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Considerations about an experimental model of chronic metabolic acidosis in rats

机译:关于大鼠慢性代谢酸中毒实验模型的思考

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During the last decades, several studies have beenpublished and have led to the data collection on the acid?basedisorder and endothelial function (Celotto et al., 2008).It was determined that extracellular acidification induced byHCl (7.4 to 6.5) promotes NO, K (ATP) and SK-mediatedvasodilation (Ca), and perhaps other K (+) channels inthe isolated thoracic aorta of the rat (Celotto et al., 2011).The scientific literature has many reports on acid-basebalance and endothelium function, but these concepts areunclear about acid-base disorders and their relationship tothe three known mechanisms of endothelium-dependentvascular reactivity: nitric oxide (NO/cGMP-dependent),prostacyclin (PGI2/cAMP-dependent) and hyperpolarization.
机译:在过去几十年中,几项研究已经发布并导致了酸上的数据收集?基于序列和内皮功能(Celotto等,2008)。确定诱导ByHCl(7.4至6.5)的细胞外酸化促进k (ATP)和SK - 介导的血致硅(CA),也许是其他K(+)频道的大鼠孤立的胸主动脉(Celotto等,2011)。科学文献有许多关于酸基培训和内皮功能的报道,但是这些概念缺乏酸基疾病及其关系,涉及三种已知的内皮依赖性反应性机制:一氧化氮(NO / CGMP依赖性),前列环素(PGI2 / CAMP依赖性)和超极化。

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