Blair M L, Jaworski R L, Want A, Piekut D T
Department of Pharmacology and Physiology, Box 711, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Rochester, NY 14642, USA.
Am J Physiol Regul Integr Comp Physiol. 2001 Apr;280(4):R1141-8. doi: 10.1152/ajpregu.2001.280.4.R1141.
The goal of this study was to determine the role of the pontine lateral parabrachial nucleus (LPBN) in the compensatory responses to blood loss. Conscious unrestrained rats with complete, partial, or sham bilateral ibotenic acid lesions of the LPBN were subjected to a hypotensive 16-ml/kg blood withdrawal via arterial catheter. Complete lesions (LPBNx) encompassed the entire LPBN and extended into the ventrolateral parabrachial region to encroach on the Kolliker-Fuse nucleus. Partial lesions were restricted to the body of the LPBN and spared the outer rim of the external lateral subnucleus of the LPBN. In all three groups, serum corticosterone concentration and plasma renin activity increased four- to fivefold after hemorrhage (P < 0.01), and immunocytochemistry demonstrated numerous Fos-positive neurons in the hypothalamic supraoptic nucleus. However, the cardiovascular responses to hypotensive blood loss differed for complete and partial lesions. Blood pressure failed to recover in LPBNx rats and was significantly lower in LPBNx (66 +/- 4 mmHg) than in rats with partial or sham lesions (98 +/- 4 and 85 +/- 5 mmHg, respectively) at 40 min posthemorrhage. In contrast, rats with partial lesions had a significant attenuation of the posthemorrhage bradycardia. This implies that a population of neurons within the body of the LPBN is essential for full expression of the bradycardia that accompanies hemorrhagic hypotension, whereas the ventrolateral parabrachial region is essential for normal restoration of arterial pressure after hypotensive hemorrhage.
