Effects of transection of cervical sympathetic trunk on cerebral infarct volume and oxygen free radical levels in rats with focal cerebral ischemia/reperfusion injury

BACKGROUND： Stellate ganglion block （SGB） plays a protective role on the brain, but the precise mechanism of action is not clear. OBJECTIVE： To simulate SGB by transection of the cervical sympathetic trunk （TCST） and to investigate the TCST effects on changes in cerebral infarct volume and oxygen free radical levels in rats with focal cerebral ischemia/reperfusion injury. DESIGN, TIME AND SETTING： A complete randomized control animal experiment was performed at the Institute of Neurological Diseases of Taihe Hospital, Yunyang Medical College from February to December 2005. MATERIALS： A total of 101 healthy Wistar rats, weighing 280-320 g, of both genders, aged 17-18 weeks, were used in this study. 2, 3, 5-triphenyltetrazolium chloride （TTC） was purchased from Changsha Hongyuan Biological Company. Superoxide dismutase （SOD）, malondialdehyde （MDA） and nitric oxide （NO） assay kits were provided by Nanjing Jiancheng Bioengineering Institute. METHODS： Rats were randomly divided into a TCST group, a model group and a sham operation group. Successful models were included in the final analysis, with at least 20 rats in each group. After TCST, rat models of focal cerebral ischemia/reperfusion injury were established in the TCST group by receiving middle cerebral artery occlusion （MCAO） by the intraluminal suture method for 2 hours, followed by 24 hours of reperfusion. Rat models of focal cerebral ischemia/reperfusion injury were made in the model group. Rats in the sham operation group underwent experimental procedures as for the model group, threading depth of 10 mm, and middle cerebral artery was not ligated. MAIN OUTCOME MEASURES： Brain tissue sections of ten rats from each group were used to measure cerebral infarct volume by TTC staining. Brain tissue homogenate of another ten rats from each group was used to detect SOD activities, MDA contents and NO levels. Rat neurological function was assessed by neurobehavioral measures. RESULTS： Cerebral infarct volume was bigger in the model group than in the TCST group （P 〈 0.05）. Twenty four hours after cerebral ischemia/reperfusion, SOD activities were lower, whereas MDA contents and NO levels were higher in the TCST and model groups, compared with the sham operation group （P 〈 0.05 or P 〈 0.01）. Compared with the model group, SOD activities were higher, whereas MDA contents and NO levels were lower in the TCST group （P 〈 0.05）. CONCLUSION： After TCST, cerebral infarct volume is reduced, SOD activities are increased, and MDA contents and NO levels are decreased compared to the model group in rats with focal cerebral ischemia/reperfusion injury. These changes may be associated with TCST.

Ketamine inhibits c-Jun protein expression in mouse hippocampus following cerebral ischemia/reperfusion injury

A model of cerebral ischemia and reperfusion was established in mice.Mice were treated with ketamine via intraperitoneal injection immediately following ischemia or ischemia/reperfusion.Ketamine did not remarkably change infarct volume in mice immediately following ischemia,but injection immediately following ischemia/reperfusion significantly decreased infarct volume.Ketamine injection immediately after ischemia or ischemia/reperfusion inhibited c-Jun protein expression in mouse hippocampus,but nuclear factor kappa B expression was unaltered.In addition,the Longa scale score for neural impairment was not reduced in mice following cerebral ischemia/reperfusion.These results indicate that ketamine can protect mice against cerebral ischemia and reperfusion injury by modulating c-Jun protein expression in mouse hippocampus.

Cervical sympathetic trunk transection affects inducible nitric oxide synthase expression in rat hippocampus following focal cerebral ischemia/reperfusion injury

BACKGROUND： The stellate ganglion block （SGB） plays a protective role in focal cerebral ischemia/reperfusion injury. The human SGB can be simulated by transection of the cervical sympathetic trunk （TCST） in rats. OBJECTIVE： To observe the effects of TCST on inducible nitric oxide synthase （iNOS） levels and cerebral infarct volume in the hippocampus of rats with cerebral ischemia/reperfusion injury, and to analyze the mechanism of action. DESIGN, TIME AND SETTING： A completely randomized, controlled, neuropathological experiment was performed at the Institute of Neurological Disease, Taihe Hospital, Yunyang Medical College between March and September 2006. MATERIALS： A total of 93 Wistar rats, aged 1718 weeks, of either gender, were used for this study. 2, 3, 5-triphenyl tetrazolium chloride was purchased from Changsha Hongyuan Biological Reagent Company China. Rabbit iNOS antibody and goat anti-rabbit IgG antibody were the products of Wuhan Boster Biological Reagent Co., Ltd., China. METHODS： Ten rats were randomly selected for the sham-operated group. Cerebral ischemia/reperfusion injury was induced by middle cerebral artery occlusion （MCAO） using the suture method in the remaining rats. Forty successful rat models were randomly and equally divided into the following two groups： （1） TCST group： subsequent to TCST, MCAO was performed for 2 hours, followed by 24 hours reperfusion; （2） model group： rats underwent experimental procedures similar to the TCST group, with the exception of TCST. Rats in the sham-operated group were subjected to experimental procedures similar to the model group; however, the thread was only introduced to a depth of 10 mm. MAIN OUTCOME MEASURES： Following 24 hours of reperfusion, functional neurological deficits were scored. Brain tissue sections from ten rats of each group were used to measure cerebral infarct volume by TTC staining. Hippocampal tissue sections of an additional ten rats from each group were used to detect iNOS levels using the streptavidin-peroxidase immunohistocbemistry method. Experimental data were expressed as absorbance values. RESULTS： Of the 93 selected rats, 50 were included in the final analysis. After MCAO for 2 hours, followed by 24 hours reperfusion, the absorbance values of iNOS-immunoreactive product were significantly greater in the model group compared to the TCST and sham-operated groups （P 〈 0.05）. However, there was no difference between the TCST and sham-operated groups （P 〉 0.05）. In addition, cerebral infarct volume in the model group was significantly greater compared to the TCST group （P 〈 0.05）. The TCST group performed with lower total functional neurological scores compared to the model group （P 〈 0.05）. CONCLUSION： TCST protects the brain against focal cerebral ischemia/reperfusion injury by possibly down-regulating hippocampal iNOS expression.