Inhibition of sympathetic responses at birth in sheep by lesion of the paraventricular nucleus

Jeffrey L. Segar, Dan L. Ellsbury, Oliva M. Smith
2002 American Journal of Physiology. Regulatory Integrative and Comparative Physiology  
is characterized by a surge in sympathetic outflow, heart rate (HR), mean arterial blood pressure (MABP) and circulating catecholamines. The paraventricular nucleus (PVN) of the hypothalamus is an important central regulatory site of sympathetic activity, but its role in the regulation of sympathoexcitation at birth is unknown. To test the hypothesis that the PVN regulates sympathetic activity at birth, experiments were performed in chronically instrumented near-term (137to 142-day gestation,
more » ... rm 145 days) sheep before and after delivery by cesarean section. Stereotaxic guided electrolytic lesioning of the PVN (n ϭ 6) or sham lesioning (n ϭ 6) was performed 48 h before study. At 30 min after birth, renal sympathetic nerve activity (RSNA) increased 128 Ϯ 26% above fetal values in the sham-lesioned animals (P Ͻ 0.05). In contrast, at a similar time point, RSNA decreased to 52 Ϯ 12% of the fetal value in the PVN-lesioned animals. Lesioning of the PVN did not affect the usual postnatal increases in MABP and epinephrine levels although HR failed to rise above fetal values. ANG II but not arginine vasopressin or norepinephrine levels increased in PVN-lesioned animals after birth, whereas all three hormones increased (P Ͻ 0.05) in sham-lesioned animals. Fetal and newborn HR baroreflex responses were similar in both groups. However, the usual postnatal attenuation of baroreflex-mediated inhibition of RSNA was blunted in the PVN-lesioned group. The results of this study demonstrate that ablation of the PVN abolishes sympathoexcitation with birth at near-term gestation. The PVN may play a critical role in physiological adaptation at birth. autonomic nervous system; fetus; newborn ACTIVATION of the sympathoadrenal system plays a vital role in regulating many of the physiological adaptations at birth, including increases in heart rate (HR), cardiac output, arterial pressure, a redistribution of organ blood flow, and thermogenesis (32, 33). The factors mediating the increase in sympathetic outflow at birth are not known but likely involve multiple factors, including hypoxia, acidosis, head compression, and cold (29, 38) . Previous studies by our group using in utero ventilation of fetal sheep suggest that rhythmic
doi:10.1152/ajpregu.00023.2002 pmid:12388455 fatcat:m5jdwppqrbaihn7gmxqxcnk7aq