Brainstem Serotonin (5‐HT) and Arterial Blood Pressure Regulation in Neonatal Rats Exposed to Intermittent Asphyxia

In neonatal rats, a systemic loss of 5‐HT exaggerates the drop in arterial blood pressure (BP) during severe hypoxia. In adult animals, intermittent hypoxia or asphyxia (IA) leads to a long‐termt increase in ventilation (V E ), sympathetic activity and BP (long‐term facilitation, LTF). The consequences of a central loss of 5‐HT on the acute BP response to asphyxia and the long‐term regulation of BP have not been studied in the neonatal period. We hypothesized that 1) a partial loss of 5‐HT neurons increases the drop in BP during asphyxia; 2) BP increases following IA; and 3) the hypertension and respiratory LTF following IA would be reduced in 5‐HT‐deficient pups. We utilized 2 week‐old Sprague Dawley rats treated i.c.v. with 5,7‐dihydroxytryptamine (n=11), lesioning 39% of brainstem 5‐HT neurons. Littermate controls were injected with saline (CTRL, n=12). We measured V E with the barometric method and BP with a femoral artery catheter. Heart rate (HR) was derived from BP. After 15 min in room air, animals were exposed to 20 1‐min challenges of moderate asphyxia (10% O 2 , 5% CO 2 ) followed by 1 hr in room air. A loss of 5‐HT neurons significantly reduced systolic (p=0.016), but not diastolic BP (p>0.1) compared to CTRL. 5‐HT‐deficiency reduced HR in both normoxic and asphyxic conditions (p<0.001). Surprisingly, the drop in BP during asphyxia was attenuated in 5‐HT‐deficient pups compared to CTRL (p=0.008). Systolic and mean BP increased significantly (p =0.003 and 0.045, respectively) following IA in 5‐HT‐deficient pups, but not in CTRL. A loss of 5‐HT neurons had no effect on the degree of respiratory LTF. Our results suggest that systolic BP is reduced by a partial deficiency of central 5‐HT neurons, an effect that can be reversed by IA.