Pharmacological characterization of rat paw edema induced by Cerastes gasperettii (cerastes) venom

• Published in: Journal of Venomous Animals and Toxins including Tropical Diseases
• Main Authors: A. K. Al-Asmari, N. M. Abdo
• Format: Article in Journal/Newspaper
• Language: English
• Published: SciELO 2006
• Subjects: inflammatory mediators; Cerastes gasperettii venom; edema; antagonist; antivenom; Arctic medicine. Tropical medicine; RC955-962; Toxicology. Poisons; RA1190-1270; Zoology; QL1-991; Arctic
• Online Access: https://doi.org/10.1590/S1678-91992006000300005; https://doaj.org/article/cc485a63f6d24c659ca54d1f8a2420fa

Inflammatory response induced by the venom of the Arabian sand viper Cerastes gasperettii was studied by measuring rat hind-paw edema. Cerastes gasperettii venom (CgV, 3.75-240 µg/paw), heated for 30s at 97°C, caused a marked dose and time-dependent edema in rat paw. Response was maximal 2h after venom administration and ceased within 24h. Heated CgV was routinely used in our experiments at the dose of 120 µg/paw. Among all the drugs and antivenoms tested, cyproheptadine and 5-nitroindazole were the most effective in inhibiting edema formation. Aprotinin, mepyramine, dexamethasone, diclofenac, dipyridamole, Nomega-nitro-L-arginine, quinacrine, and nordihydroguaiaretic acid showed statistically (p<0.001) significant inhibitory effect, but with variations in their inhibition degree. Equine polyspecific and rabbit monospecific antivenoms significantly (p<0.001) reduced edema when locally administered (subplantar) but were ineffective when intravenously injected. We can conclude that the principal inflammatory mediators were serotonin, histamine, adenosine transport factors, phosphodiesterase (PDE), cyclooxygenase, lipoxygenase and phospholipase A2 (PLA2), in addition to other prostaglandins and cytokines.