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Objective: by detecting cerebral ischemia reperfusion at different stages, different types within the lung, liver and kidney tissue of nitric oxide synthase (NOS) activity variation as well as medications given after the intervention rotundine reveal nitric oxide together enzyme in cerebral ischemia-reperfusion lung, liver and kidney tissue damage in the role, and to explore rotundine protection mechanism. Method: improved Pulsinelli four-vessel occlusion method to establish global cerebral ischemia-reperfusion injury model, were divided into three groups: sham operation group (S group), cerebral ischemia and reperfusion group (IR) and Luo pass given the treatment group (T). The two groups after reperfusion time is divided into 2h, 6h, 12h, 24h, and 48h five subgroups. T group clipping given immediately after rotundine injection (20mg/kg) intraperitoneal injection, after each interval 6h give the equivalent volume of drug treatment. Animals in each group (S group immediately after IR and T group at the corresponding time points respectively reperfusion 2h, 6h, 12h, 24h, 48h), the rats were killed quickly, collect specimens for the determination of nitric oxide synthase (NOS) activity, production, and histological sections. Results: (1) Compared with the sham group (S), ischemia-reperfusion group (IR) total nitric oxide synthase (NOS) activity in 2h, 12h, 24h high than the S group, the difference was statistically significance (P <0.05). The first peak (P lt; 0.05), which formed in 2h mainly to the main structure of nitric oxide synthase (eNOS) rose (P lt; 0.05) 6h back down to the level of the sham group (P gt ; 0.05) and late (gt; 6h), nitric oxide synthase (NOS) activity to rise again, and 12h increased the most significant (P lt; 0.01), second peak of inducible nitric oxide mainly synthase (iNOS) increased (P <0.01) and is still high (P <0.05) at 24h, 48h close to the S group level (P gt; 0.05); (2) and ischemia-reperfusion group (IR constitutive nitric oxide synthase (eNOS) activity group) compared to the treatment group (T) at 2h further increased (P <0.01), the activity of inducible nitric oxide synthase (iNOS) in 12h, 24h decreased significantly (P <0.01); (3) sham group (S group) lung, liver, kidney pathological structures no exception; the IR group pathological changes and organ function (Cr, ALT) compared with S group, there were varying degrees of damage, at 12h the most serious; the T group organization pathology and organ damage is minor compared with the IR group significantly improved. Conclusion: (1) nitric oxide synthase (NOS) involved after cerebral ischemia-reperfusion lung, liver, kidney and multiple organ damage process. The activity of the different types of nitric oxide synthase (NOS) in different stages of cerebral ischemia and reperfusion of the lung, liver and kidney tissues, plays a different role: the eNOS activity level of tissue damage is inversely proportional to the high activity mild tissue damage; opposite, iNOS activity correlated with the degree of tissue damage is proportional to the high activity, the most serious injury. (2) the role of rotundine by adjusting the different types of nitric oxide synthase (NOS) activity early protective effect factor increase eNOS activity, post suppress damage factor iNOS activity, of acute cerebral ischemia-reperfusion injury in rats lung, liver and kidney tissues plays a protective role.
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