Hindbrain serotonergic neurons in prolonged hypotensive hemorrhage

Blood loss elicits a syncopal‐like response characterized by sympathetic withdrawal. Compensatory responses slowly recovery if blood loss is terminated prior to decompensation. Studies suggest that serotonin release contributes to the syncopal response during anesthesia and to blood pressure (BP) recovery after acute hemorrhage in awake rats. We determined if hindbrain serotonergic lesion slows the sympathoinhibitory response to blood loss and the compensatory response to hypovolemic shock in awake rats. Two wks after serotonin lesion (9 nmoles 5,7‐dihyroxytryptamine in caudal raphe) male Sprague Dawley rats were fit with vascular catheters and a renal sympathetic recording electrode (65 mg/kg sodium pentobarbital). The next day, BP, heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded during hemorrhage (3.2 ml/kg/min for 6 minutes, then 0.53 ml/kg/min for 4 min then withdrawal to maintain BP at 55 mmHg for 15 min). Lesioned rats had a slowed syncopal response (BP: −12.7 ± 1.2 vs. −21.0 ± 0.9 mm Hg/sec, P <0.001; HR: −35.6 ± 4.2 vs. −59.9 ± 3.5 bpm/sec, P <0.001; RSNA 3.2 ± 0.4 vs. 14.6 ± 3.1 % baseline/sec, P <0.001). BP of lesioned rats also recovered more slowly (68.5 ± 0.05 vs. 76.2 ± 3.0 mmHg between 25–60 min after start of hemorrhage, P <0.05), despite a similar blood loss (3.5 ± 0.1 vs. 3.2 ± 0.1 % BW). HR and RSNA did not differ. Hindbrain serotonergic neurons mediate sympathoinhibition during acute blood loss as well as BP compensation during hypovolemic shock, the latter possibly through hormonal mechanisms. Supported by HL72354