ABSTRACT
Contribution of histamine H1- and H2-receptors to the effect of compound 48/80, a potent histamine releaser, upon asphyxiation and body temperature in mice was investigated in the present experiments. Compound 48/80 showed an apparent protective potency against hypoxia and significantly prolonged the latencies for convulsions and death in a dose-dependent manner. Compound 48/80 also decreased the body temperature, which was in relation with the antihypoxic effect. Both the H1-receptor antagonist, dimethindene, and the H2-receptor antagonist, ranitidine, attenuated the hypothermic effect of compound 48/80, indicating the involvement of central histamine through both the H1- and H2-receptors. Ranitidine had no effect on the protective effect of compound 48/80 against hypoxia-induced lethality, whereas dimethindene completely antagonized it. These results suggest that the protective effect of compound 48/80 against hypoxia is mediated through histamine H1-receptors and is not related to its ability to induce hypothermia.
Subject(s)
Male , Mice , Animals , Hypoxia/drug therapy , Body Temperature/drug effects , Seizures/prevention & control , Mice, Inbred BALB C , Receptors, Histamine H1/physiology , Receptors, Histamine H2/physiology , p-Methoxy-N-methylphenethylamine/pharmacologyABSTRACT
De acuerdo a los esquemas conocidos, no se admite la existencia de aclorhidria con mucosa gástrica normal. Reportamos en un grupo de habitantes de altura, aclorhidria con mucosa gástrica normal verificada endoscópica e histológicamente. Asimismo, la aclorhidria basal e histamino resistente se acompaña de una mayor gastrinemia en comparación con un grupo normoclorhídrico, apreciándose una relación inversa entre acidez y gastrina. Una marcada disminución de células parietales o ausencia de receptores de gastrina e histamina estarían determinando la aclorhidria, y una hiperfunción o hiperplasia de células G la gastrinemia incrementada