Rogean Rodrigues Nunes1, Gastão Fernandes Duval Neto2, Júlio César Garcia de Alencar3, Suyane Benevides Franco3, Nayanna Quezado de Andrade3, Danielle Maia Holanda Dumaresq4, Sara Lúcia Cavalcante5. 1. TSA; MSc and PhD in Anesthetics; Postgraduate in Cardiology, Universidade Federal do Ceará (UFC); Jointly Responsible for the Center for Teaching and Training (CET) of Hospital Geral de Fortaleza (HGF); Medicine Professor of Fachristus; Postgraduate in Clinical Engineering, Universidade de Fortaleza (Unifor); Vice-Chair of the Research Ethics Committee, Hospital São Carlos, Fortaleza, Ceará. Electronic address: rogean@fortalnet.com.br. 2. TSA; Full Professor; PhD; Department of General Surgery, Universidade Federal de Pelotas (UFPel). 3. Medical Student, UFC. 4. TSA; MSc, UFC; Responsible for CET-IJF; Chairman of the Pediatric Anesthesia Committee, Sociedade Brasileira de Anestesiologia (SBA) - 2011; Medicine Professor of Fachristus, Fortaleza, Ceará 5. PhD; Professor, Faculdade de Medicina, UFC; Corresponsible for the CET of the HGF from Hospital São Carlos, Fortaleza Ceara, Brazil.
Abstract
BACKGROUND AND OBJECTIVES: Several studies demonstrate that cerebral preconditioning is a protective mechanism against a stressful situation. Preconditioning determinants are described, as well as the neuroprotection provided by anesthetic and non-anesthetics agents. CONTENT: Review based on the main articles addressing the pathophysiology of ischemia-reperfusion and neuronal injury and pharmacological and non-pharmacological factors (inflammation, glycemia, and temperature) related to the change in response to ischemia-reperfusion, in addition to neuroprotection induced by anesthetic use. CONCLUSIONS: The brain has the ability to protect itself against ischemia when stimulated. The elucidation of this mechanism enables the application of preconditioning inducing substances (some anesthetics), other drugs, and non-pharmacological measures, such as hypothermia, aimed at inducing tolerance to ischemic lesions.
BACKGROUND AND OBJECTIVES: Several studies demonstrate that cerebral preconditioning is a protective mechanism against a stressful situation. Preconditioning determinants are described, as well as the neuroprotection provided by anesthetic and non-anesthetics agents. CONTENT: Review based on the main articles addressing the pathophysiology of ischemia-reperfusion and neuronal injury and pharmacological and non-pharmacological factors (inflammation, glycemia, and temperature) related to the change in response to ischemia-reperfusion, in addition to neuroprotection induced by anesthetic use. CONCLUSIONS: The brain has the ability to protect itself against ischemia when stimulated. The elucidation of this mechanism enables the application of preconditioning inducing substances (some anesthetics), other drugs, and non-pharmacological measures, such as hypothermia, aimed at inducing tolerance to ischemic lesions.