Why the study?
Does the integrity of neural projections from medullary noradrenergic neurons to the median preoptic nucleus mediate hypertonic saline solution-induced cardiovascular and sympathetic recovery in hypovolemic hemorrhagic rats?
Does the integrity of neural projections from medullary noradrenergic neurons to the median preoptic nucleus mediate hypertonic saline solution-induced cardiovascular and sympathetic recovery in hypovolemic hemorrhagic rats?
The recovery of mean arterial pressure and sympathoinhibition following hypertonic saline infusion in hemorrhagic rats depends on intact neural projections from medullary noradrenergic neurons to the median preoptic nucleus.
Supports central noradrenergic mediation of hypertonic saline effects in rats; leaves open applicability to human hypovolemic shock.
The infusion of hypertonic saline solution (HSS) is known to be beneficial to the treatment of hypovolemic hemorrhage (HH). The central mechanism of HSS-induced cardiovascular and autonomic recovery of animals subjected to HH remains unclear. Hence, the present study evaluated the involvement of median preoptic nucleus (MnPO) and medullary noradrenergic neurons (A1 and A2) in HSS-induced cardiovascular and sympathetic responses in hemorrhagic rats. The wistar rats were subjected to specific lesion of noradrenergic neurons through the nanoinjections of anti-DβH-saporin into caudal ventrolateral medulla (A1 neurons) and nucleus of the solitary tract (A2 neurons). After recovery, mean arterial pressure (MAP) and renal sympathetic nervous activity were recorded. The HH was performed through blood withdrawal until a MAP of 60 mmHg was attained. In sham rats, HSS infusion (3M NaCl) reestablished MAP without change in HH-induced sympathoinhibition. The muscimol (agonist of GABAA receptor) was nanoinjected in MnPO during HH and MnPO inhibition abolished the recovery of MAP and HSS-induced sympathoinhibition. Simultaneous lesions of A1 and A2 abolished MAP restoration and sympathoinhibition after HSS infusion. These results suggest that the recovery of MAP and HSS-induced sympathoinhibition in hemorrhaged rats depend on intact neural projections from A1 and A2 to MnPO.
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Naves et al. (2018) studied this question.
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