A Pharmacological Examination of the Cardiovascular Effects of Malayan Krait (Bungarus candidus) Venoms

摘要: Cardiovascular effects (e.g., tachycardia, hypo- and/or hypertension) are often clinical outcomes of snake envenoming. Malayan krait (Bungarus candidus) envenoming has been reported to cause cardiovascular that may be related abnormalities in parasympathetic activity. However, the exact mechanism for this effect yet determined. In present study, we investigated vivo and vitro B. candidus venoms from Southern (BC-S) Northeastern (BC-NE) Thailand. SDS-PAGE analysis showed some differences protein profile venoms. (50 µg/kg-100 µg/kg, i.v.) caused dose-dependent hypotension anaesthetised rats. The highest dose sudden (phase I) followed by a return mean arterial pressure baseline levels decrease heart rate with transient hypertension II) prior small blood III). Prior administration monovalent antivenom significantly attenuated induced (100 i.v.). hypotensive BC-NE venom was abolished hexamethonium (10 mg/kg, or atropine (5 BC-S (0.1 µg/ml) concentration-dependent relaxation (EC50 = 8 ± 1 13 3 µg/mL, respectively) endothelium-intact aorta. concentration-response curves were markedly shifted right pre-incubation L-NAME (0.2 mM), removal endothelium, suggesting endothelium-derived nitric oxide (NO) is likely responsible venom-induced aortic relaxation. Our data indicate due combination vascular mediators (i.e., NO) autonomic adaptation via nicotinic muscarinic acetylcholine receptors.