Cavaliere M J, Puga F R, Calore E E, Calore N M, Pelegrino J R, da Rosa A R, Weg R
Instituto Adolfo Lutz, Divisão de Patologia, São Paulo, Brazil.
J Toxicol Clin Toxicol. 1998;36(4):295-300. doi: 10.3109/15563659809028024.
To determine the protective effect of pralidoxime on muscle fiber necrosis induced by organophosphate acute intoxication in rats.
Adult male Wistar rats were given oral organophosphate compounds dissolved in glycerol formal: dichlorvos, isofenphos, metamidophos, and diazinon. Half of the animals also received pralidoxime mesylate (20 mg/kg, intraperitoneal). Control animals received only the solvent. Twenty-four hours after treatment, the diaphragm muscle was collected for histological counts of necrotic muscle fibers in transverse sections.
Metamidophos- and isofenphos-treated animals showed the highest percentage of necrotic muscle fibers: 1.66 +/- 1.112 and 1.34 +/- 0.320, respectively. Diazinon-treated animals had a lower percentage of necrotic fibers: 0.40 +/- 0.032 (p < 0.05) compared to the first 2 products, and dichlorvos-treated animals showed the smallest: 0.05 +/- 0.021 (p < 0.05) when compared to the other 3 products. Pralidoxime reduced necrotic fibers about 20 times in metamidophos-treated animals, 10 times in isofenphos-treated animals and 6 times in diazinon-treated animals. Pralidoxime administration did not increase plasma cholinesterase activity in any group, although symptoms were reduced.
Oxime reduced diaphragmatic muscle necrosis in experimental organophosphate intoxication, despite little effect on plasma cholinesterase. Since respiratory insufficiency is an important cause of mortality and morbidity in organophosphate intoxications, early oxime administration may be particularly beneficial.
确定氯解磷定对大鼠有机磷急性中毒所致肌纤维坏死的保护作用。
成年雄性Wistar大鼠经口给予溶解于福尔马林甘油中的有机磷化合物:敌敌畏、异柳磷、甲胺磷和二嗪农。半数动物还接受甲磺氯解磷定(20 mg/kg,腹腔注射)。对照动物仅给予溶剂。治疗24小时后,采集膈肌用于横切片坏死肌纤维的组织学计数。
甲胺磷和异柳磷处理的动物显示坏死肌纤维百分比最高:分别为1.66±1.112和1.34±0.320。与前两种产物相比,二嗪农处理的动物坏死纤维百分比更低:0.40±0.032(p<0.05),与其他三种产物相比,敌敌畏处理的动物坏死纤维百分比最小:0.05±0.021(p<0.05)。氯解磷定使甲胺磷处理的动物坏死纤维减少约20倍,异柳磷处理的动物减少10倍,二嗪农处理的动物减少6倍。尽管症状减轻,但氯解磷定给药并未增加任何组的血浆胆碱酯酶活性。
肟类药物可减轻实验性有机磷中毒时的膈肌坏死,尽管对血浆胆碱酯酶影响不大。由于呼吸功能不全是有机磷中毒致死和致残的重要原因,早期给予肟类药物可能特别有益。