Role of decreased cardiac output in isoproterenol‐induced cardiovascular teratogenesis in chick embryos

Abstract

Abstract Studies employing microcinematography, time‐lapse microphotography, electrocardiography, and bioelectrical impedance cardiography indicate that a decrease in cardiac output may be important in isoproterenol‐induced cardiovascular teratogenesis in the chick embryo and merits further investigation. It has been demonstrated by microcinematography that the rate of flow through embryonic chick hearts (Hamburger‐Hamilton developmental stages 24–26) treated with 7.5 × 10 −4 M isoproterenol is less than that observed before or without drug administration. Bioelectrical impedance cardiograms have confirmed the above observations. Furthermore, isoproterenol induced momentary asystoles and depressed heart rates for as long as 1–2 hours. Pretreatment of embryos with practolol, a β‐1 adrenergic receptor antagonist, induced more normal cardiac performance after isoproterenol administration. Time‐lapse microphotographs demonstrated morphological alterations, indicating possible venous pressure changes in the vitelline system. Those findings are consistent with a hypothesis that practolol prevents isoproterenol‐induced acute heart failure in the embryonic chick.