G Letechipía-Vallejo1, I González-Burgos, M Cervantes. 1. División de Estudios de Posgrado, Facultad de Medicina Doctor Ignacio Chávez, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Michoacán, Mexico.
Abstract
BACKGROUND: Melatonin has been proposed as a neuroprotective agent on the basis of its ability to function as a free radical scavenger, provided that lipoperoxidation and other free radical damage induced by reactive oxygen species resulting from cerebral ischemia are relevant pathophysiologic processes of ischemic neuronal damage. METHODS: The effects of melatonin or vehicle on neurologic deficit scores (Todd scale; maximal deficit score = 100, daily during 7 days after the ischemic episode) and neuronal population of hippocampal CA1-CA4 fields (cresyl violet stain, at the eighth day after the ischemic episode) were evaluated in adult male cats subjected to a 15-min period of acute global cerebral ischemia induced by cardiorespiratory arrest, and in cats subjected to a sham procedure. Continuous intravenous (iv) administration of either melatonin 10 mg/kg/h in 10% ethanol in saline or the vehicle alone (3 mL/kg/h) for 6 h starting 30 min after the end of the period of global cerebral ischemia was used as treatment. RESULTS: Global cerebral ischemia resulted in a severe loss of neurons in hippocampal CA1-CA4 fields (9, 13, 30 and 28% remaining neurons, respectively) of ischemic vehicle-treated cats in comparison with sham cats (100%). By contrast, remaining neurons in these regions were between 81 and 100% in the ischemic melatonin-treated cats, values that are nonsignificantly different as compared with sham cats. Values of remaining neurons in CA1-CA4 fields in ischemic melatonin-treated cats were significantly higher than those in ischemic vehicle-treated cats. Neurologic deficit scores in ischemic vehicle-treated cats (42-77 at day 1, 6-39 at day 7) were significantly higher than those in ischemic melatonin-treated cats (16-38 at day 1, 0-6 at day 7) on the days after the ischemic episode. CONCLUSIONS: Overall, the results support the neuroprotective effect of melatonin against the neuronal cerebral damage induced by acute global cerebral ischemia.
BACKGROUND:Melatonin has been proposed as a neuroprotective agent on the basis of its ability to function as a free radical scavenger, provided that lipoperoxidation and other free radical damage induced by reactive oxygen species resulting from cerebral ischemia are relevant pathophysiologic processes of ischemic neuronal damage. METHODS: The effects of melatonin or vehicle on neurologic deficit scores (Todd scale; maximal deficit score = 100, daily during 7 days after the ischemic episode) and neuronal population of hippocampal CA1-CA4 fields (cresyl violet stain, at the eighth day after the ischemic episode) were evaluated in adult male cats subjected to a 15-min period of acute global cerebral ischemia induced by cardiorespiratory arrest, and in cats subjected to a sham procedure. Continuous intravenous (iv) administration of either melatonin 10 mg/kg/h in 10% ethanol in saline or the vehicle alone (3 mL/kg/h) for 6 h starting 30 min after the end of the period of global cerebral ischemia was used as treatment. RESULTS: Global cerebral ischemia resulted in a severe loss of neurons in hippocampal CA1-CA4 fields (9, 13, 30 and 28% remaining neurons, respectively) of ischemic vehicle-treated cats in comparison with sham cats (100%). By contrast, remaining neurons in these regions were between 81 and 100% in the ischemicmelatonin-treated cats, values that are nonsignificantly different as compared with sham cats. Values of remaining neurons in CA1-CA4 fields in ischemicmelatonin-treated cats were significantly higher than those in ischemic vehicle-treated cats. Neurologic deficit scores in ischemic vehicle-treated cats (42-77 at day 1, 6-39 at day 7) were significantly higher than those in ischemicmelatonin-treated cats (16-38 at day 1, 0-6 at day 7) on the days after the ischemic episode. CONCLUSIONS: Overall, the results support the neuroprotective effect of melatonin against the neuronal cerebral damage induced by acute global cerebral ischemia.
Authors: Zachary M Weil; Kate Karelina; Alan J Su; Jacqueline M Barker; Greg J Norman; Ning Zhang; A Courtney Devries; Randy J Nelson Journal: Neurobiol Dis Date: 2009-08-05 Impact factor: 5.996
Authors: Xin Wang; Bryan E Figueroa; Irina G Stavrovskaya; Yi Zhang; Ana C Sirianni; Shan Zhu; Arthur L Day; Bruce S Kristal; Robert M Friedlander Journal: Stroke Date: 2009-03-19 Impact factor: 7.914