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Production of nitric oxide and change of nitric Oxide synthase activity in brains mitochondria of the rats with focal cerebral ischemia/reperfusion

Jian Xu

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Abstract

AIM and METHOD:To determine the production of nitric oxide(NO) and change of NO synthase(NOS) activity in mitochondria isolated from the rat brains of the ischemia/reperfusion rat model produced by transient occlusion of middle cerebral artery on the following the points: 2 h after occlusion of artery and 30 min, 2h, 4h after reperfusion. RESULTS: After the occlusion of middle cerebral artery, the respiratory control rate(RCR) of mitochondria significantly decreased and slightly increased at 4h after reperfusion. Meantime, the production of NO in mitochondria increased significantly. But with the increase of perfusion, production of NO gradually decreased and reached normal level as in the control group. It also shows that cerebral ischemia increased NOS's activity significantly in the mitochondria and still kept a higher level than the control group although it decreased gradually after reperfusion. But the iNOS's activity did not show obvious change. The change of total NOS's activity depends on the change of cNOS's activity. CONCLUSION: The activation of NO/NOS system in the mitochondria might play an important role in the reperfusion injury during reperfusion of ischemic brain.

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AIM and METHOD:To determine the production of nitric oxide(NO) and change of NO synthase(NOS) activity in mitochondria isolated from the rat brains of the ischemia/reperfusion rat model produced by transient occlusion of middle cerebral artery on the following the points: 2 h after occlusion of artery and 30 min, 2h, 4h after reperfusion. RESULTS: After the occlusion of middle cerebral artery, the respiratory control rate(RCR) of mitochondria significantly decreased and slightly increased at 4h after reperfusion. Meantime, the production of NO in mitochondria increased significantly. But with the increase of perfusion, production of NO gradually decreased and reached normal level as in the control group. It also shows that cerebral ischemia increased NOS's activity significantly in the mitochondria and still kept a higher level than the control group although it decreased gradually after reperfusion. But the iNOS's activity did not show obvious change. The change of total NOS's activity depends on the change of cNOS's activity. CONCLUSION: The activation of NO/NOS system in the mitochondria might play an important role in the reperfusion injury during reperfusion of ischemic brain.

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Available abstract

AIM and METHOD:To determine the production of nitric oxide(NO) and change of NO synthase(NOS) activity in mitochondria isolated from the rat brains of the ischemia/reperfusion rat model produced by transient occlusion of middle cerebral artery on the following the points: 2 h after occlusion of artery and 30 min, 2h, 4h after reperfusion. RESULTS: After the occlusion of middle cerebral artery, the respiratory control rate(RCR) of mitochondria significantly decreased and slightly increased at 4h after reperfusion. Meantime, the production of NO in mitochondria increased significantly. But with the increase of perfusion, production of NO gradually decreased and reached normal level as in the control group. It also shows that cerebral ischemia increased NOS's activity significantly in the mitochondria and still kept a higher level than the control group although it decreased gradually after reperfusion. But the iNOS's activity did not show obvious change. The change of total NOS's activity depends on the change of cNOS's activity. CONCLUSION: The activation of NO/NOS system in the mitochondria might play an important role in the reperfusion injury during reperfusion of ischemic brain.

Key concepts: Nitric oxide synthase, Nitric oxide, Ischemia, Mitochondrion, Anesthesia, Occlusion, Reperfusion injury, Internal medicine

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Production of nitric oxide and change of nitric Oxide synthase activity in brains mitochondria of the rats with focal cerebral ischemia/reperfusion — Research Paper | ScholarLens