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

Department of Pharmacology, Phramongkutklao College of Medicine, Bangkok 10400, Thailand
Department of Physiology, Phramongkutklao College of Medicine, Bangkok 10400, Thailand
Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok 65000, Thailand
Queen Saovabha Memorial Institute, The Thai Red Cross Society, Bangkok 10330, Thailand
Jeffrey Cheah School of Medicine and Health Sciences, Monash University Sunway Campus, Bandar Sunway 46150, Malaysia
Authors to whom correspondence should be addressed.
Academic Editor: Andreimar M. Soares
Toxins 2017, 9(4), 122;
Received: 13 March 2017 / Revised: 23 March 2017 / Accepted: 24 March 2017 / Published: 29 March 2017
(This article belongs to the Section Animal Venoms)
PDF [2167 KB, uploaded 31 March 2017]


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

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Chaisakul, J.; Rusmili, M.R.A.; Hodgson, W.C.; Hatthachote, P.; Suwan, K.; Inchan, A.; Chanhome, L.; Othman, I.; Chootip, K. A Pharmacological Examination of the Cardiovascular Effects of Malayan Krait (Bungarus candidus) Venoms. Toxins 2017, 9, 122.

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