Indian red scorpion venom-induced augmentation of cardio-respiratory reflexes and pulmonary edema involve the release of histamine

Dutta, Abhaya; Deshpande, Shripad B.

doi:10.1016/j.toxicon.2010.11.010

Cited by 20 publications

(10 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The NO involvement by venom is also reported for the augmentation of cardiovascular reflexes (Kanoo et al 2009). Further, venom-induced changes are shown to be mediated through kinins, prostaglandins and histamine (Bagchi and Deshpande 1998;Dutta and Deshpande, 2011;Kanoo et al 2009. Thus, venominduced toxicity may be due to the activation of NO synthesis directly by venom or via the inflammatory mediators such as kinins, histamine, prostaglandins, etc.…”

Section: Discussionmentioning

confidence: 99%

Involvement of NO-guanylyl cyclase pathway for the depression of spinal monosynaptic reflex by Mesobuthus tamulus venom in neonatal rat in vitro

Maurya¹,

Deshpande²

2011

Life Sciences

Self Cite

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Involvement of NO-guanylyl cyclase pathway for the depression of spinal monosynaptic reflex by Mesobuthus tamulus venom in neonatal rat in vitro

Maurya¹,

Deshpande²

2011

Life Sciences

Self Cite

View full text Add to dashboard Cite

“…Metabolic data from Murthy's group include cardiac sarcolemmal defects, reduced insulin secretion, and alterations in both carbohydrate and fat metabolism (see inter alia, Murthy 1982;Murthy and Ag 1986;Murthy and Medh 1986;). Deshpande's group has shown that venom-induced pulmonary edema and augmentation of cardiac reflexes are produced through a variety of cellular processes, including the stimulation of central serotonin (5-HT 1A ) subtypes , kinin activation of a nitric oxide/cGMP pathway (Kanoo et al 2009), and histamine release mediated by H 1 receptors on mast cells (Dutta and Deshpande 2011). From animal studies, a number of different treatments have been proposed.…”

Section: Pathophysiology and Clinical Aspectsmentioning

confidence: 99%

Scorpion Venom Research Around the World: Indian Red Scorpion

Strong

Mukherjee²,

Shah³

et al. 2014

Toxinology

View full text Add to dashboard Cite

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.

show abstract

“…One possibility is that degranulation of mast cells is driven by some neuroendocrine factors such as substance P released from sensory nerve fiber terminals activated by scorpion venom; the other possibility is that degranulation of mast cells is triggered directly by scorpion venom (Matos et al 1999;Liu et al 2007). Other possibility is that scorpion venom enhances the synthesis of kinins; kinins activate the mast cells to release histamine to bring about the pulmonary edema (Dutta and Deshpande 2011).…”

Section: Mast Cells and Eosinophilsmentioning

confidence: 99%

Scorpion Venom Interactions with the Immune System

2013

View full text Add to dashboard Cite

Scorpion envenomation (SE) is a common medical problem in many countries; it is an important cause of morbidity and mortality, especially among children. In certain cases scorpion stings lead to multiorgan failure that may be fatal; the manifestations include acute respiratory distress syndrome and systemic inflammatory response syndrome. Neurotoxins are the most active components of the scorpion venom responsible for the toxic effects induced after SE. They induce a massive release of neurotransmitters during stimulation of sympathetic and parasympathetic of the autonomic nervous system. The pathophysiological disturbances caused by scorpion venom are not exclusively assigned to the released neurotransmitters. The activation and release of inflammatory mediators (cytokines, kinins, eicosanoids, reactive oxygen species, and nitric oxide) may also play an important role in the pathophysiology of envenomation after stings and may be responsible for some of the inflammatory manifestations and organ failure. The massive release of these mediators from injured and activated cells promotes the inflammatory response and may be responsible for its exacerbation and its maintenance. The present chapter focuses on the role of inflammatory mediators and on elucidation of the potential mechanisms by which the immune system affects the pathophysiology following SE. Understanding of involved inflammatory cascade in scorpion envenoming syndromes may have future therapeutic and diagnostic benefits.

show abstract

Indian red scorpion venom-induced augmentation of cardio-respiratory reflexes and pulmonary edema involve the release of histamine

Cited by 20 publications

References 22 publications

Involvement of NO-guanylyl cyclase pathway for the depression of spinal monosynaptic reflex by Mesobuthus tamulus venom in neonatal rat in vitro

Involvement of NO-guanylyl cyclase pathway for the depression of spinal monosynaptic reflex by Mesobuthus tamulus venom in neonatal rat in vitro

Scorpion Venom Research Around the World: Indian Red Scorpion

Scorpion Venom Interactions with the Immune System

Contact Info

Product

Resources

About