Resumen de Direct negative chronotropic and inotropic efects of curare on isolated and perfused frog's heart

Abdel J. Fuenmayor, Brenda Valero, María A. Farías, Rambal Fuenmayor, Rosalba Caruso, Grisel Rada, Mary Quijada, Abdel M. Fuenmayor

• español

  e afirma que el curare no tiene efectos sobre el corazón porque en este órgano no hay receptores muscarínicos. Durante un tra bajo experimental, observarnos que al administ rar d-tubocurarina en altas dosis a unos sapos, se producían cambios en la actividad cardiaca. Decidimos estudiar los efectos de la d-tubocurarina s obre la frecuencia cardiaca y la contractilidad de 8 corazones d e batracio aislados y perfundidos. Después de probar los efectos de la d-tubocurarina, agregamos acetilcolina, atropina, atenonol o verapamil para investigar el mecanismo de acción de la d-tubocur arina. Encontramos que 1) la d- tubocurarina en altas dosis (1 a 15 mcg) produce una disminución significativa de la frecuencia y la contractibilidad cardíacas; 2) la d-tubocurarina no bloquea el efecto de la acetilcolina, y 3)que la atropina, el atenonol y el verapamil no bloquean el efecto de la d-tubocurarina. Concluimos que la d- tubocurarina, administrada en dosis altas, produce una disminuci ón de la frecuencia y la contractilidad cardíacas directamente relacionadas con las dosis y que dicho efecto no está mediado por receptores muscarínicos, beta- 1 o de canales lentos de calci o.

• English

  It has been stated that curare has no direct effect upon the he art because the cardiac muscle is deprived of nicotine receptors . While performing an experimental work, we noticed that when high doses of curare were administered to frogs, a change in cardiac acti vity occurred. In order to elucidate whether the cardiac effects of cu rare were the results of a direct action or a reflex response, we studied the effects of increasing doses of d-tubocurarine on the rate and contractility of 8 isolated and perfused frogs' hearts. After testing ale d-tubocurarine effects on the heart rate and contractility, we added either acetylcholine, atropine, atenonol or verapamil in o rder to find out whether any change occurred in th e cardiac effects produced by d-tubocurarine.

  Thirty seven measurements were carried out arid it was found that 1) high doses between 1 and 15 micrograms) of d-tubocurarine produced a highly significant decrease in h eart rate an contractility; 2) d-tubocurarine did not avoid the acet ylcholine effect; 3) atropine, atenonol and verapamil did not in terfere with d-tubocurarine effects. We conclude that high doses of d-tubocurarine produce «dosis-dependent» heart rate and contractili ty reductions. These effects are not mediated by muscarinic receptors, beta- 1 receptors or the slow calcium channels.