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The Protective Effect of Pretreatment with Two Medicines on Cerebral Tissue of Mongolian Gerbils Injured by Cerebral Ischemia-reperfusion

Difen Wang

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Abstract

Objective: To study the protective effects of lidocaine and propofol pretreatment to cerebral tissue of gerbils undergone schemia-reperfusion injury. Methods:Thirty-four Mongolian gerbils were randomly divided into four groups:A)Control group with sham operation( n =7);B)ischemia group ( n =9);C)Lidocaine pretreatment group( n =9);D)Propofol pretreatment group( n =9).Lidocaine 30 mg/kg or propofol 100 mg/kg were given to the animals in groups C and D respectively(ip)24 h before ischemia. Ischemia-reperfusion operation:clamping bilatered common carotid arteries for 10 min after the animals were anesthetized with urethane at the dose of 1 g/kg ip,and then unclamped for reperfusion for 50 min.The animals in group A were only exposed with their bilatered common carotid arteries but not clamped.Detection procedures:The animals were decapitated and forebrain cerebral cortex was removed for the determination of superoxid dismutase(SOD)and glutathione(GSH)activities and contents of malondial dehyde(MDA),endothelin(ET)and calcitonin gene-related peptide(CGRP).One sample of left forebrain cerebral cortex (1 mm×1 mm) was removed randomly in each group to observe the ultramicroscopic changes of cerebral tissue with electronic microscope. Results: MDA and ET contents were significantly lower and SOD,GSH activities were higher in groups C and D than those in group B ( P 0.01, P 0.05, P 0.01, and P 0.05, respectively); CGRP contents in groups C and D were higher than those in group B, but the differences were not significant statistically( P 0.05). No significant difference was found between two pretreatment groups. Compared with group B, the ultramicroscopic pathological changes of cerebral tissue structures were lighter to different degrees in groups C and D, and there was no difference between the latter two groups in respect of pathological changes. Conclusions: Lidocaine and propofol pre-treatment 24 h before cerebral ischemia might have effects to some degree to protect cerebral tissue from ischemia-reperfusion caused injury. The protection has relation to the rise of SOD, GSH activities and the decrease of ET. The protection results are not significantly different between the pretreatments of the two medicines.

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Objective: To study the protective effects of lidocaine and propofol pretreatment to cerebral tissue of gerbils undergone schemia-reperfusion injury. Methods:Thirty-four Mongolian gerbils were randomly divided into four groups:A)Control group with sham operation( n =7);B)ischemia group ( n =9);C)Lidocaine pretreatment group( n =9);D)Propofol pretreatment group( n =9).Lidocaine 30 mg/kg or propofol 100 mg/kg were given to the animals in groups C and D respectively(ip)24 h before ischemia. Ischemia-reperfusion operation:clamping bilatered common carotid arteries for 10 min after the animals were anesthetized with urethane at the dose of 1 g/kg ip,and then unclamped for reperfusion for 50 min.The animals in group A were only exposed with their bilatered common carotid arteries but not clamped.Detection procedures:The animals were decapitated and forebrain cerebral cortex was removed for the determination of superoxid dismutase(SOD)and glutathione(GSH)activities and contents of malondial dehyde(MDA),endothelin(ET)and calcitonin gene-related peptide(CGRP).One sample of left forebrain cerebral cortex (1 mm×1 mm) was removed randomly in each group to observe the ultramicroscopic changes of cerebral tissue with electronic microscope. Results: MDA and ET contents were significantly lower and SOD,GSH activities were higher in groups C and D than those in group B ( P 0.01, P 0.05, P 0.01, and P 0.05, respectively); CGRP contents in groups C and D were higher than those in group B, but the differences were not significant statistically( P 0.05). No significant difference was found between two pretreatment groups. Compared with group B, the ultramicroscopic pathological changes of cerebral tissue structures were lighter to different degrees in groups C and D, and there was no difference between the latter two groups in respect of pathological changes. Conclusions: Lidocaine and propofol pre-treatment 24 h before cerebral ischemia might have effects to some degree to protect cerebral tissue from ischemia-reperfusion caused injury. The protection has relation to the rise of SOD, GSH activities and the decrease of ET. The protection results are not significantly different between the pretreatments of the two medicines.

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Available abstract

Objective: To study the protective effects of lidocaine and propofol pretreatment to cerebral tissue of gerbils undergone schemia-reperfusion injury. Methods:Thirty-four Mongolian gerbils were randomly divided into four groups:A)Control group with sham operation( n =7);B)ischemia group ( n =9);C)Lidocaine pretreatment group( n =9);D)Propofol pretreatment group( n =9).Lidocaine 30 mg/kg or propofol 100 mg/kg were given to the animals in groups C and D respectively(ip)24 h before ischemia. Ischemia-reperfusion operation:clamping bilatered common carotid arteries for 10 min after the animals were anesthetized with urethane at the dose of 1 g/kg ip,and then unclamped for reperfusion for 50 min.The animals in group A were only exposed with their bilatered common carotid arteries but not clamped.Detection procedures:The animals were decapitated and forebrain cerebral cortex was removed for the determination of superoxid dismutase(SOD)and glutathione(GSH)activities and contents of malondial dehyde(MDA),endothelin(ET)and calcitonin gene-related peptide(CGRP).One sample of left forebrain cerebral cortex (1 mm×1 mm) was removed randomly in each group to observe the ultramicroscopic changes of cerebral tissue with electronic microscope. Results: MDA and ET contents were significantly lower and SOD,GSH activities were higher in groups C and D than those in group B ( P 0.01, P 0.05, P 0.01, and P 0.05, respectively); CGRP contents in groups C and D were higher than those in group B, but the differences were not significant statistically( P 0.05). No significant difference was found between two pretreatment groups. Compared with group B, the ultramicroscopic pathological changes of cerebral tissue structures were lighter to different degrees in groups C and D, and there was no difference between the latter two groups in respect of pathological changes. Conclusions: Lidocaine and propofol pre-treatment 24 h before cerebral ischemia might have effects to some degree to protect cerebral tissue from ischemia-reperfusion caused injury. The protection has relation to the rise of SOD, GSH activities and the decrease of ET. The protection results are not significantly different between the pretreatments of the two medicines.

Key concepts: Calcitonin gene-related peptide, Ischemia, Propofol, Glutathione, Anesthesia, Medicine, Reperfusion injury, Lidocaine

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