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.