The ovine fetal endocrine reflex responses to haemorrhage are not mediated by cardiac nerves.
This study was designed to test the hypothesis that cardiac receptors tonically inhibit the secretion of renin, arginine vasopressin (AVP) and adrenocorticotropic hormone (ACTH) in late-gestation fetal sheep. Eight chronically catheterised fetal sheep between 122 and 134 days gestation were subjected to injection or infusion of saline or 4 % procaine into the pericardial space. Fetal blood pressure and heart rate were monitored and fetal blood samples were drawn to measure the response to these injections. Injection of procaine into the pericardial space effectively blocked cardiac nerves, as evidenced by a reduction in the variability of fetal heart rate and by the blockade of reflex reductions in fetal heart rate after intravenous injection of phenylephrine (an alpha-adrenergic agonist which raises blood pressure). Injection of saline had no discernable effects on any of the measured variables. A single injection of procaine, followed by a slow infusion, produced a transient blockade of cardiac nerves. Multiple injections of procaine produced a sustained blockade of cardiac nerves and a sustained rise in fetal plasma renin activity and ACTH. In none of the experiments did procaine significantly alter fetal plasma AVP concentrations. In 11 fetuses between 121 and 134 days gestation, we combined the cardiac nerve blockade with slow haemorrhage to test the cardiac nerves as mediators of the endocrine response to haemorrhage in utero. Cardiac nerve blockade exaggerated the fetal blood gas response to haemorrhage somewhat but did not significantly alter the magnitude of the ACTH, AVP, or plasma renin activity response to haemorrhage. We conclude that cardiac nerves in the late-gestation fetal sheep have minor influences on plasma renin activity and ACTH in normovolaemic fetuses, but that changes in cardiac nerve activity do not mediate the endocrine responsiveness to haemorrhage.
Wood
Charles E
CE
Department of Physiology, University of Florida College of Medicine, Gainesville, FL 32610-0274, USA. cwood@phys.med.ufl.edu
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D004195:Disease Models, Animal; D004702:Endocrine Glands / Q000503:physiopathology*; D005260:Female; D005333:Fetus / Q000503:physiopathology*; D006321:Heart / Q000294:innervation* / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006340:Heart Rate, Fetal / Q000187:drug effects; D006470:Hemorrhage / Q000503:physiopathology*; D010101:Oxygen Consumption / Q000502:physiology; D010496:Pericardium; D010656:Phenylephrine / Q000494:pharmacology; D011247:Pregnancy; D011343:Procaine / Q000494:pharmacology; D012083:Renin / Q000378:metabolism; D012756:Sheep
D000316:Adrenergic alpha-Agonists; D001127:Arginine Vasopressin; D010656:Phenylephrine; D011343:Procaine; D000324:Adrenocorticotropic Hormone; D012083:Renin