Collares C B, Ribeiro-da-Silva G
Departamento de Farmacologia, Faculdade de Ciências Médicas, UNICAMP, Campinas, Brasil.
Braz J Med Biol Res. 1988;21(1):107-10.
This paper reports on the metabolic alkalosis produced in rats by canatoxin, a neurotoxic principle extracted from Canavalia ensiformis seeds. Rats receiving canatoxin showed increased blood bicarbonate concentration with alkaline pH and no change in pCO2. A fall in pO2 was also seen. A dose-dependent relationship between pO2 decrease and bicarbonate increase was also observed with the toxin, suggesting that hypoxia may result from respiratory compensation. Canatoxin-induced hypoxia was both lipoxygenase and cyclo-oxygenase dependent but metabolic alkalosis was only blocked with cyclo-oxygenase inhibitors. Canatoxin activates the lipoxygenase pathway and probably increases leukotriene (LT) production. Since LT may release cyclo-oxygenase products, this may explain the metabolic alkalosis observed with canatoxin.
本文报道了刀豆毒素（一种从刀豆种子中提取的神经毒性成分）在大鼠体内引起的代谢性碱中毒。接受刀豆毒素的大鼠血液碳酸氢盐浓度升高，pH呈碱性，而pCO2无变化。同时还观察到pO2下降。毒素引起的pO2下降与碳酸氢盐升高之间也存在剂量依赖关系，提示低氧可能是呼吸代偿的结果。刀豆毒素诱导的低氧既依赖脂氧合酶又依赖环氧化酶，但代谢性碱中毒仅被环氧化酶抑制剂阻断。刀豆毒素激活脂氧合酶途径，可能增加白三烯（LT）的生成。由于LT可能释放环氧化酶产物，这或许可以解释刀豆毒素所致的代谢性碱中毒。
