Mieko Okada1, Luiz Fernando Reis Falcão2, David Ferez3, José Luiz Martins4, Paolo Ruggero Errante5, Francisco Sandro Menezes Rodrigues5, Afonso Caricati-Neto6, Márcia Marinho7, Guilherme Fenelon8, Itamar Souza Oliveira-Júnior9. 1. Fellow PhD degree, Postgraduate Program in Translational Medicine, Universidade Federal de São Paulo (UNIFESP), Brazil. Acquisition, analysis and interpretation of data; technical procedures; statistical analysis, manuscript writing. 2. PhD, Associate Professor, Division of Anesthesia, Pain and Intensive Medicine, Department of Surgery, UNIFESP, Sao Paulo-SP, Brazil. Interpretation of data, statistical analysis, manuscript writing, critical revision. 3. PhD, Associate Professor, Division of Anesthesia, Pain and Intensive Medicine, Department of Surgery, UNIFESP, Sao Paulo-SP, Brazil. Interpretation of data, critical revision. 4. PhD, Full Professor, Division of Anesthesia, Pain and Intensive Medicine, Department of Surgery, UNIFESP, Sao Paulo-SP, Brazil. Interpretation of data, manuscript writing, critical revision. 5. Fellow PhD degree, Postgraduate Program in Pharmacology, UNIFESP, Sao Paulo-SP, Brazil. Histopathological examinations, analysis of data. 6. PhD, Associate Professor, Department of Pharmacology, UNIFESP, Sao Paulo-SP, Brazil. Manuscript writing, critical revision. 7. PhD, Full Professor, Veterinary Medicine School, UNESP, Araçatuba-SP, Brazil. Biochemistry data analysis, statistical analysis, critical revision. 8. Associate Professor, Division of Cardiology, Department of Surgery, UNIFESP, Sao Paulo-SP, Brazil. Conception and design of the study, manuscript writing, critical revision. 9. Full Professor, Division of Anesthesia, Pain and Intensive Medicine, Department of Surgery, and Associate Professor, Postgraduate Program in Translational Medicine, UNIFESP, Sao Paulo-SP, Brazil. Conception and design of the study, critical revision, final approval of the version to be published.
Abstract
PURPOSE: To investigate the effects of atenolol in inflammatory mediator and oxidative stress in a myocardial injury by intestinal ischemia/reperfusion in rat model. METHODS: Adult Wistar male rats were randomly (n=8), anesthetized and divided in: Sham: submitted to operation only; group SS+IR: intravenous saline infusion following superior mesenteric artery occlusion during 60 minutes (ischemia) and open for 120 minutes (reperfusion); group AT+IR: intravenous atenolol infusion (2 mg/kg) following superior mesenteric artery occlusion during 60 minutes (ischemia) and open for 120 minutes (reperfusion); and group AT+I+AT+R: intravenous atenolol infusion following superior mesenteric artery occlusion during 60 minutes (ischemia) and in the time 45 minutes other atenolol doses were administrated and the artery was open for 120 minutes (reperfusion), all animals were submitted to muscular relaxation for mechanical ventilation. In the end of experiment the animals were euthanized and the hearts tissue were morphology analyzed by histology and malondialdehyde by ELISA, and the plasma were analyzed for tumor necrosis factor-alpha by ELISA. RESULTS: The group SS+IR demonstrated the higher malondialdehyde levels when compared with the atenolol treated-groups (p=0.001) in the heart tissue. The tumor necrosis factor-alpha level in plasma decrease in the treated groups when compared with SS+IR group (p=0.001). Histology analyses demonstrate pyknosis, edema, cellular vacuolization, presence of inflammatory infiltrate and band contraction in the heart tissue of the rats. CONCLUSION: Atenolol significantly reduce the degree of cardiac damage after intestinal ischemia-reperfusion.
PURPOSE: To investigate the effects of atenolol in inflammatory mediator and oxidative stress in a myocardial injury by intestinal ischemia/reperfusion in rat model. METHODS: Adult Wistar male rats were randomly (n=8), anesthetized and divided in: Sham: submitted to operation only; group SS+IR: intravenous saline infusion following superior mesenteric artery occlusion during 60 minutes (ischemia) and open for 120 minutes (reperfusion); group AT+IR: intravenous atenolol infusion (2 mg/kg) following superior mesenteric artery occlusion during 60 minutes (ischemia) and open for 120 minutes (reperfusion); and group AT+I+AT+R: intravenous atenolol infusion following superior mesenteric artery occlusion during 60 minutes (ischemia) and in the time 45 minutes other atenolol doses were administrated and the artery was open for 120 minutes (reperfusion), all animals were submitted to muscular relaxation for mechanical ventilation. In the end of experiment the animals were euthanized and the hearts tissue were morphology analyzed by histology and malondialdehyde by ELISA, and the plasma were analyzed for tumor necrosis factor-alpha by ELISA. RESULTS: The group SS+IR demonstrated the higher malondialdehyde levels when compared with the atenolol treated-groups (p=0.001) in the heart tissue. The tumor necrosis factor-alpha level in plasma decrease in the treated groups when compared with SS+IR group (p=0.001). Histology analyses demonstrate pyknosis, edema, cellular vacuolization, presence of inflammatory infiltrate and band contraction in the heart tissue of the rats. CONCLUSION:Atenolol significantly reduce the degree of cardiac damage after intestinal ischemia-reperfusion.