SOME PHARMACOLOGICAL STUDIES ON THE EFFECTS OF CERASTES VIPERA (SCHARA SAND VIPER) SNAKE-VENOM

The effects of the venom of the Sahara sand viper (Cerastes vipera) were studied on isolated chick biventer cervicis, isolated rat atria and vas deferens preparations, and on the electrocardiogram of anaesthetized rats. Effects on H-3-noradrenaline uptake were studied using rat brain synaptosomes. At 50 mu g/ml and 100 mu g/ml, the venom caused a transient increase in rate and force of contractions of the rat atria followed by an irreversible depression. These effects were not prevented by atenolol, atropine or a combination of the two. In the presence of 25 mu M lignocaine, the effects of venom on rat atria were reversible by washing. At 100 mu g/ml, the venom transiently increased responses of vas deferens preparations to indirect stimulation, but had little effect on responses to noradrenaline, KCI, and ATP. In the presence of an alpha(1)-adrenoceptor antagonist (prazosin) or a P-2-purinergic receptor antagonist (suramin), the venom still significantly increased twitch height and responses to noradrenaline but not to KCl or ATP. The effect of the venom did not change after exposure to a combination of prazosin, suramin and tetrodotoxin. The venom (100 mu g/ml) significantly decreased twitches to indirect and direct stimulation in chick biventer cervicis preparations. Responses to exogenously applied acetylcholine, carbachol and KCI were also decreased. Venom blocked the synaptosomal uptake of 3H-noradrenaline (IC50 = 5 mu g/ml), and caused severe bradycardia in vivo. Some of the direct effects on muscle preparations are possibly due to the venom's phospholipase A(2) activity.