Capacity of intrinsic cardiac neurons to modify the acutely autotransplanted mammalian heart.
The capacity of the intrinsic cardiac nervous system to modify the acutely autotransplanted heart was investigated in eight anesthetized open-chest canine preparations in which the adrenal glands had been removed from the circulation. Cardiac effects elicited by isoproterenol and nicotine were also examined before and after heart-lung transplantation. Cardiac augmentation induced by isoproterenol was similar before and immediately after cardiopulmonary transplantation, indicating that the surgery did not obtund cardiac myocyte function significantly. The initial bradycardia induced by nicotine was greater before transplantation. The subsequent augmentation in left atrial systolic pressure, as well as right and left ventricular intramyocardial systolic pressures, induced by nicotine were similar before and after transplantation. When nicotine was administered to transplanted preparations after atropine administration, cardiac augmentation was induced. Cardiac augmentation was not induced by nicotine after subsequent beta-adrenergic blockade. These data indicate that nicotine-sensitive adrenergic neurons which accompany the transplanted heart are capable of inducing considerable cardiac augmentation. Power spectral analysis of heart rate and left ventricular chamber rate of pressure rise variability indicated an almost complete lack of power in these indexes after, as opposed to before, transplantation. Together with intrinsic cardiac cholinergic neurons, intrinsic cardiac adrenergic neurons may be responsible for physiologically and pharmacologically induced alterations in cardiac variables that occur in acutely transplanted hearts.
Murphy
D A
DA
Department of Surgery, Dalhousie University, Halifax, Nova Scotia, Canada.
O'Blenes
S
S
Hanna
B D
BD
Armour
J A
JA
D000311:Adrenal Glands / Q000502:physiology; D000320:Adrenergic Fibers / Q000187:drug effects / Q000502:physiology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D016279:Atrial Function, Left / Q000187:drug effects / Q000502:physiology; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001919:Bradycardia / Q000139:chemically induced / Q000503:physiopathology; D002799:Cholinergic Fibers / Q000187:drug effects / Q000502:physiology; D004285:Dogs; D004562:Electrocardiography / Q000187:drug effects; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D016027:Heart Transplantation / Q000502:physiology*; D016041:Heart-Lung Transplantation / Q000502:physiology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009538:Nicotine / Q000494:pharmacology; D012815:Signal Processing, Computer-Assisted; D013233:Stellate Ganglion / Q000187:drug effects / Q000502:physiology; D014182:Transplantation, Autologous; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology; D017725:Ventricular Pressure / Q000187:drug effects / Q000502:physiology
D000319:Adrenergic beta-Antagonists; D009538:Nicotine; D001285:Atropine; D007545:Isoproterenol