Citation

Dutta A, Deshpande SB. Toxicon 2011; 57(2): 193-198.

Affiliation

Department of Physiology, Institute of Medical Sciences, BanarasHindu University, Varanasi-221005, India.

Copyright

(Copyright © 2011, Elsevier Publishing)

DOI

10.1016/j.toxicon.2010.11.010

PMID

21112349

Abstract

Pulmonary edema is a consistent feature of Mesobuthus tamulus (MBT) envenomation. Kinins, prostaglandins and other inflammatory mediators are implicated in it. Since, histamine also increases capillary permeability, this study was undertaken to evaluate whether MBT venom utilizes histamine to produce pulmonary edema and augmentation of cardio-respiratory reflexes evoked by phenylbiguanide (PBG). Blood pressure, respiratory excursions and ECG were recorded in urethane anaesthetized adult rats. Injection of PBG (10 μg/kg) produced apnoea, hypotension and bradycardia and the responses were augmented after exposure to venom (100 μg/kg). There was increased pulmonary water content in these animals. Pretreatment with pheniramine maleate (H(1)-antagonist, 3 mg/kg) blocked both venom-induced augmentation of PBG-response and pulmonary edema. In another series, compound 48/80 (mast cell depletor) was treated for 4 days then the PBG responses were elicited as before. At the end of the experiments, mast cells were counted from the peritoneal fluid. The venom-induced pulmonary edema and the augmentation of PBG-reflex were not observed in compound 48/80 treated animals. Further, mast cells in the peritoneal fluid were absent in this group as compared to vehicle treated group (29 ± 7.9 cells/mm(3)). These observations indicate that venom-induced pulmonary edema and augmentation of PBG reflexes are mediated through mast cells by involving H(1)-receptors.

Language: en