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Objective To investigate the effects of local mild hypothermia on the expression of EMAP-Ⅱ and proEMAP-Ⅱ after cerebral ischemia and reperfusion in rats and to explore the possible neuroprotection mechanism of mild hypothermia.Methods Forty-four male Wistar rats were divided randomly into a sham-operation group (Sham),a normothermia group (NT) and a hypothermia group (HT).Middle cerebral artery occlusion was performed using Longa's method,and reperfusion was allowed after 2 hours of occlusion.Mild hypothermia (33.0 ± 0.5)℃ for 6 hours was initiated at the start of reperfusion,followed by rewarming.Brains were harvested after 6,12,24,48 and 72 hours of reperfusion and used for HE staining to evaluate cellular apzoptosis and immunohistochemical staining for detecting the expression EMAP-Ⅱ and proEMAP-Ⅱ.Results The expression of EMAP-Ⅱ and proEMAP-Ⅱ in the ischemic penumbra was significant at 6 hours in the normothermia and hypothermia groups.It peaked at 12 hours in the normothermia group and 24 hours in the hypothermia group,and then decreased gradually.At 72 hours the expression of EMAP-Ⅱ and proEMAP-Ⅱ in the ischemic penumbras was very close to that in the sham group.EMAP-Ⅱ-positive cells were significantly fewer in the hypothermia group than in the normothermia group at all time points.ProEMAP-Ⅱ-positive cells were significantly more numerous in the normothermia group than in the hypothermia group at 6,12 and 24 hours.Conclusions Mild hypothermia (33.0 ± 0.5) ℃ has a valid neuroprotective effect which involves reducing EMAP-Ⅱ and proEMAP-Ⅱ expression in the ischemic penumbra and inhibiting apoptosis and inflammatory reactions after cerebral ischemia and reperfusion,at least in rats.
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Objective To study the expression of EI-1 in myocardium during cerebral ischemia and reper-fusion, and to investigate the mechanism of cerebral cardiac syndrome. Method Two hundred and eight SD rats weighting 220～250 gram, were divided into three groups: sham control group (n=48), cerebral ischemia group (n=80), cerebral ischemia/reperfusion group (n=80). The area of cerebral ischemia, and the concentration of sennn ET-1 and CK-MB, and the content of myocardial ET-1 were determined in 0,6, 12,24,48,72 h after cerebral ischemia and reperfusion, and were analyzed by t-test or F-test. Results Cerebral necrosis area was ob-served at 6 h after cerebral ischemia in cerebral ischemia group, and peaked at 12 h (P>0.05). The concentra-tion of CK-MB increased gradually after cerebral ischmia, peaked at 12 h (P<0.05), and then gradually de-creased. The serum concentration of ET-1 peaked at 6 h and then gradually decreased. The content of ET-1 in my-ocardium began to increase at 6 h after cerebral ischemia, and peaked at 12 h (P<0.05). In cerebral ischemia/reperfusion group, all of cerebral necrosis size, CK-MB concentration and myocardial ET-1 concent paelced at 12 h and then gradually decreased (P<0.05). Change of ET-1 concentration in blood was similar to that in cerebral ischemia group. Compared with cerebral ischemia group, the size of cerebral necrosis reduced obviously at 24 h,48 h,72 h in cerebral ischemia/reperfusion group (P<0.05). The concentration of CK-MB in cerebral ischemia/ reperfusion group was higher than that in cerebral isehemia group (P<0.05). The peak time of myocardial ET-1 was shatened in cerebral ischemia/reperfusion group. The change of serum ET-1 was not different between two groups. Conclusions Large area of cerebral ischemia, might cause myocardial injury. ET-1 is involved in the course of myocardial injury following cerebral ischemia. Though cerebral reperfusion can protect brain,but it make myocardial injury more serious,and ET-1 might participate in this course.
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To evaluate the protective effect of MgSO_4 during cerebral ischemia reperfusion,twentyfour SD rats were divided randomly into control group (n=7),ischemic reperfusion group (n=9)and MgSO_4 treatment group (n=8)with Pnlsinelli and Brierley's animal ischemic reperfusion model. Compared with the control and ischemic reperfusion group,cerebral tissue contents of water and malondialdehyde reduced markedly (P