0.05).NAA reached the lowest level at 24hours and Ch and Cr at 3days,and then NAA,Ch and Cr gradually increased with time.The increase in NAA was especially obvious which increased by 1.5 times at 2 months than that at 24hours after cerebral ischemia.The earliest detection of lactate was at 10 minutes within the infarct.The lactate concentration elevated and peaked at 12 hours,and a partial recovery of the reduction of lactate was seen at 3 days.However,the elevation in lactate was no longer observed during the period of up to 2 month follow-up.Conclusion:(1) 1HMRS can early detect the metabolite changes induced by middle cerebral artery occlusion in rats.(2).Abnormalities in chronic stage of cerebral ischemia in rats could also be found and gave important information for evaluating neuroprotective strategies.

BACKGROUND: Some researches report that diffusion-weighted imaging (DWI) can appear abnormal signal in minutes after cerebral ischemia.OBJECTIVE: To investigate the manifestation and regularity of diffusion coefficient in middle cerebral artery occlusion (MCAO) of rats after cerebral ischemia.DESIGN: Randomized controlled study.SETTING: Neurological Department of Clinical College of ChongqingMedical University.MATERIALS: The experiment was conducted at the Radiological Department of the First Affiliated Hospital of Chongqing Medical University from April to July 2004. Totally 18 adult Wistar rats with clean grade were randomly divided into three groups: control group, sham operation group and cerebral ischemia group with 6 rats in each group.METHODS: The origin of right middle cerebral artery was blocked with filament into right internal carotid. In the sham-operated group, the filament was just inserted into the common carotid artery not into the origin of middle cerebral artery, rats in normal control group were not treated with anything after anesthesia. MRI experiments were performed on a 1.5 T GE signa Highspeed NMR spectrometer to obtain DWI and ADC values at the time-point of 7, 15, 30, 60 minutes, 3,6, 12, 24 hours, 3, 7, 15 days, 1 and 2 months after operation.MAIN OUTCOME MEASURES: Changes of ADCs in infarct hemisphere and contralateral hemisphere.RESULTS: There was no significant change in MRI T1-and T2-weighted imaging in rats at 7 minutes post-infarction, but abnormal high intensity was emerged during the period of 1 hour to 3 hours, and enlarged over time. Finally, the infarction area located the right basal ganglia and the frontal-parietal lobes at 12 hours and increased less significantly later.Focal abnormal high signal was noted in DWI 7 minutes after cerebral ischemic insult, and the ADC values was decreased at the same time,reduced gradually after significant recover at 30 minutes, dropped to the lowest level at 12 hours and again increased at 24 hours, since then all the ADC values were remained high throughout follow-up, which increased by 5 times at 2 months than that at 12 hours. Correspondingly,rADC values showed the contrary pattern of evolution.CONCLUSION: It is reflected that ADC is highly sensitive not only to onset of cerebral ischemia but also to chronic cerebral ischemia.

Objective To explore the protective effect of Mip1 on cerebral edema by observing the Mip1 expression of perihematoma in intracerebral hemorrhage (ICH) rat model. Methods Ninety male SD rats were randomly divided into sham-operated group (n=15) and ICH group (n=75). ICH group was equally subdivided into 6 h, 12 h, 1 d, 3 d, and 7 d groups according to cerebral hemorrhage time, 15 in each group. Hematoma was formed by infusing autologous femoral artery blood into the right caudate nucleus. Rats were killed at the above time points, brain tissues around hematoma were taked. The pathological morphological changes in brain tissue around hematoma were observed using HE staining. The water content of brain (BWC) was measured with dry/wet weight method, and immunohistochemistry was used to analyze the average optical density value of Mip1 protein in perihematoma. Results Neuronal cell body of perihematoma was significantly decreased after ICH, the cytoplasm light staining, Nissl body reduced obviously in cytoplasm, and edema fissure appeared around cells, however, no obvious changes of nerve cells were detected in sham-operated group. Brain edema gradually increased at 6 h, and reached peak at 3 d (all P<0.05), then up to normal at 7 d after intracerebral hemorrhage (P>0.05). A large amount of brown Mip1 positive cells were found to distribute in cytoplasm and nucleus of perihematoma after intracerebral hemorrhage. The Mip1 protein expression level was higher in 6 h after intracerebral hemorrhage than that in sham-operated group (all P<0.05), and returned to normal level at 7 d (P>0.05). Conclusion The high expression of Mip1 after ICH is in line with the trend of the brain edema development, and shows that the activation of Mip1 may participate in the pathological process of hemorrhagic cerebral edema.

With the advent of the modern medical mode,rehabilitation medicine teaching becomes an important part of the whole system of medical education.Theory on rehabilitation medicine education infiltrates clinical specialities and brings about a great advance in promoting subject development throughly during clinical education.

BACKGROUND: Brain metabolic abnormality can be observed after cerebral ischemia.OBJECTIVE: To observe the changes of biochemical metabolism of rats with focal cerebral ischemia with 1H magnetic resonance spectroscopy (MRS) in order to reflect the metabolite abnormalities of rats during cerebral ischemic recovery phase.DESIGN: Randomized controlled study.SETTING: Departments of Neurology and department of Radiology of First Affiliated Hospital of Chongqing Medical University.MATERIALS: The experiment was conducted at the Radiological Department of First Affiliated Hospital of Chongqing Medical University from April to July 2004. Totally 24 adult Wistar rats with clean grade were randomly divided into three groups, namely: control group, sham operation group and cerebral ischemia group, with 8 rats in each group.METHODS: The focal cerebral ischemic model was established by occluding the right internal carotid artery in cerebral ischemia group and the filament were just inserted into the internal carotid artery not into the middle cerebral artery in sham operation group, nothing was done except for anesthetizing in the control group. 1H MRS was performed within the area of cerebral infarction and the homologous area of the contralateral hemisphere using 1.5T GE signa Highspeed MRI spectrometer in cerebral ischemic and shamed operation group at the following time point of 30 minutes, 1, 3, 6, 12, 24 hours, 3, 7, 15 days, 1 and 2 months after cerebral ischemia, and in the control group at the same time point.MAIN OUTCOME MEASURES: Changes of lactate, N-acetyl-aspartate (NAA), choline and creatine in infarct hemisphere and contralateral hemisphere.RESULTS: Totally 24 rats were selected in the study, but two died of anesthesia in sham operation group and four of serious brain edema in cerebral ischemia group, only 18 rats entered the final analysis with 8 in normal control group, 6 in sham operation group and 4 in cerebral isThe marked increase in NAA, choline and creatine was recognizable in bilateral spectra 30 minutes after cerebral ischemia and decreased to the period of 3-6 hours, but there was no significant difference in NAA, choline at 6 hours and reached the lowest level at 24 hours (45.21±0.37), choline (93.80±0.56) and creatine (69.33±0.44) at 3 days, and then NAA, choline and creatine gradually increased over time. The increase in NAA was especially obvious which increased by 2.5 times at 2 months than that at 24The earliest detection of lactate was at 10 minutes within the infarct. The lactate concentration elevated at 1 day and peaked at 12 hours, and a partial recovery of the reduction of lactate was seen at 3 days, and the lactate increase within the infarct region was significant compared with that of the homologous area (66.83±0.43,44.35±0.35, t=2.379, P ＜ 0.05). However, the elevation in lactate was no longer observed during the period of up to 2month follow-up.ischemia and reflect the metabolites changes in brain of rats after cerebral cerebral ischemic recovery phase objectively.

Acute ischemic stroke is one of the main causes of long-term morbidity and mortality in developed and developing countries.Collateral circulation,as a compensatory method after ischemia,is affected by many factors and plays an important role in the prevention and treatment of acute ischemic stroke.The influence of collateral circulation on the clinical prognosis and treatment choice of patients with acute ischemic stroke has become a hot topic.Good collateral state can not only reduce the severity of early stroke,but also improve functional recovery after 3 months after stroke.This article reviews the effects of collateral circulation on the prognosis of acute ischemic stroke.