Role of A1 and A2 Noradrenergic Neurons and Median Preoptic Nucleus in Cardiovascular Recovery Induced by Hypertonic Saline Infusion in Hypovolemic Hemorrhagic Rats

Previous studies showed the involvement of Median Preoptic Nucleus (MnPO) and medullary catecholaminergic neurons (A1 and A2) in cardiovascular responses to changes in plasma osmolality. The present study examines the role of A1 and A2 noradrenergic neurons and MnPO in cardiovascular recovery induced by hypertonic saline infusion (HSI) in hypovolemic hemorrhagic rats. All experiments were performed in Wistar rats. Lesions of A1 and A2 neurons were obtain by nanoinjections of anti‐DBH‐saporin (6.3 ng/60nl). In other group nanoinjections muscimol (GABA agonist ‐ 4 mM) were used to blockade MnPO. Bleeding was induced by the withdrawal of blood for over 10 min until MAP reaches approximately 60 mmHg. After 20 min of hemorrhagic period, HSI administration was performed (3M NaCl; 1.8 ml/kg; i.v). On the day of experiment, rats were anesthetized with thiopental (40 mg/kg, i.v.) and instrumented for mean arterial pressure (MAP) recording. In sham‐rats we observed a recovery of MAP (112 ± 4.6 mmHg, 10 min after HSI). The blockade of MnPO prevented restoration of MAP induced by HSI (60 ± 6.2, 10 min after HSI; p <0.05). Similar to observed in sham rats, HSI induced a recovery of MAP in A1 (101 ± 8.5 mmHg; 10 min after HSI) and A2 lesioned rats (121.4 ± 5.3 mmHg, 10 min after HSI). In A2 pressor response was greatest. The MnPO injections sites and A1 or A2 lesions extensions were confirmed by histology analysis. These results showed that the MnPO plays an important role in HSI induced resuscitation in hemorrhagic shock. However, A1 and A2 noradrenergic neurons seem not to be directly involved in the cardiovascular recovery induced by HSI in hemorrhagic rats. Financial Support: CNPq, FAPEG