Schade D S
Ciba Found Symp. 1982;87:235-53. doi: 10.1002/9780470720691.ch13.
Catecholamines (noradrenaline and adrenaline) are catabolic hormones secreted during stress. They initiate many metabolic processes including increased production of both ketoacids and lactic acid. Support for a direct participation of these hormones in the development and/or maintenance of ketoacidosis includes: (1) the high incidence of stress (approx. 70%) as a precipitating factor for ketoacidosis; (2) the elevated plasma levels of noradrenaline (norepinephrine) in patients with ketoacidosis; (3) the rise in plasma concentrations of ketone bodies during catecholamine infusion; and (4) the reduction in the incidence of ketoacidosis with beta-adrenergic pharmacological blockade. Support for a direct participation of catecholamines in the development and/or maintenance of lactic acidosis includes: (1) the common association of stress and lactic acidosis; (2) the rise in plasma lactate concentration during adrenaline (epinephrine) infusion; (3) the precipitation of lactic acidosis by adrenaline intoxication and phaeochromocytoma; and (4) the vasoconstrictor effects of catecholamines leading to tissue anoxia and lactic acid production. Thus, in susceptible patients, catecholamines may be principal determinants of whether ketoacidosis and/or lactic acidosis develops.
儿茶酚胺(去甲肾上腺素和肾上腺素)是应激期间分泌的分解代谢激素。它们启动许多代谢过程,包括酮酸和乳酸生成增加。支持这些激素直接参与酮症酸中毒发生和/或维持的证据包括:(1)应激作为酮症酸中毒促发因素的高发生率(约70%);(2)酮症酸中毒患者血浆去甲肾上腺素(去甲肾上腺素)水平升高;(3)儿茶酚胺输注期间酮体血浆浓度升高;(4)β-肾上腺素能药理学阻断可降低酮症酸中毒的发生率。支持儿茶酚胺直接参与乳酸酸中毒发生和/或维持的证据包括:(1)应激与乳酸酸中毒的常见关联;(2)肾上腺素(肾上腺素)输注期间血浆乳酸浓度升高;(3)肾上腺素中毒和嗜铬细胞瘤引发乳酸酸中毒;(4)儿茶酚胺的血管收缩作用导致组织缺氧和乳酸生成。因此,在易感患者中,儿茶酚胺可能是酮症酸中毒和/或乳酸酸中毒是否发生的主要决定因素。