London, United Kingdom 2013 Fig 1 CV staining of the brain sections 1) Light stained part represents infarct area. 2) Column 1, each plot represents a CV staining layer of brain sections in MH2. Column 2, each plot represents a CV staining layer of brain sections in MH6. Column 3, each plot represents a CV staining layer of brain sections in NT. E-Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 251 9 Experimental studies Effect of Mild Delayed Hypothermia on a Focal Model of Permanent Cerebral Ischemia in Spontaneously Hypertensive rats W. Fan1, A.Y Ge2, J Ding3, J.C Guo4, X.Q Wu5, H.F Bao6, F.H Zhuo7 Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, CHINA1, De-partment of Neurology, Zhongshan Hospital, Fudan University, shanghai, CHINA2, Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, CHINA3, National Key Laboratory of Medical Neurobiology, Medical College, Fudan University, shanghai, CHINA4, Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, CHINA5, Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, CHINA6, Department of Neurology, Zhongshan Hospital, Fudan University, shanghai, CHINA7 Background: Mild hypothermia (MH) has been shown to reduce damage resulting from transient fo-cal ischemia in animal models with normal blood pressure. Little information is available, however, regarding the protective potential of MH against permanent brain ischemia in hypertensive animals. Therefore we established a model of permanent middle cerebral artery occlusion (pMCAO) in spon-taneously hypertensive rats (SHR) to investigate the effect of MH on ischemic injury. Methods: 33 SHR were randomly divided into 4 groups: 2 hours delayed MH group (MH2, n=8, 33+/-0.5°C MH induced 2 hrs after pMCAO until rats killed; 6 hrs delayed MH group (MH6, n=9, 33+/-0.5°C MH induced 6 hrs after pMCAO until rats killed); normothermia group (NT, n=8, rats kept in 25°C after pMCAO); and sham group (SH, n=8, rats kept in 25°C after sham operation). The pMCAO model was established by a suture-occluded method. Neurological behavior impairment score (NBI) was evaluated at 5 hrs, 24 hrs and 36 hrs after operations and all rats were killed at 36 hrs. Continuous coronal brain sections were stained by cresyl violet for calculation of infarct volume and evaluation of brain edema. NeuN staining was used to detect loss of neurons in infarct core (IC) and peri-in-farct area (PI). Results: There were no significant differences in NBI among MH2, MH6 and NT. Compared with NT, infarct volume was decreased by 23.75% (P<0.01) and 18.72% (P<0.05); brain edema by 25.32% (P<0.05) and 21.52% (P<0.05) in MH2 and MH6, respectively. In PI, MH2 and MH6 had an increased count of NeuN positive cells compared with NT by 21.67% (P<0.01) and 15.67% (P<0.05), respectively. While in IC, no difference had been found in neuron loss among MH2, MH6 and NT. The infarct volume, brain edema and neuron loss did not differ between MH2 and MH6. In SH, no NBI and pathological impairment had been found. Conclusion: In SHR, pro-longed mild hypothermia induced at 2 or 6 hours after pMCAO is neuroprotective.
Karger_ESC London_2013
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