RESUMEN
In 13 guinea pigs the pulmonary circulation was isolated from the systemic circulation and perfused with Tris buffer alone or with isoproterenol. The lungs were initially ventilated with 100% O2 and then switched to 100% N2 to induce alveolar hypoxia. The effluent was collected from the aorta and assayed for histamine. In the control group (n = 7) the histamine levels rose markedly with hypoxia. In the group perfused with Tris buffer and isoproterenol (n = 6) the rise in histamine levels was markedly diminished. Therefore, the authors conclude that isoproterenol, in their in vivo model, had a dramatic effect on hypoxia (non-immunologic) mediated histamine release.
Asunto(s)
Liberación de Histamina/efectos de los fármacos , Hipoxia/metabolismo , Isoproterenol/farmacología , Animales , Cobayas , Histamina/sangre , Nitrógeno , OxígenoRESUMEN
In 16 guinea pigs the pulmonary circulation was isolated from the pulmonary systemic circulation and perfused with Tris buffer or with Tris buffer containing cromolyn sodium. The lungs were first ventilated with 100% O2 and then 100% N2 to induce alveolar hypoxia. The effluent was collected from the aorta and assayed for histamine by the fluorometric method. In all seven animals perfused with Tris alone (no cromolyn) a marked elevation of the effluent histamine was demonstrated. In the group perfused with buffer containing cromolyn there was a substantial diminution in the response to hypoxia. Therefore, cromolyn sodium partially blocked hypoxia-mediated histamine release.