CAPACITY OF INTRINSIC CARDIAC NEURONS TO MODIFY THE ACUTELY AUTOTRANSPLANTED MAMMALIAN HEART

Citation
Da. Murphy et al., CAPACITY OF INTRINSIC CARDIAC NEURONS TO MODIFY THE ACUTELY AUTOTRANSPLANTED MAMMALIAN HEART, The Journal of heart and lung transplantation, 13(5), 1994, pp. 847-856
Citations number
NO
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
10532498
Volume
13
Issue
5
Year of publication
1994
Pages
847 - 856
Database
ISI
SICI code
1053-2498(1994)13:5<847:COICNT>2.0.ZU;2-3
Abstract
The capacity of the intrinsic cardiac nervous system to modify the acu tely autotransplanted heart was investigated in eight anesthetized ope n-chest canine preparations in which the adrenal glands had been remov ed from the circulation. Cardiac effects elicited by isoproterenol and nicotine were also examined before and after heart-lung transplantati on. Cardiac augmentation induced by isoproterenol was similar before a nd immediately after cardiopulmonary transplantation, indicating that the surgery did not obtund cardiac myocyte function significantly. The initial bradycardia induced by nicotine was greater before transplant ation. The subsequent augmentation in left atrial systolic pressure, a s well as right and left ventricular intramyocardial systolic pressure s, induced by nicotine were similar before and after transplantation. When nicotine was administered to transplanted preparations after atro pine administration, cardiac augmentation was induced. Cardiac augment ation was not induced by nicotine after subsequent beta-adrenergic blo ckade. These data indicate that nicotine-sensitive adrenergic neurons which accompany the transplanted heart are capable of inducing conside rable cardiac augmentation. Power spectral analysis of heart rate and left ventricular chamber rate of pressure rise variability indicated a n almost complete lack of power in these indexes after, as opposed to before, transplantation. Together with intrinsic cardiac cholinergic n eurons, intrinsic cardiac adrenergic neurons may be responsible for ph ysiologically and pharmacologically induced alterations in cardiac var iables that occur in acutely transplanted hearts.