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首页> 外文期刊>Annals of the New York Academy of Sciences >Reperfusion of chronic tissue ischemia: nitrite and dipyridamole regulation of innate immune responses
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Reperfusion of chronic tissue ischemia: nitrite and dipyridamole regulation of innate immune responses

机译：慢性组织缺血再灌注：亚硝酸盐和双嘧达莫对先天免疫反应的调节

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Chronic and intermittent ischemic vascular disorders represent a burgeoning clinical challenge. Previous studies have focused on the idea that therapeutic angiogenesis strategies could alleviate tissue ischemia; however, it is now appreciated that vascular disease is not simply limited to vascular wall cells but also influenced by simultaneously occurring inflammatory responses. Our laboratory has discovered that pharmacological treatment of permanent tissue ischemia with dipyridamole significantly augments ischemic tissue reperfusion, angiogenesis, and arteriogen-esis over time. We have found that the beneficial effects of dipyridamole therapy are due to its ability to increase tissue nitric oxide bioavailability that corrects tissue redox imbalance. Importantly, we have also discovered that dipyridamole treatment invoking nitric oxide (NO) production significantly downregulates various innate immune response genes during chronic ischemic tissue injury. These findings demonstrate that dipyridamole-induced production of nitrite/NO significantly decreases inflammatory responses while increasing vascular growth in ischemic tissues.
机译：慢性和间歇性缺血性血管疾病代表了新兴的临床挑战。先前的研究集中于治疗性血管生成策略可以减轻组织缺血的观点。然而，现在可以理解，血管疾病不仅限于血管壁细胞，还受到同时发生的炎症反应的影响。我们的实验室发现，用双嘧达莫对永久性组织缺血进行药理治疗会随着时间的推移显着增强缺血组织的再灌注，血管生成和动脉粥样硬化。我们发现双嘧达莫治疗的有益作用是由于其具有增加组织一氧化氮生物利用度的能力，该生物利用度可纠正组织氧化还原失衡。重要的是，我们还发现在慢性缺血性组织损伤过程中，调用一氧化二氮（NO）生成的双嘧达莫处理可显着下调各种先天免疫应答基因。这些发现表明，双嘧达莫诱导的亚硝酸盐/ NO生成明显降低了炎症反应，同时增加了缺血组织中的血管生长。

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