The effects of lignocaine on actions of the venom from the yellow scorpion Leiurus quinquestriatus'' in vivo and in vitro

Abstract

The effects of lignocaine on actions of the venom from the yellow scorpion, Leiurus quinquestriatus, in vivo and in vitro. Toxicon, 19. Many toxins from scorpion venoms activate sodium channels, thereby enhancing neurotransmitter release. The aim of the present work was to determine if the in vivo and in vitro e ects of Leiurus quinquestriatus venom (LQQ) could be ameliorated by lignocaine, a sodium channel blocker. In urethane anaesthetised rabbits, LQQ venom (0.5 mg kgÿ1, i.v.) caused initial hypotension and bradycardia followed by hypertension, pulmonary oedema, electrocardiographic changes indicating conduction defects, ischaemia, infarction, and then hypotension and death. Lignocaine (1 mg kgÿ1 i.v. bolus initially, followed by i.v. infusion of 50 mg kgÿ1 minÿ1) signi®cantly attenuated the majority of the venom-evoked e ects and reduced mortality. Addition of LQQ venom (1, 3 and 10 mg mlÿ1) to chick biventer cervicis, guinea pig ileum, and rat vas deferens preparations, increased the height of electrically-induced twitches, elevated resting tension, and caused autorhythmic oscillations. Lignocaine (3 10ÿ4±1.2 10ÿ3 M) greatly attenuated these venom-evoked actions in the three preparations. Antagonists of appropriate neurotransmitters were also tested to determine the contribution of released transmitters to LQQ e ects. Atropine signi®cantly decreased the venom-elicited e ects on guinea pig ileum preparations, while prazosin and guanethidine signi®cantly reduced the venom's actions on rat vas deferens. In chick biventer cervicis preparations, tubocurarine and hexamethonium signi®cantly attenuated the venom-induced e ects. This study supports the hypothesis that many e ects of LQQ venom involve the release of neurotransmitters and may be ameliorated by treatment with lignocaine.