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组织缺氧引起的乳酸酸中毒是休克最重要的病生理之一。酸中毒能降低心肌收缩力和心输出量,增加内源性儿茶酚胺(CA)的合成与释放。CA(如多巴胺,DA)能改善降低了的血液动力学。但作者最近发现,严重的代谢性酸中毒能加快DA向去甲肾上腺素和肾上腺素的转化速度,去甲肾上腺素增高能抑制由输注DA而致的心输出量的增加。还原型谷胱甘肽(GSH)有细胞解毒作用、膜稳定作用和辅酶活性。应用外源性GSH能改善某些休克的血液动力学及其代谢。作者用酸中毒的狗,观察了DA灌流前、后GSH对血液动力学和血浆CA浓度改变的影响。
Lactic acidosis caused by hypoxia is one of the most important pathophysiology of shock. Acidosis can reduce myocardial contractility and cardiac output, increase endogenous catecholamine (CA) synthesis and release. CA (eg, dopamine, DA) improves reduced hemodynamics. However, the authors recently found that severe metabolic acidosis can speed up the conversion of DA to norepinephrine and epinephrine. Increased norepinephrine can inhibit the increase in cardiac output caused by infusion of DA. Reduced glutathione (GSH) has cell detoxification, membrane stabilization and coenzyme activity. Exogenous GSH can improve the hemodynamics and metabolism of certain shock. The author used acid-poisoned dogs to observe the effect of GSH on hemodynamics and plasma CA concentration before and after DA perfusion.