Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

摘要: The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied the neonatal period. We hypothesized that a partial loss 5-HT would reduce arterial blood pressure (BP) at rest, increase fall BP during hypoxia, and long-term facilitation breathing (vLTF) following AIH. exposed 2-wk-old, 5,7-dihydroxytryptamine-treated controls AIH (10% O2; n = 13 control, 14 treated), hypercapnia (5% CO2; 12 11), or hypercapnic (AIHH; 10% O2, 5% 15 17). gave five 5-min challenges hypercapnia, twenty ∼20-s AIHH mimic sleep apnea. Systolic (sBP), diastolic BP, mean pressure, heart rate (HR), ventilation (Ve), metabolic (Vo2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% from medullary raphe. Compared with controls, pups deficient had reduced resting sBP (∼6 mmHg), (∼5 HR (56 beats/min), experienced drop hypoxia. vLTF both groups, reflected increased Ve Ve/Vo2, decreased Pco2. neurons, but was 1 h AIHH. Our data suggest relatively small compromises HR, no influence on ventilatory plasticity by may be useful for reversing cardiorespiratory defects related system dysfunction.