title: Potentation of the cardiac response to aminophylline by oxyfedrine.
abstract: The influence of oxyfedrine on the cardiostimulatory effects of aminophylline was studied in the isolated perfused guinea-pig heart.  It was found that oxyfedrine potentiated the stimulatory effects of aminophylline on isometric contraction, dF/dt, coronary flow and heart rate.  This potentation was abolished after pretreatment with propranolol.  Histamine, though to a lesser extent, also potentiated the effects of aminophylline.  When oxyfedrine and histamine were infused simultaneously in the presence of propranolol, the response of the heart to aminophylline was also potentiated; the magnitude of this potentiation was comparable to that obtained with histamine alone, indicating that propranolol abolished only the action of oxyfedrine but not that of histamine.  The mechanical effects of aminophylline were accompanied by a slight (15 per cent) but significant inhibition of phosphodiesterase, which was not further augmented by oxyfedrine.  The results suggest that the potentiating effects of oxyfedrine or histamine on the cardiostimulatory actions of aminophylline are elicited by their stimulatory actions on adenylate cyclase activity.
mesh_terms: D000628:Aminophylline / Q000494:pharmacology*; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D004357:Drug Synergism; D005260:Female; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D009206:Myocardium / Q000201:enzymology; D010477:Perfusion; D010726:Phosphodiesterase Inhibitors; D011412:Propanolamines / Q000494:pharmacology*; D011427:Propiophenones / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology
chemical_list: D010726:Phosphodiesterase Inhibitors; D011412:Propanolamines; D011427:Propiophenones; D000628:Aminophylline; D006632:Histamine; D011433:Propranolol; D007545:Isoproterenol