Mudraya I S, Kirpatovsky V I, Martov A G, Obuchova T V
Urological Research Institute, Moscow, Russia.
J Endourol. 2001 Jun;15(5):533-9. doi: 10.1089/089277901750299357.
Ureteral endoprostheses are used for dilatation of strictures in order to maintain upper urinary tract (UUT) function for a longer period.
Three kinds of short (3-4-cm) endoprostheses were inserted into the ureter of mongrel dogs with intact UUT or experimental ureter strictures. The UUT function was evaluated by means of radiographic examinations and in terms of following measures of contractility: intraluminal pressure, electroureterography (EUG), and multichannel impedance ureterography (MIUG). Studies were performed 1, 3 to 6 months, and 1 to 3 years after prostheses implantation.
Similar urodynamic changes were registered in prosthetically treated ureters of dogs with initially intact UUTs and those with ureteral strictures. These disorders consisted of increased UUT intraluminal pressure and different functioning of the upper and lower regions of the ureter. The bioelectric and contractile activity of the upper UUT regions was reinforced, accelerated, and dysrhythmic, while peristaltic ureter wall function below the endoprosthesis was rare and weak.
The changes observed are typical for ureteral prosthetics. The UUT urodynamic alterations could be attributable entirely to the excluding of the ureteral segment from active contraction and were the result of the local absence of the ureteral wall closing mechanism. One must keep in mind that UUT endoprostheses produce a high load on the ureter wall. The transition from UUT hyperfunction to contractile function decompensation may depend on the intrinsic compensatory reserves of the ureter.
输尿管内支架用于扩张狭窄，以更长时间维持上尿路（UUT）功能。
将三种短（3 - 4厘米）的内支架植入杂种犬的输尿管，这些犬的上尿路完整或存在实验性输尿管狭窄。通过影像学检查以及以下收缩性指标评估上尿路功能：腔内压力、输尿管电描记术（EUG）和多通道阻抗输尿管描记术（MIUG）。在支架植入后1个月、3至6个月以及1至3年进行研究。
在最初上尿路完整的犬和存在输尿管狭窄的犬中，接受支架治疗的输尿管出现了相似的尿动力学变化。这些紊乱包括上尿路腔内压力升高以及输尿管上下段功能不同。上尿路区域的生物电和收缩活动增强、加速且节律紊乱，而支架下方输尿管壁的蠕动功能罕见且微弱。
观察到的变化是输尿管支架植入的典型表现。上尿路尿动力学改变可能完全归因于输尿管节段主动收缩的排除，并且是输尿管壁关闭机制局部缺失的结果。必须牢记，上尿路内支架会给输尿管壁带来高负荷。从上尿路功能亢进转变为收缩功能失代偿可能取决于输尿管的内在代偿储备。
