Indian red scorpion (Buthus tamulus) venom-induced augmentation of cardiac reflexes is mediated through the mechanisms involving kinins in urethane anaesthetized rats

Bagchi, Sipra; Deshpande, Shripad B.

doi:10.1016/s0041-0101(97)00121-9

Cited by 36 publications

(34 citation statements)

References 18 publications

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“…The data with aprotinin elsewhere fully support for the elevation of endogenous kinins by BT venom. [5,6] In addition to kinin, PGs are also implicated in venom-induced changes. [6,16] Besides these inflammatory mediators, venom contains histamine, serotonin, and other peptides which produce pain.…”

Section: Discussionmentioning

confidence: 99%

“…[5,6] In addition to kinin, PGs are also implicated in venom-induced changes. [6,16] Besides these inflammatory mediators, venom contains histamine, serotonin, and other peptides which produce pain. There is possibility that all these chemical mediators stimulate or excite the vagal receptors or afferents to induce the inhibitory effect on the respiratory center resulting in respiratory failure and death of the animal.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6] Reports from this laboratory have shown that the animals died within 60 min of exposure to BT venom. [3] The cause of death was attributed to the respiratory failure and respiratory arrest.…”

Section: Introductionmentioning

confidence: 99%

“…[3] In studies elsewhere, acute myocarditis, conduction blockade, cardiac arrhythmias, and pulmonary edema were also implicated for the lethal effects of venom. [1,[2][3][4][5][6] It has been shown that BT venom increased the phenyl diguanide-sensitive vagal activity indicating the role of vagus. [4] The vagal activity although was completely blocked by ondansetron, a 5-HT 3 receptor antagonist, only aprotinin was able to prevent the pulmonary edema formation and the increased vagal activity.…”

Section: Introductionmentioning

confidence: 99%

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Role of vagus in mediating the toxicity induced by Mesobuthus tamulus venom in rats

Pandey¹,

Tiwari²,

Deshpande³

2017

Natl J Physiol Pharm Pharmacol

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Background: Mesobuthus tumulus (red scorpion, MBT) envenomation is a serious health problem in tropical countries and is responsible for high morbidity and mortality. Aims and Objectives: Earlier reports about the role of vagus in producing MBT venom-induced toxicity are conflicting. Therefore, in this study, the role of vagus in MBT venom-induced toxicity in rats was evaluated. Materials and Methods: The rats were divided into three groups. In group I, only saline was injected. This group served as control. In group II, MBT venom was injected. In group III, MBT venom was injected in vagotomized rats. Mean arterial pressure (MAP), ECG (for heart rate [HR]), respiratory rate, pulmonary water content, and survival time were determined in all groups. Results: Exposure to MBT venom in rats produced prolonged apnea with intermittent shallow breathing and was accompanied by an instantaneous decrease, followed by an increase and then a progressive decrease in MAP and HR leading to death within 60 min. There was increased pulmonary water content (82% vs. 74% in controls). MBT venom in vagotomized rats produced immediate changes as before, but these changes recovered to reasonably good level within 30 min and the animals survived for >120 min. Pulmonary water content in vagotomized rats was similar to control group. Conclusion: The results indicate that vagus plays a vital role for the toxic effects produced by MBT venom.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Role of vagus in mediating the toxicity induced by Mesobuthus tamulus venom in rats

Pandey¹,

Tiwari²,

Deshpande³

2017

Natl J Physiol Pharm Pharmacol

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“…Vasodilators, including captopril and nifedipine, have been used to correct both venom-induced hyper-and hypotension (Krishnan et al 2007), although the use of captopril, an ACE inhibitor, has been questioned since it has been shown that captopril-induced cardiopulmonary changes are similar to venom (Bagchi and Deshpande 1998). However, the most successful drug treatment has been the use of prazosin, an a-adrenergic blocker, championed by Bawaskar (Bawaskar and Bawaskar 1996).…”

Section: Pathophysiology and Clinical Aspectsmentioning

confidence: 99%

Scorpion Venom Research Around the World: Indian Red Scorpion

Strong

Mukherjee²,

Shah³

et al. 2014

Toxinology

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The Indian red scorpion is the medically most important scorpion on the Indian subcontinent, and a sting is often lethal without treatment, especially to young children. The correct identification of this species is Hottentotta tamulus; the more commonly known names, Buthus tamulus and Mesobuthus tamulus, and the suggestions of subspecies (Pocock) are incorrect and should be discouraged. Mild cases of H. tamulus envenoming show vasoconstriction and hypertension resulting from a massive release of catecholamines. Severe cases result in hypotension, pulmonary edema and myocardial dysfunction. Animal studies indicate that catecholamine release is as a consequence of prolonged sodium channel activation and potassium channel inhibition. Pulmonary edema results from many subcellular events, including kinin activation and stimulation of central serotonin receptor subtypes. Treatment with a specific antibody (with or without the a-adrenoreceptor blocker, prazosin, dependent on symptoms and clinical severity) is presently the preferred therapy. The few venom constituents that have been characterized in detail include iberiotoxin, a specific blocker of high conductance, calcium-activated potassium channels; tamapin, a specific blocker of low conductance calcium activated potassium channels (K Ca 2.2 subtype); and the short peptide insectotoxins, ButaIT and BtlTx3.

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