Changes in the arterial blood pressure, heart rate and normal ECG parameters of rat after envenomation with Egyptian cobra (Naja haje) venom

Omran, Mohamed A.; Abdel-Nabi, Ismail M.

doi:10.1177/096032719701600606

Cited by 9 publications

(6 citation statements)

References 22 publications

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“…, 1996). Further, preclinical models identified R wave increases caused by drugs and chemicals of known or assumed pro‐arrhythmic properties (Sandusky and Meyers, 1985; Omran and Abdel‐Nabi, 1997; Watanabe et al. , 1999).…”

Section: Mechanisms Of Ventricular Fibrillationmentioning

confidence: 99%

“…The incidence of familial dilated cardiomyopathy (Codd et al, 1989;Manolio et al, 1992) is larger than that of congenital short QT syndrome, clinically healthy relatives of patients show subclinical abnormalities (Baig et al, 1998) and the disease is associated with a clear risk of fatal arrhythmias (Jordaens et al, 1996). Further, preclinical models identified R wave increases caused by drugs and chemicals of known or assumed pro-arrhythmic properties (Sandusky and Meyers, 1985;Omran and Abdel-Nabi, 1997;Watanabe et al, 1999). Nevertheless, while the hypotheses about adverse drug actions associated with these electrocardiographic changes might be as plausible as or even more plausible than the hypothesis of QTc shortening causing abrupt ventricular fibrillation, there is no evidence suggesting that we should take them seriously.…”

Section: Mechanisms Of Ventricular Fibrillationmentioning

confidence: 99%

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Facts, fancies and follies of drug‐induced QT/QTc interval shortening

Malik

2010

British J Pharmacology

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Parallels exist between drug-induced QT/QTc prolongation and shortening. However, these parallels are largely superficial and the experience with drug-induced QTc prolongation and its potential proarrhythmic link cannot be directly applied to drug-related QTc shortening. The congenital short QT syndrome (SQTS) is clearly much less prevalent than congenital, long QT syndrome, possibly some 1000 times. If the same discrepancy exists between arrhythmic susceptibility to drug-induced QTc prolongation and shortening, it is questionable whether regulatory burden should be imposed on drugs that might cause serious arrhythmia, once in many millions of exposures. Further, majority of torsadegenic drugs block the IKr current which is susceptible to the drug blockade because of the corresponding channel geometry. There is no parallel known for drug-induced QTc shortening. Also, all drugs that prolong QTc interval massively cause torsade de pointes tachycardia in more than exceptional isolated instances. On the contrary, digitalis that causes substantial QTc shortening is not known to trigger frequently ventricular arrhythmias. Moreover, most available population QTc data were obtained with Bazett's correction which produces erroneous QTc shortening at slow heart rates. Safety limits derived from such data are inappropriate. Because practically all new drugs undergo the so-called thorough QT study, drug-induced QTc shortening will not go unnoticed for any new pharmaceutical. Describing drug-related QTc shortening in the label seems sufficient to avoid treatment of the rare SQTS subjects. Intensive investigations of QTc-shortening drugs (similar to those of drugs with positive thorough QT studies) do not seem to be warranted.

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Section: Mechanisms Of Ventricular Fibrillationmentioning

confidence: 99%

Section: Mechanisms Of Ventricular Fibrillationmentioning

confidence: 99%

Facts, fancies and follies of drug‐induced QT/QTc interval shortening

Malik

2010

British J Pharmacology

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“…Neurotoxic and systemic symptoms develop within few hours, and deaths have occurred within 6-16 hours after large snakes' bites, despite the use of antivenom and mechanical ventilation (38). Several authors have reported that sublethal doses of N. haje venom induced potent histopathological, histochemical, and pathophysiological alterations in the heart, liver, kidney, and brain of rats (4,12,(22)(23)(24). These pathological changes included severe degrees of cellular damage concomitant with marked signs of both myolytic and coagulative necrosis (27)(28)(29).…”

Section: Introductionmentioning

confidence: 99%

Biochemical and morphological analysis of cell death induced by Egyptian cobra (Naja haje) venom on cultured cells

Fabb

Dickson

2004

J. Venom. Anim. Toxins incl. Trop. Dis

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ABSTRACT. We investigated the in vitro process of cell death caused by Egyptian cobra venom on primary human embryonic kidney (293T) and mouse myoblast (C2C12) cell lines. The aim of these studies was to provide further information about triggering cell death, and suggest methods for eliminating unwanted cells, such as tumour cells. Both cell lines were treated with 10, 20, and 50 µg/ml of Egyptian cobra (Naja haje) venom in serum free media (SFM) and incubated for 8 hours. Total activities of the lactate dehydrogenase (LDH) and creatine kinase (CK) released in the culture during venom incubation were used as an indicator of the venom in vitro cytotoxicity. Cell injury was morphologically recognized and apoptosis determined by a Fluorescing Apoptosis Detection System and confirmed by staining nuclear DNA with DAPI. Our data clearly demonstrated marked cytotoxic effects and acute cell injury for both cell lines. Release of LDH and CK into the culture media induced by the venom correlates well with the morphological changes and extent of cell death. Mostly, these consequences were time and dose-dependent in both cell lines. The results obtained from this study indicated that cobra venom cause cell death by two different mechanisms: necrosis and induction of apoptosis. The apoptotic mechanism, accompanied by cell necrosis, mediated cell destruction of both tested cell lines; however, necrosis was predominant in the C2C12 cell line while apoptosis, in 293T cells. This unusual form of cell death induced by cobra venom may represent a combination of apoptosis and necrosis within the same cell. This is a first-hand investigation showing the apoptotic effects of N. haje venom at the cellular level. However, the contribution of the apoptotic pathway may be dependent on concentration and/or time of exposure to snake venom.

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“…The most important manifestation of the cardiac effects of cobra venom arise from alterations in electrical or contractile properties of the heart. The effect of Egyptian cobra (Naja haje) on BP and chronotropic response of the heart might be dose dependent as reported in a study based on an experiment conducted on rats (10). In that study, a hypothesis was inferred that the differences in the concentration of the neurotoxic and cardiotoxic components of the venom in the blood of envenomated rats affect the entire vascular system, regulating the mean arterial BP and cardiac muscles in different ways.…”

Section: Discussionmentioning

confidence: 95%

Autonomic Dysfunction Manifesting as Severe Hypertension Following Cobra Envenomation: An Unusual Occurrence

Singh¹,

Balasubramanian²,

Gupta³

2018

J Emerg Med Case Rep

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Introduction: Envenomation due to an elapid snake (krait or cobra) bite is a common life-threatening medical emergency in India and is associated with significant morbidity and mortality. Common cobra (Naja naja) and common krait (Bungarus caeruleus) are the common snake species whose bites are associated with neuroparalysis, which is a key feature of envenomation. Autonomic dysfunction (AD) is another feature of envenomation with varied clinical presentations such as abdominal pain, vomiting, sweating, mydriasis, mild to moderate hypertension (HTN) or hypotension, and cardiac arrhythmia. The occurrence of AD manifesting as severe HTN and tachycardia is unusual following an elapid snake bite. This presentation has been frequently reported with krait envenomation but can also be observed with cobra envenomation. Case Report: We present the case of a 31-year-old male with common cobra (Naja naja) envenomation presenting with neuroparalysis along with severe HTN and tachycardia. The patient had a gradual and sustained recovery with anti-snake venom and other supportive care. Conclusion: Increasing incidences of cobra envenomation warrant that understanding its atypical presentation and its early recognition are of paramount importance as they may alter treatment decisions influencing the overall morbidity and mortality.

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Changes in the arterial blood pressure, heart rate and normal ECG parameters of rat after envenomation with Egyptian cobra (Naja haje) venom

Cited by 9 publications

References 22 publications

Facts, fancies and follies of drug‐induced QT/QTc interval shortening

Facts, fancies and follies of drug‐induced QT/QTc interval shortening

Biochemical and morphological analysis of cell death induced by Egyptian cobra (Naja haje) venom on cultured cells

Autonomic Dysfunction Manifesting as Severe Hypertension Following Cobra Envenomation: An Unusual Occurrence

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