Szabó C, Csáki C, Benyó Z, Marczis J, Reivich M, Kovách A G
Department of Neurology, Medical School University of Pennsylvania, Philadelphia, USA.
Circ Shock. 1994 Nov;44(3):104-10.
Middle cerebral artery rings (MCA) were prepared from control and hemorrhagic hypotension and retransfusion-subjected (HHR) cats, with or without superoxide dismutase (SOD) treatment. Two-mm-long MCA segments were suspended in organ chambers containing Krebs-Henseleit solution (37 degrees C, gassed with 95% O2-5% CO2) for isometric force measurements. HHR was produced by bleeding to 90, 70, and 50 mmHg MAP and maintained for 15 min at each level, followed by retransfusion. HHR resulted in a marked attenuation of the acetylcholine- and ATP-induced endothelium-dependent relaxations of the MCA in vitro. Relaxations induced by the nitric oxide (NO) donor SIN-1 remained unaltered. In vitro treatment of the vessels with SOD (150 U/ml), facilitated the acetylcholine-induced relaxations both in the control arteries and in the vessels after HHR. In the vessel rings from cats that received in vivo SOD (10 mg/kg initial bolus, followed by 0.1-mg/kg/min infusion) during HHR, cholinergic relaxations were more pronounced than in the HHR untreated cats. The ATP-induced relaxations, however, remained attenuated after SOD treatment, except for the highest dose (10(-5) M) that was applied.
Superoxide release attenuates the endothelium-dependent relaxation by acetylcholine both in control arteries and after HHR in vitro. The protective effect of in vivo SOD treatment on cerebrovascular endothelium-dependent reactivity in cats suggests that superoxide free radicals contribute to the development of the endothelium dysfunction in MCA rings after HHR.
从对照猫以及经历出血性低血压和再输血（HHR）的猫身上制备大脑中动脉环（MCA），部分进行超氧化物歧化酶（SOD）处理，部分未处理。将2毫米长的MCA节段悬挂于含有 Krebs-Henseleit 溶液（37℃，用 95% O₂ - 5% CO₂ 通气）的器官浴槽中进行等长力测量。通过将平均动脉压（MAP）降至 90、70 和 50 mmHg 并在每个水平维持 15 分钟，随后再输血来产生 HHR。HHR 导致体外 MCA 对乙酰胆碱和 ATP 诱导的内皮依赖性舒张显著减弱。一氧化氮（NO）供体 SIN-1 诱导的舒张未改变。用 SOD（150 U/ml）对血管进行体外处理，可促进对照动脉以及 HHR 后血管对乙酰胆碱诱导的舒张。在 HHR 期间接受体内 SOD（初始推注 10 mg/kg，随后以 0.1 mg/kg/min 输注）的猫的血管环中，胆碱能舒张比未处理的 HHR 猫更明显。然而，除了应用的最高剂量（10⁻⁵ M）的 ATP 外，SOD 处理后 ATP 诱导的舒张仍减弱。
超氧化物释放减弱了对照动脉以及体外 HHR 后血管对乙酰胆碱的内皮依赖性舒张。体内 SOD 处理对猫脑血管内皮依赖性反应性的保护作用表明，超氧自由基促成了 HHR 后 MCA 环中内皮功能障碍的发展。
