Asunto(s)
Cromonar/farmacología , Cumarinas/farmacología , Ácidos Grasos no Esterificados/metabolismo , Glucosa/metabolismo , Animales , Caproatos/metabolismo , Cobayas , Atrios Cardíacos/metabolismo , Hipoxia/metabolismo , Contracción Miocárdica/efectos de los fármacos , Consumo de Oxígeno , Palmitatos/metabolismoAsunto(s)
Benzodiazepinas/farmacología , Frecuencia Cardíaca/efectos de los fármacos , Corazón/efectos de los fármacos , Parasimpatolíticos , Piperazinas/farmacología , Animales , Carbacol/administración & dosificación , Carbacol/antagonistas & inhibidores , Carbacol/farmacología , Relación Dosis-Respuesta a Droga , Cobayas , Atrios Cardíacos/efectos de los fármacos , MasculinoAsunto(s)
Miocardio/patología , Reserpina/farmacología , Inanición/patología , Animales , Femenino , Glucógeno/análisis , Cobayas , Corazón/efectos de los fármacos , Atrios Cardíacos , Ventrículos Cardíacos , Lípidos/análisis , Masculino , Miocardio/análisis , Músculos Papilares , Fosfolípidos/análisis , Factores de Tiempo , Conservación de Tejido , Triglicéridos/análisisRESUMEN
The effects of free and albumin-bound arachidonic acid, which is the precursor of the prostaglandins E2 and F2alpha, were studied on the spontaneous rate, contractile force and myocardial fatty acid metabolism in isolated, spontaneously beating atria of guinea pigs. Both free and albumin-bound arachidonic acid (10(-6)-10(-3) M) produced a dose-dependent positive chronotropic and a modest inotropic action. Tachyphylaxis to the positive chronotropic action of arachidonic acid developed in the course of repeated applications. Beta-Adrenoceptor blockade (pincolol) and pretreatment with reserpine or prostaglandin-synthetase inhibitors (indomethacin, fenoprofen, aspirin, 5,8,11,14-eicosatetraynoic acid) failed to affect the chronotropic activity of arachidonic acid significantly. The action of arachidonic acid was independent of the decarboxylation of the fatty acid. Linoleic and oleic acids did not show any positive chronotropic activity. The data are interpreted as suggesting that changes induced by arachidonic acid might be partly due to peroxides formed from arachidonic acid.
Asunto(s)
Ácidos Araquidónicos/farmacología , Corazón/efectos de los fármacos , Animales , Ácidos Araquidónicos/metabolismo , Interacciones Farmacológicas , Ácidos Grasos Insaturados/metabolismo , Ácidos Grasos Insaturados/farmacología , Femenino , Cobayas , Frecuencia Cardíaca/efectos de los fármacos , Técnicas In Vitro , Masculino , Metaproterenol/farmacología , Contracción Miocárdica/efectos de los fármacos , Miocardio/metabolismo , Pindolol/farmacología , Prostaglandinas/biosíntesis , Unión Proteica , Reserpina/farmacología , Albúmina Sérica/metabolismo , TaquifilaxisAsunto(s)
AMP Cíclico/metabolismo , Atrios Cardíacos/efectos de los fármacos , Frecuencia Cardíaca/efectos de los fármacos , Morfina/farmacología , Antagonistas de Prostaglandina/farmacología , Animales , Cobayas , Técnicas In Vitro , Masculino , Miocardio/metabolismo , Prostaglandinas E/farmacología , Estimulación QuímicaRESUMEN
For the oxyntic cell of the stomach the hypothesis was forwarded by Grossmann and Konturek [1] that, if one of its three receptors is blocked, the physico-chemical properties of the two others are changed in such a way that they respond less sensitively to their specific stimulation. This hypothesis was tested for the heart by studying the effect of histamine-H2-receptor- and beta-receptor-blockade on the orciprenaline-, histamine-, and prostaglandin E1-stimulated frequency of the spontaneously beating isolated guinea-pig atrium. Therefore cumulative dose response curves were established for orciprenaline, histamine and prostaglandin E1 (PGE1) alone or in the presence of metiamide or pindolol. (1) The beta-blocker pindolol inhibited the effect of orciprenaline in a competitive manner, without having an effect on histamine- and PGE1-stimulation. (2) The histamine H2-receptor blocker metiamide inhibited the histamine response competitively. (3) In contrast to pindolol, metiamide inhibited the PGE1-stimulated rise in atrial frequency, most obviously non- or uncompetitively. From these results it is evident that in the heart the particular inhibitors, at least at the receptor site, act rather specifically without affecting neighbouring receptors and that metiamide influences the PGE1-response in a way different from the receptor site.