Picture of boy being examining by doctor at a tuberculosis sanatorium

Understanding our future through Open Access research about our past...

Strathprints makes available scholarly Open Access content by researchers in the Centre for the Social History of Health & Healthcare (CSHHH), based within the School of Humanities, and considered Scotland's leading centre for the history of health and medicine.

Research at CSHHH explores the modern world since 1800 in locations as diverse as the UK, Asia, Africa, North America, and Europe. Areas of specialism include contraception and sexuality; family health and medical services; occupational health and medicine; disability; the history of psychiatry; conflict and warfare; and, drugs, pharmaceuticals and intoxicants.

Explore the Open Access research of the Centre for the Social History of Health and Healthcare. Or explore all of Strathclyde's Open Access research...

Image: Heart of England NHS Foundation Trust. Wellcome Collection - CC-BY.

Some pharmacological studies on the effects of Cerastes vipera (Sahara sand viper) snake-venom

Alzahaby, M. and Rowan, E.G. and Young, L.C. and Al-Zahaby, A.S. and Abu-Sinna, G. and Harvey, A.L. (1995) Some pharmacological studies on the effects of Cerastes vipera (Sahara sand viper) snake-venom. Toxicon, 33 (10). pp. 1299-1311. ISSN 0041-0101

Full text not available in this repository. Request a copy from the Strathclyde author

Abstract

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 3H-noradrenaline uptake were studied using rat brain synaptosomes. At 50 μg/ml and 100 μg/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 μM lignocaine, the effects of venom on rat atria were reversible by washing. At 100 μg/ml, the venom transiently increased responses of vas deferens preparations to indirect stimulation, but had little effect on responses to noradrenaline, KCl, and ATP. In the presence of an α1-adrenoceptor antagonist (prazosin) or a P2-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 μg/ml) significantly decreased twitches to indirect and direct stimulation in chick biventer cervicis preparations. Responses to exogenously applied acetylcholine, carbachol and KCl were also decreased. Venom blocked the synaptosomal uptake of 3H-noradrenaline (IC50 = 5 μg/ml), and caused severe bradycardia in vivo. Some of the direct effects on muscle preparations are possibly due to the venom's phospholipase A2 activity.