Hemodynamic Changes Provoked through Intravascular Injection of the Echis carinatus Venom in Rats
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Published on: December 19, 2013
S Zaeri1, H Fatemikia2, M Kamyab3
1Department of Pharmacology, Bushehr University of Medical Sciences, Bushehr, Iran.
Insights
The Iranian Echis carinatus snake venom causes severe hypotension and bradycardia in rats, leading to death. Antivenom administration is effective only when given immediately after envenomation.
Area of Science:
- Toxicology
- Cardiovascular Physiology
- Pathology
Background:
- Echis carinatus envenomation is known for hematological and nephrotoxic effects.
- Limited data exists on cardiovascular changes induced by Iranian Echis carinatus venom.
Purpose of the Study:
- To evaluate the venom-induced hemodynamic manifestations of Iranian Echis carinatus in rats.
- To assess the efficacy of antivenom and other drugs in counteracting these effects.
Main Methods:
- Intravenous administration of Echis carinatus venom (120 µg/kg) to rats.
- Continuous recording of hemodynamic parameters (blood pressure, heart rate, pulmonary rate).
- Evaluation of pre-treatment effects of antivenom, heparin, epinephrine, atropine, dexamethasone, and ketorolac.
Main Results:
- Venom induced significant hypotension, transient hypertension, bradycardia, and decreased pulmonary rate, leading to death.
- Immediate pre-treatment with Iranian polyvalent antivenom, heparin, and epinephrine neutralized hypotension.
- Atropine, dexamethasone, and ketorolac showed no protective effects.
- Histological examination revealed lung damage (mononuclear infiltration, congestion), renal deterioration (tubular necrosis), and mild hepatic inflammation.
Conclusions:
- Iranian Echis carinatus venom causes life-threatening hypotension and bradycardia.
- Early administration of specific antivenom is crucial for effective treatment.
- The venom primarily affects the cardiovascular system, lungs, and kidneys, with minimal cardiac histological changes.
Abstract:
Echis carinatus (E. carinatus) is known for its hematological and nephrotoxic properties in the envenomed patients. Based on the limited data upon the cardiovascular changes associated with this dangerous venomous snake in Iran, the current study purposed to evaluate the venom-induced hemodynamic manifestations in rats. Venom (120 µg/kg) was administered intravenously within one minute through the left femoral vein, and the hemodynamic parameters were continuously recorded using a pressure transducer (MLT844, ADInstruments, Australia). The venom caused prominent hypotension leading to death a few minutes after a transient uprise in blood pressure. It also induced a decrease in heart and pulmonary rates, yet it had no arrhythmogenic properties. Additionally, pre-treatment with the pepsin-derived Iranian polyvalent antivenom (30 µl/Kg) completely neutralized the hemodynamic responses but had no effect when instilled two minutes after venom injection. Heparin (300 IU/kg) and epinephrine (1.5 µg/kg) prevented dramatic hypotension when used 10 minutes before venom instillation; however, atropine (1 mg/kg), dexamethasone (1 mg/kg), and ketorolac (10 mg/ml) had no effects. All treated rats were killed post-injection. Histologically, the lung was the most vulnerable organ with mononuclear infiltration, microcystic formation, and significant capillary congestion. Prominent renal pathological deterioration also occurred, including mesangial cell infiltration and diffuse bleeding, leading to acute tubular necrosis. Modest portal inflammation and vascular congestion were observed in the hepatic tissue of the envenomed rats. The crude venom of Iranian Echis carinatus caused hypotension leading to bradycardia, a decrease in pulmonary rate, and death without significant histological changes to the heart.
