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Ultra-low dose beta-irradiation induces constriction of rabbit carotid arteries via the endothelium.

机译:超低剂量的β射线照射可通过内皮引起兔颈动脉收缩。

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摘要

PURPOSE: To investigate the action of ultra-low dose beta-radiation (ULDBR) on isolated segments of blood vessels. MATERIALS AND METHODS: We used the pharmacological model of isolated rabbit carotid arteries with intact or mechanically removed endothelium. Specific vascular responses to beta-irradiation were registered after addition of (90)Sr in the concentration range between 12 and 96 microCi l(-1) to the organ bath containing physiological salt solution (PSS). RESULTS: Intact vascular rings, preconstricted with 20 mM K(+)-PSS, developed an additional constriction upon the addition of (90)Sr depending on the absorbed radiation dose (21.5, 42.9, 85.8, and 171.6 microGy) and the dose rate (51.5, 103.0, 206.0 and 412.0 microGy h(-1)). The vasoconstriction due to (90)Sr was absent in the endothelium-denuded vascular segments indicating the endothelium dependent action of ULDBR. Irradiation did not alter the endothelium dependent relaxation of rabbit carotid arteries induced by acetylcholine. The endothelium dependent responses to ULDBR were abolished after increasing the extra-cellular K(+) to 40 mM. CONCLUSIONS: ULDBR acts on rabbit carotid arteries as a pharmacological signalling agent because ULDBR effects were completely reversible. ULDBR-mediated contractile responses of the vessels are endothelium dependent. The resistance of acetylcholine endothelium-dependent relaxation of rabbit carotid arteries to ULDBR indicates that the polyphosphoinositide-nitric oxide (NO) signalling cascade is not impaired by ULDBR in endothelial cells.
机译:目的:研究超低剂量β射线(ULDBR)对孤立血管段的作用。材料与方法:我们使用完整或机械去除内皮的孤立兔颈动脉的药理模型。向含有生理盐溶液(PSS)的器官浴中添加浓度范围在12到96 microCil(-1)之间的(90)Sr后,记录对β辐射的特定血管反应。结果:完整的血管环,预先约束有20 mM K(+)-PSS,根据吸收的辐射剂量(21.5、42.9、85.8和171.6 microGy)和剂量率,在添加(90)Sr时会产生另外的约束(51.5、103.0、206.0和412.0 microGy h(-1))。在内皮剥脱的血管段中没有由于(90)Sr引起的血管收缩,这表明ULDBR的内皮依赖性作用。辐照不会改变乙酰胆碱诱导的兔颈动脉内皮依赖性舒张。将细胞外K(+)增加至40 mM后,对ULDBR的内皮依赖性反应消失。结论:由于ULDBR的作用是完全可逆的,因此ULDBR可作为药理信号转导剂作用于兔颈动脉。 ULDBR介导的血管收缩反应是内皮依赖性的。兔颈动脉对乙酰胆碱内皮依赖性舒张的抗性表明ULDBR在内皮细胞中不会损害多磷酸肌醇一氧化氮(NO)信号级联。

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