Detre Z, Leithner C, Winter M, Sinzinger H, Silberbauer K, Fódy L, Jellinek H
Artery. 1980;8(4):398-403.
In the early phase of malignant renal hypertension induced by aortic ligature, a transient activation of transmural aortic permeability is observed. The transmural permeability shows its maximum during the first week of hypertension returning in the third week to normal or even subnormal values, whereas the blood pressure is still rising. The permeability disturbance precedes the structural transformation of the arterial wall. Although the aortic segments above and below the ligature are exposed to different blood pressure and hemodynamic stresses their patterns of permeability disturbance are the same. If the kidney below the aortic ligature is removed no permeability disturbance can be observed. Aortic wall PGI2-formation both above and below the ligature is elevated in the first phase of hypertension. The PGI2-synthesis returns to normal values during the 5th week. Our data suggest that in the early phase of renovascular hypertension there is an increased aortic antiaggregatory activity and that PGI2 is probably not the compound responsible for increased transmural permeability. Moreover, the blood pressure and the hemodynamic forces have no decisive importance in the induction of the aortic transmural permeability disturbance.
在主动脉结扎诱导的恶性肾性高血压早期,可观察到跨壁主动脉通透性的短暂激活。跨壁通透性在高血压的第一周达到最大值,在第三周恢复到正常甚至低于正常的值,而血压仍在上升。通透性紊乱先于动脉壁的结构转变。尽管结扎上方和下方的主动脉段暴露于不同的血压和血流动力学应力,但它们的通透性紊乱模式是相同的。如果切除主动脉结扎下方的肾脏,则观察不到通透性紊乱。结扎上方和下方的主动脉壁PGI2形成在高血压的第一阶段均升高。PGI2合成在第5周恢复到正常值。我们的数据表明,在肾血管性高血压的早期,主动脉抗聚集活性增加,并且PGI2可能不是导致跨壁通透性增加的化合物。此外,血压和血流动力学力在主动脉跨壁通透性紊乱的诱导中没有决定性作用。