Acute cardiovascular effects of Naja oxiana venom in anesthetized rats

Document Type : Original Articles

Authors

1 Department of Pharmacology, School of Medicine, Bushehr University of Medical Sciences, Bushehr, Iran

2 College of Veterinary Medicine, Gyeongsang National University, Jinju, KR

3 Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Iran

4 Department of Human Vaccine and Serum,Razi Vaccine and Serum Research Institute,Agricultural Research,Education and Organization Organization,Karaj,Iran

5 Department of Pathology,Bushehr University of Medical Sciences,Bushehr,Iran

6 Department of Pharmacology,School of Medicine,Bushehr University of Medical Sciences,Bushehr,Iran

10.32592/ARI.2025.80.2.597

Abstract

Cobra bite is common in northwest province of Iran located in the Middle East Area. Naja naja oxiana envenomation is presented with neurologic manifestations like ptosis, drooling and so on. The aim of this preliminary study was to examine the hemodynamic abnormalities induced with intravascular injection of this venom in rats. Additionally, the neutralizing effects of different premedications were investigated.
Twenty male wistar rats weighting between 200-250 grams were randomly divided in to four groups (n=5). Group one was selected as control while the others were envenomed intravenously with crude venom (300µg/kg, 600 µg/kg and 1500 µg/kg) dissolved in normal saline (200µl) in two minutes. Atropine, dexamethasone, heparin and aminoguanidine were injected intraperitoneally ten minutes before envenomations to counteract its deleterious effects. All animals were sacrificed with cervical dislocation and their abdominal area were visualized for bleeding. Different organs (lung, heart and kidney) were removed and prepared for Hematoxylin and Eosin staining to reveal the pathological events.
N.oxiana venom (1500 µg/kg) induced significant ionotropic changes following intravenous infusion and all animals expired eight minutes later due to hypotension. There was no arrhythmia but heart rate was decreased statistically (p<0.001) in this group. Pretreatment with aminoguanidine (29±2.1%) and heparin (21±1.2%) prevented hypotension at 8 minutes but all animals eventually died at 20 minutes. Disruption of the alveolar walls of the lung with presence of the red blood cells and inflammatory components were observed while there were no pathological abnormalities with light microscope in other organs. It should be noted that according to our ionotropic and chronotropic results the last group was selected to continue our examinations.
In this preliminary study, it was observed that in large doses it could produce significant negative ionotropic effects in rats. According to our results, it seems that systemic vasodilation has a major role since pretreatment of heparin and aminoguanidine diminished this effect profoundly while there were no pathological abnormalities in other organs except lungs. It seems that increasing the doses of the heparin and aminoguanidine could prolong the survival of the envenomed rats in short time since all animals were died 20 minutes later.

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