Biancardi, Vivian [UNESP]da Silva, Luana Tenorio [UNESP]Bicego, Kenia C. [UNESP]Gargaglioni, Luciane H. [UNESP]2014-05-202014-05-202010-02-28Respiratory Physiology & Neurobiology. Amsterdam: Elsevier B.V., v. 170, n. 2, p. 150-156, 2010.1569-9048http://hdl.handle.net/11449/2755We investigated the specific role of LC noradrenergic (NA) neurons in the cardiorespiratory and thermal responses to hypoxia. Aiming this, LC NA neurons were selectively destroyed by microinjecting 6-OHDA bilaterally in the LC of male rats. Pulmonarl ventilation ((V) over dotE, plethysmograph), core body temperature (Tc, dataloggers), mean arterial pressure (MAP) and heart rate (fH) were measured during normoxia followed by 7% O(2) in air. Tyrosine hydroxylase (TH) immunoreactivity was performed to verify the chemical lesions effectiveness. Hypoxia caused increase in (V) over dotE, decrease in Tc and did not affect fH in both sham-operated and 6-OHDA-lesioned groups. In addition, hypoxia decreased MAP in the sham-operated group and did not affect MAP in the 6-OHDA-lesioned group. LC lesion did not affect (V) over dotE, MAP, fH and Tc. Thus, these results indicate that LC noradrenergic neurons do not play a role in cardiorespiratory control and thermoregulation under basal and hypoxic conditions. (C) 2009 Elsevier B.V. All rights reserved.150-156engAnapyrexiaNoradrenaline6-HydroxydopamineArtigo10.1016/j.resp.2009.12.004WOS:000275259400003Acesso restrito