Temple A R
Pediatrics. 1978 Nov;62(5 Pt 2 Suppl):873-6.
The principal pathophysiologic effect of toxic doses of salicylates are characterized by (1) stimulation of the respiratory center of the brain, leading to hyperpnea and respiratory alkalosis; (2) uncoupling of oxidative phosphorylation, leading to increased oxygen utilization and glucose demand, increased oxygen utilization and glucose demand, increased glyconeogenesis, and increased heat production; (3) inhibition of Krebs cycle enzymes, leading to decreased glucose availability and increased organic acids; (4) alterations in lipid metabolism and amino acid metabolism, enhancing metabolic acidosis; and (5) increased fluid and electrolyte losses, leading to dehydration, sodium depletion, potassium depletion, and loss of buffer capacity. The principal toxic manifestations of respiratory alkalosis and metabolic acidosis, altered glucose availability and depletion, fluid and electrolyte losses, and hypermetabolism result in serious morbidity and are potentially fatal. Therapy of salicylate intoxication should be aimed principally at replacement of fluid electrolytes, correction of acidemia, administration of glucose, and prevention of further salicylate absorption and enhancement of salicylate elimination.
（1）刺激大脑呼吸中枢，导致呼吸急促和呼吸性碱中毒；（2）氧化磷酸化解偶联，导致氧利用和葡萄糖需求增加、糖异生增加以及产热增加；（3）抑制三羧酸循环酶，导致葡萄糖供应减少和有机酸增加；（4）脂质代谢和氨基酸代谢改变，加重代谢性酸中毒；（5）液体和电解质丢失增加，导致脱水、钠耗竭、钾耗竭和缓冲能力丧失。呼吸性碱中毒和代谢性酸中毒、葡萄糖供应改变和耗竭、液体和电解质丢失以及高代谢的主要中毒表现会导致严重发病，并有潜在致命风险。水杨酸盐中毒的治疗应主要针对补充液体电解质、纠正酸血症、给予葡萄糖以及防止水杨酸盐进一步吸收和促进水杨酸盐排泄。
