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Journal Article

Citation

Bucaretchi F, Collares EF. Braz. J. Med. Biol. Res. 1996; 29(2): 205-211.

Affiliation

Departamento de Pediatria, Universidade Estadual de Campinas, Brasil.

Copyright

(Copyright © 1996, Associacao Brasileira De Divulgacao Cientifica)

DOI

unavailable

PMID

8731350

Abstract

The effect of Phoneutria nigriventer spider venom (PNV) on the gastric emptying of liquids was studied in 240 young adult Wistar rats (2-3 months of age) divided into subgroups of 8 animals each. The study was performed in 3 stages. Initially, PNV was injected into rats at doses of 0.19, 0.38 or 0.76 mg/kg and the effect on gastric emptying was assessed 30 min later. In the second stage, a time-course study was performed by injecting 0.76 mg PNV/kg and measuring the effect on gastric emptying 15, 60 and 120 min post-venom. In the last stage, in order to investigate the possible mechanisms of PNV influence on gastric emptying, one group of rats underwent subdiaphragmatic vagotomy and then received 0.76 mg PNV/kg while three other groups were pretreated iv with either prazosin (0.4 mg/kg), domperidone (1.0 mg/kg) or propranolol (0.6 mg/kg) and then given 0.38 or 0.76 mg PNV/kg. In this last stage, gastric retention was measured 30 min post-venom. Each animal received a saline test meal solution containing phenol red as a marker (60 micrograms/ml). Ten min after administering the test meal by gavage, gastric retention was determined by measuring the residual test meal marker concentration and the animals were sacrified. PNV (0.76 mg/kg) provoked a significant delay in gastric emptying of liquids 15, 30 and 60 min after its administration. Propranolol partially interfered with gastric emptying in rats that had received 0.38 and 0.76 mg PNV/kg. Vagotomy and pretreatment of the rats with prazosin and domperidone had no effect. We conclude that the delay in the liquid gastric emptying observed in severely envenomed rats was probably due, at least in part, to a venom-stimulated release of catecholamines which inhibited gastric motility by activating smooth muscle beta-adrenergic receptors.


Language: en

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