Reversal of aconitine-induced tachycardia by prostaglandins in the rabbit Langendorff preparation.
The ability of PGA2, E1, E2, and F2alpha to alter: (a) the refractory period (as judged by the maximal driving frequency); (b) the rate of automatically beating aconitine-treated papillary muscles; and (c) the rate of both untreated and aconitine-treated Langendorff preparations, was studied. The addition of PGA2 (3.0 mumol), PGE2 (2.84 mumol), and PGF2alpha (2.1 mumol) to the perfusate returned heart rate to pre-aconitine levels in the Langendorff preparation, but this action was frequently accompanied by atrioventricular dissociation. In contrast, PGE1 (2.82 mumol) was ineffective in antagonising aconitine-induced tachycardia. In the normally beating rabbit Langendorff, PGF2alpha (2.1 mumol) produced a slight but statistically significant negative chronotropic effect. Neither cardiac contractile force nor maximal driving frequency was altered by the addition of prostaglandins. These results suggest that PGA2, PGE2, and especially PGF2alpha may exert antiarrhythmic activity by direct action(s) upon in vitro rabbit myocardial preparations.
D000157:Aconitine / Q000037:antagonists & inhibitors*; D031841:Aconitum / Q000031:analogs & derivatives*; D000818:Animals; D005260:Female; D006339:Heart Rate / Q000187:drug effects*; D066298:In Vitro Techniques; D008297:Male; D010210:Papillary Muscles / Q000187:drug effects; D011453:Prostaglandins / Q000494:pharmacology*; D011817:Rabbits; D013268:Stimulation, Chemical; D013997:Time Factors
D011453:Prostaglandins; D000157:Aconitine