxidants (and cytokines) may lead to increased SS red cell adhesion. We hypothesize that endothelial activation is indispensable in SS red cell adhesion to the endothelium and that antioxidants will have an inhibitory effect on this interaction. We examined the effect of selected antioxidants in ex vivo mesocecum vasculature, a well-established model that allows measurement of hemodynamic parameters and, by intravital microscopy, can allow quantification of adhesion. We tested antioxidant enzymes (SOD and catalase) and an intravascular SOD mimetic, polynitroxyl albumin (PNA), in the presence of platelet-activating factor (PAF); the latter causes endothelial oxidant generation and endothelial activation, which characterize SCA. In ex vivo preparations, PAF not only induced marked endothelial oxidant generation, it also enhanced SS red cell adhesion, resulting in frequent blockage of small-diameter venules. The adhesion, inversely related to venular diameter, and vasoocclusion were markedly inhibited by antioxidants, resulting in improved hemodynamics. PNA, the most effective antioxidant, also abolished SS red cell adhesion in non-PAF-activated preparations. Thus SS red cell adhesion and related vasoocclusion may be ameliorated by antioxidant therapy with a stable and long-acting molecule (e.g., PNA).
机译：在镰状细胞性贫血（SCA）中，炎症事件（即血管内镰状和短暂性血管闭塞）会导致慢性内皮活化。除镰刀行为外，镰刀（SS）红细胞还表现出与血管内皮的异常相互作用，这被认为在引发血管闭塞方面具有重要作用。由氧化剂（和细胞因子）引起的内皮粘附分子的上调可能导致SS红细胞粘附增加。我们假设内皮细胞的活化在SS红细胞对内皮细胞的粘附中是必不可少的，并且抗氧化剂会对此相互作用产生抑制作用。我们检查了离体的中肠盲肠脉管系统中选定的抗氧化剂的作用，该模型是一个行之有效的模型，可以测量血流动力学参数，并且通过活体显微镜检查可以定量粘附。在血小板活化因子（PAF）存在的情况下，我们测试了抗氧化酶（SOD和过氧化氢酶）和血管内SOD模仿物多硝基木清蛋白（PNA）。后者引起内皮氧化剂的产生和内皮活化，这是SCA的特征。在离体制剂中，PAF不仅诱导明显的内皮氧化剂生成，而且还增强了SS红细胞的附着力，导致小直径小静脉的频繁阻塞。抗氧化剂可显着抑制与小静脉直径成反比的粘连和血管闭塞，从而改善血液动力学。 PNA，最有效的抗氧化剂，也消除了非PAF活化制剂中SS红细胞的粘附。因此，可以通过使用稳定且长效的分子（例如，PNA）的抗氧化剂治疗来改善SS红细胞的粘附和相关的血管闭塞。

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