RESUMO
Anaphylactic shock decreased the coronary perfusion pressure, systemic arterial pressure and cardiac output in anesthetised dogs. After combined inhibition of cyclo-oxygenase and lipoxygenase with linoleate-hydroxamic acid, the anaphylactic coronary constriction and morphological cardiac lesions were considerably diminished. Activation of the lipoxygenase pathway seems to play a major role in development of the coronary constriction in anaphylaxis.
Assuntos
Anafilaxia/fisiopatologia , Vasos Coronários/fisiopatologia , Resistência Vascular/fisiologia , Anafilaxia/sangue , Anafilaxia/etiologia , Anafilaxia/patologia , Animais , Ácido Araquidônico/antagonistas & inibidores , Ácido Araquidônico/sangue , Pressão Sanguínea/fisiologia , Débito Cardíaco/fisiologia , Vasos Coronários/ultraestrutura , Cães , Imunização/métodos , Indometacina/farmacologia , Ácido Linoleico , Ácidos Linoleicos/farmacologia , Fatores de TempoRESUMO
The preliminary inhibition of prostanoid biosynthesis by indomethacin (10 mg/kg, intravenously) strongly changes the typical anaphylactic shock reaction produced by the intracoronary injection of the challenging dose of the antigen in the dogs sensitized with normal horse serum. A rapid fall of blood pressure and cardiac output at the first stage of the anaphylactic reaction is sharply diminished, the reaction of the coronary vessels is inversed. Instead of dilatation, vasoconstriction occurred increasing with the repeated administration of the antigen. The data obtained suggest that the initial hypotension under anaphylactic shock is due to prostanoid production while the coronary spasm is the result of lipoxygenase activation.
Assuntos
Anafilaxia/tratamento farmacológico , Vasos Coronários/efeitos dos fármacos , Indometacina/uso terapêutico , Resistência Vascular/efeitos dos fármacos , Anafilaxia/etiologia , Anafilaxia/fisiopatologia , Animais , Cateterismo Cardíaco , Circulação Coronária/efeitos dos fármacos , Circulação Coronária/fisiologia , Vasos Coronários/fisiopatologia , Cães , Avaliação Pré-Clínica de Medicamentos , Hemodinâmica/efeitos dos fármacos , Hemodinâmica/fisiologia , Imunização/métodos , Fatores de Tempo , Resistência Vascular/fisiologiaRESUMO
In experimental myocardial infarction in dogs caused by 60-minute occlusion of the coronary artery with the subsequent 24-hour reperfusion, the administration of quercetin solution (50 mg/kg) was found to improve the contractile function of the left ventricular myocardium, to decrease the incidence of heart rate and conductivity disorders, to contribute to limitation of the ischemic damage area, to exert the protective effect on the ultrastructure of the coronary arteries that can promote the preservation of the vessels' integrity, the improvement of the coronary circulation and the prevention of intravascular thrombus formation.
Assuntos
Doença das Coronárias/tratamento farmacológico , Coração/efeitos dos fármacos , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Quercetina/uso terapêutico , Animais , Pressão Sanguínea/efeitos dos fármacos , Pressão Sanguínea/fisiologia , Cateterismo Cardíaco , Doença das Coronárias/fisiopatologia , Cães , Avaliação Pré-Clínica de Medicamentos , Feminino , Coração/fisiopatologia , Masculino , Microscopia Eletrônica , Infarto do Miocárdio/tratamento farmacológico , Infarto do Miocárdio/fisiopatologia , Traumatismo por Reperfusão Miocárdica/fisiopatologia , Miocárdio/ultraestrutura , Fatores de TempoRESUMO
The effects of intracoronary LTC4 administration have been studied in narcotized dogs with an intact chest. LTC4 in doses of 0.5-40 micrograms produced a dose-dependent decrease in coronary flow, inhibition of myocardial contractility and disturbance of cardiac rhythm. A decrease in myocardial contractility was shown to take place before the signs of myocardial ischemia had appeared that could not be entirely due to the decrease in coronary blood flow. Ultrastructural changes in the endothelium of the coronary vessels have also been observed under the action of LTC4.
