Brainstem areas activated by intermittent apnea in awake unrestrained rats.
Autor: | Ferreira CB; Department of Physiology, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil., Schoorlemmer GH; Department of Physiology, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil., Rossi MV; Department of Physiology, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil., Takakura AC; Department of Pharmacology, Institute of Biomedical Science, University of São Paulo, 05508-000 São Paulo, SP, Brazil., Barna BF; Department of Physiology and Biophysics, Institute of Biomedical Science, University of São Paulo, 05508-000 São Paulo, SP, Brazil., Moreira TS; Department of Physiology and Biophysics, Institute of Biomedical Science, University of São Paulo, 05508-000 São Paulo, SP, Brazil., Cravo SL; Department of Physiology, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil. Electronic address: sldcravo@unifesp.br. |
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Jazyk: | angličtina |
Zdroj: | Neuroscience [Neuroscience] 2015 Jun 25; Vol. 297, pp. 262-71. Date of Electronic Publication: 2015 Apr 08. |
DOI: | 10.1016/j.neuroscience.2015.04.007 |
Abstrakt: | We investigated the role of the autonomic nervous system to cardiovascular responses to obstructive apnea in awake, unrestrained rats, and measured expression of Fos induced by apnea in the brainstem. We implanted a tracheal balloon contained in a rigid tube to allow the induction of apnea without inducing pain in the trachea. During bouts of 15s of apnea, heart rate fell from 371±8 to 161±11bpm (mean±SEM, n=15, p<0.01) and arterial pressure increased from 115±2 to 131±4mmHg (p<0.01). Bradycardia was due to parasympathetic activity because it was blocked by the muscarinic antagonist, methylatropine. The pressor response was due to vasoconstriction caused by sympathetic activation because it was blocked by the α1 antagonist, prazosin. Apnea induced Fos expression in several brainstem areas involved in cardiorespiratory control such as the nucleus of the solitary tract (NTS), ventrolateral medulla (VLM), and pons. Ligation of the carotid body artery reduced apnea-induced bradycardia, blocked heart rate responses to i.v. injection of cyanide, reduced Fos expression in the caudal NTS, and increased Fos expression in the rostral VLM. In conclusion, apnea activates neurons in regions that process signals from baroreceptors, chemoreceptors, pulmonary receptors, and regions responsible for autonomic and respiratory activity both in the presence and absence of carotid chemoreceptors. (Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.) |
Databáze: | MEDLINE |
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