Previous studies have demonstrated the protective effect of hypoxic preconditioning on acute ce-rebral infarction, but the mechanisms underlying this protection remain unclear. To investigate the protective mechanisms of hypoxic preconditioning in relation to its effects on angiogenesis, we in-duced a photochemical model of cerebral infarction in an inbred line of mice (BALB/c). Mice were then exposed to hypoxic preconditioning 30 minutes prior to model establishment. Results showed significantly increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra at 24 and 72 hours post infarction, mainly in neurons and vascular endothelial cells. Hy-Hypoxic preconditioning increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra and the expression of vascular endothelial growth factor was positively related to that of CD31. Moreover, hypoxic preconditioning reduced the infarct volume and improved rological function in mice. These findings indicate that the protective role of hypoxic preconditioning in acute cerebral infarction may possibly be due to an increase in expression of vascular endothelial growth factor and CD31 in the ischemic penumbra, which promoted angiogenesis.

缺氧预适应过程中的小鼠脑一氧化氮下调

Downregulation of nitric oxide in the brain of mice during their hypoxic preconditioning.J Appl Physiol 91:1193～1198,2001.An animal model of hypoxic preconditioning was produced in mice by repeated exposure to autohypoxic condition.The animals' tolerance times to hypoxia were 1.7,1.8,2.1 and 2.3 times longer in runs 2,3,4 and 5,respectively,than that in run 1,and their oxygen consumption and heart and respiration rates were progressively and significantly slowed down during the repetitive exposure to hypoxia.L-arginine concentration,nitric oxide (NO) synthase-positive cells,NO synthase activity,and NO content in the whole brain and the subregions telencephalon,diencephalons,and brain stem were significantly increased during the first exposure and were,instead of continuing to increase,significantly decreased in run 4 after the second and third exposure.Tolerance times under the hypoxic condition were significantly shortened and prolonged when preadministration of L-arginine and its analog,respectively,was made.These results indicate that NO in the brain is downregulated under condition of hypoxic preconditioning and negatively involved in increased tolerance to hypoxia.

缺氧预适应过程中的小鼠脑一氧化氮下调

Downregulation of nitric oxide in the brain of mice during their hypoxic preconditioning.J Appl Physiol 91:1193～1198,2001.An animal model of hypoxic preconditioning was produced in mice by repeated exposure to autohypoxic condition.The animals' tolerance times to hypoxia were 1.7,1.8,2.1 and 2.3 times longer in runs 2,3,4 and 5,respectively,than that in run 1,and their oxygen consumption and heart and respiration rates were progressively and significantly slowed down during the repetitive exposure to hypoxia.L-arginine concentration,nitric oxide (NO) synthase-positive cells,NO synthase activity,and NO content in the whole brain and the subregions telencephalon,diencephalons,and brain stem were significantly increased during the first exposure and were,instead of continuing to increase,significantly decreased in run 4 after the second and third exposure.Tolerance times under the hypoxic condition were significantly shortened and prolonged when preadministration of L-arginine and its analog,respectively,was made.These results indicate that NO in the brain is downregulated under condition of hypoxic preconditioning and negatively involved in increased tolerance to hypoxia.