缺氧一再给氧时家兔主动脉NO的变化及机制研究

目的 :观察缺氧一再给氧时家兔主动脉一氧化氮 (nitric oxide,NO)含量的变化并探讨其机制。方法 :培养的家兔主动脉内皮细胞 (endothelialcell,EC)随机分为四组 :(1 )对照 (C)组一通入空气 ;(2 )缺氧 (H)组一通入 95% N2 与 5% CO2 气 ;(3 )缺氧一再给氧 (H/ R)组一在缺氧的基础上通入 95% O2 与 5% CO2 气 ;(4 )超氧化物歧化酶 (superoxide dismutase,SOD)与缺氧一再给氧 (SOD H/ R)组一在 3之家加入 SOD,余同 3。测定 NO- 2 含量间接反映 NO含量。结果 :缺氧、再给氧时 H、H/ R组 NO含量均降低 ,以 H/R组更加显著 ,SOD可使 NO含量增加。结论 :缺氧可损伤 EC,使 NO生成减少 ;再给氧可促进缺氧的损伤。NO减少的机制与缺氧一再给氧时自由基产生增多有关。

CHANGS IN NITRIC OXIDE LEVEL OF RABBIT AORTA TO HYPOXIA-REOXYGENATION AND ITS MECHANISM

Objective:To observe the changes in nitric oxide (No)level of rabbit aorta to hypoxia-reoxygenation and study its mechanism.Methods:Cultured rabbit's aortic endothelial cells(EC)were divided into four groups:1.Control(c)group:with the air put in to.2.hypoxia(H)group:with 95%N 2 and 5%CO 2.put into 3.hypoxia-reoxygenation(H/R)group:with 95%o 2 and 5%co 2 put in to after hypoxia.4.Superoxide dismutase(SOD)and hypoxia-reoxygenation(SOD H/R)group:SOD administrated was before hypoxia-reoxygenation.NO level was measured by measuring NO - 2 contents.Results:NO level of H and H/R groups was decreased,especially in H/R group.The administration of SOD could increase NO level.Conclusion:Hypoxia could induced EC injury,and decrease No production.Reoxygenation worsened the hypoxic injury.Oxygen free radicals may be one of the main mechanisms involved in the NO decrease of hypoxia-reoxygenation injury.