Weischer C H
Int J Clin Pharmacol Ther Toxicol. 1980 Nov;18(11):494-9.
In the present study we examined the utility, sensitivity and specificity of the cadmium- and heat-induced hemolysis, investigating the effects of diclofenac, salicylate and lidocaine, carticaine and procaine on the rabbit erythrocyte membrane. In the cadmium-induced hemolysis, which has not been reported, as far as we know, as a test model for local anesthetics, the studied local anesthetics have, to a large extent, protective effects on the erythrocyte membranes, probably based on an osmotic action at drug concentrations of 10(-4) to 10(-2) M. On the other hand, these local anesthetics amplify the heat-induced hemolysis to a variable extent. The studied antirheumatic drugs showed in the cadmium-induced hemolysis that they cannot have the same binding sites as the local anesthetics investigated. In the cadmium-induced hemolysis, the reaction products of the antirheumatic drugs with the membrane protein presumably cannot cause an increase in surface area/volume ratio of the erythrocytes, which is generally regarded as a cause for stabilization. This interpretation could be an explanation for the increase of the cadmium-induced hemolysis by the antirheumatic drugs studied. On the other hand, the antirheumatic drugs inhibited to a variable extent the heat-induced hemolysis.
在本研究中,我们检测了镉和热诱导溶血的实用性、敏感性和特异性,研究了双氯芬酸、水杨酸盐、利多卡因、卡替卡因和普鲁卡因对兔红细胞膜的影响。据我们所知,镉诱导的溶血作为局部麻醉药的一种测试模型尚未见报道,在所研究的局部麻醉药中,在药物浓度为10(-4)至10(-2)M时,很大程度上对红细胞膜具有保护作用,可能基于渗透作用。另一方面,这些局部麻醉药在不同程度上会加剧热诱导的溶血。所研究的抗风湿药物在镉诱导的溶血中表明,它们与所研究的局部麻醉药没有相同的结合位点。在镉诱导的溶血中,抗风湿药物与膜蛋白的反应产物大概不会导致红细胞表面积/体积比增加,而这通常被认为是稳定化的一个原因。这种解释可能是所研究的抗风湿药物导致镉诱导溶血增加的原因。另一方面,抗风湿药物在不同程度上抑制了热诱导的溶血。