Assuntos
Alcalose/diagnóstico , Antiácidos/intoxicação , Overdose de Drogas/diagnóstico , Fármacos Gastrointestinais/intoxicação , Bicarbonato de Sódio/intoxicação , Taquicardia Ventricular/etiologia , Alcalose/induzido quimicamente , Alcalose/fisiopatologia , Alcalose/terapia , Antiácidos/antagonistas & inibidores , Diagnóstico Diferencial , Overdose de Drogas/fisiopatologia , Overdose de Drogas/terapia , Gastrite/tratamento farmacológico , Fármacos Gastrointestinais/antagonistas & inibidores , Azia/tratamento farmacológico , Humanos , Masculino , Medicina Tradicional/efeitos adversos , Pessoa de Meia-Idade , Automedicação/efeitos adversos , Índice de Gravidade de Doença , Bicarbonato de Sódio/antagonistas & inibidores , Taquicardia Ventricular/prevenção & controle , Taquicardia Ventricular/terapia , Resultado do TratamentoRESUMO
Dopaminergic compounds affect gastric secretion and response to experimental gastric mucosal injury. We showed previously that the novel dopamine D4 receptor antagonist, clozapine, significantly reduces gastric acid secretion and restraint stress-induced gastric lesions. Because the selectivity of clozapine for D4 receptors has recently been questioned, we tested the ability of a known D1 receptor blocker, SCH23390, to affect clozapine-induced reduction in gastric acid secretion. SCH23390 given i.p. or i.c.v., at doses that did not affect gastric acid secretion, significantly blocked the anti-secretory effect of clozapine, administered either peripherally or centrally. These data suggest that neither clozapine nor SCH23390 exhibit as high a degree of selectivity for the dopamine D4 and D1 receptor, respectively, as previously believed.
Assuntos
Antiácidos/antagonistas & inibidores , Benzazepinas/farmacologia , Clozapina/antagonistas & inibidores , Antagonistas de Dopamina/farmacologia , Animais , Interações Medicamentosas , Ácido Gástrico/metabolismo , Injeções Intraperitoneais , Injeções Intraventriculares , Masculino , Ratos , Ratos Sprague-Dawley , Taxa Secretória/efeitos dos fármacosRESUMO
The inhibitory effect of elastase on experimental atherosclerosis has been reported in numerous studies. In our investigation, performed in the rat, a pancreatic extract provided with elastolytic activity has been shown to possess an anti-aggregative effect in vitro and ex vivo and anti-thrombotic properties. In addition, the elastase was capable of inhibiting endothelial exfoliation induced by the desquamatory agent sodium citrate. This agent was tested for its microhaemorrhoeological activity in acute and subacute experiments. In both these conditions, elastase was able to increase the flexibility of red blood cells and their resistance to lysis provoked by hypotonic solutions. In animals fed on an atherogenic diet, this substance limited the lipoprotein accumulation in the aorta wall. Moreover, it reduced the enhanced calcium content, induced by vitamin D administration, in the tissue of arteries. These data indicate that elastase can counteract some pathobiological aspects that characterize atherosclerotic events.
