BACKGROUND: We designed this study to determine whether a combination of dexmedetomidine and sevoflurane postconditioning provides additive neuroprotection in a rat model of transient global cerebral ischemia. METHODS: Forty rats were randomly allocated to 4 groups. Control group (group C, n=10) received no treatment. Dexmedetomidine group (group D, n=10) received dexmedetomidine of 100 μg/kg intraperitoneally 30 minutes before ischemia. Sevoflurane postconditioning group (group P, n=10) underwent 2 sevoflurane inhalations after ischemia. Each inhalation consisted of 5 minutes of 2.5% sevoflurane and a subsequent washout time of 10 minutes. Sevoflurane postconditioning plus dexmedetomidine group (group PD, n=10) received received dexmedetomidine and 2 sevoflurane inhalations 30 minutes before ischemia and after ischemia, respectively. In all the groups, ischemia was induced by a bilateral common carotid artery occlusion plus hemorrhagic hypotension and was maintained for 8 minutes. Histologic outcomes and apoptosis-related proteins were measured 7 days after ischemia in the CA1 area of the rat hippocampus. RESULTS: Groups D, P, and PD contained more viable cells and less apoptotic cells in the hippocampal CA1 area than group C (P<0.01). There was a significant difference in the Bax and Bcl-2 expression between group C and other groups (P<0.05). But the number of viable and apoptotic cells, and the Bax and Bcl-2 expression were not statistically different between group D or P and group PD. CONCLUSIONS: A combination of preischemic dexmedetomidine and sevoflurane postconditioning provides no additional neuroprotective benefit over preischemic dexmedetomidine or sevoflurane postconditioning alone.
BACKGROUND: We designed this study to determine whether a combination of dexmedetomidine and sevoflurane postconditioning provides additive neuroprotection in a rat model of transient global cerebral ischemia. METHODS: Forty rats were randomly allocated to 4 groups. Control group (group C, n=10) received no treatment. Dexmedetomidine group (group D, n=10) received dexmedetomidine of 100 μg/kg intraperitoneally 30 minutes before ischemia. Sevoflurane postconditioning group (group P, n=10) underwent 2 sevoflurane inhalations after ischemia. Each inhalation consisted of 5 minutes of 2.5% sevoflurane and a subsequent washout time of 10 minutes. Sevoflurane postconditioning plus dexmedetomidine group (group PD, n=10) received received dexmedetomidine and 2 sevoflurane inhalations 30 minutes before ischemia and after ischemia, respectively. In all the groups, ischemia was induced by a bilateral common carotid artery occlusion plus hemorrhagic hypotension and was maintained for 8 minutes. Histologic outcomes and apoptosis-related proteins were measured 7 days after ischemia in the CA1 area of the rat hippocampus. RESULTS: Groups D, P, and PD contained more viable cells and less apoptotic cells in the hippocampal CA1 area than group C (P<0.01). There was a significant difference in the Bax and Bcl-2 expression between group C and other groups (P<0.05). But the number of viable and apoptotic cells, and the Bax and Bcl-2 expression were not statistically different between group D or P and group PD. CONCLUSIONS: A combination of preischemic dexmedetomidine and sevoflurane postconditioning provides no additional neuroprotective benefit over preischemic dexmedetomidine or sevoflurane postconditioning alone.
Authors: Hyungseok Seo; Ho-Geol Ryu; Je Do Son; Jeong-Soo Kim; Eun Jin Ha; Jeong-Eun Kim; Hee-Pyoung Park Journal: Medicine (Baltimore) Date: 2016-12 Impact factor: 1.889
Authors: Hasan Ali Kiraz; Fatih Poyraz; Gülay Kip; Özlem Erdem; Metin Alkan; Mustafa Arslan; Abdullah Özer; Volkan Şivgin; Faruk Metin Çomu Journal: Libyan J Med Date: 2015-01 Impact factor: 1.657