Ureteral Compliance and Histology in Partial Obstruction in a Canine Model

Abstract

Standardized partial ureter obstruction was achieved in 35 mongrel dogs in whom ureteral compliance and its relationship to histologic changes were studied over a period of 26 weeks. The partially obstructed ureter became dilated with thickened wall and showed muscle hypertrophy and connective tissue proliferation. The normal stellate configuration of the ureteral lumen gradually flattened and became entirely circular by the eighth week. The compliance of the obstructed ureter increased gradually after one, 2, 4, and 8 weeks but decreased thereafter at 12 and 26 weeks. At 8 weeks, the ureter was significantly more compliant than both, the unobstructed control ureter (p less than 0.005) and the 12 week and 26 week partially obstructed ureters (p less than 0.005 & p less than 0.05 respectively). The increase in ureteral compliance was proportional to the amount of muscle hypertrophy during the first 8 weeks while the subsequent decrease in compliance (at 12 and 26 weeks) was proportional to the amount of connective tissue proliferation. This study documents ureteral response, both functional and histologic, to partial obstruction in a canine model over 26 week duration.

Tissue damage and regeneration of ureteric smooth muscle in rats with obstructive uropathy

“…The degree of smooth muscle hypertrophy progressed consistently during ureteric obstruction. These results agree with the clinical changes during hydroureter [ 14] and those of other animal studies [ 2, 3]. Fibrotic tissue in the smooth muscle layer was detected 21 days after ligation and increased during ureteric obstruction, eventually occupying > 90% of the area of the muscle layer in all the ligated ureters 42 days after ligation ( Fig.…”

“…During ureteric obstruction the dilated ureter shows hypertrophy of the ureteric smooth muscle and proliferation of connective tissues [ 1–5]. Although the genetic and cellular characteristics of bladder outlet obstruction have been well studied [ 6] and the hypertrophy of ureteric smooth muscle in obstructive uropathy is well known [ 1–5], the role of hyperplasia of myocytes in the obstructed ureter is rarely reported [ 7]. In addition, the degeneration and regeneration of the smooth muscle layer during ureteric obstruction has not been discussed.…”

Establishment and observation of a new and ideal reversible model of PUUO

“…At present, there are a few surgical methods to create PUUO in animals, such as the Ulm and Miller’s psoas muscle approach, 3 Cheng and Chevalier’s tube approach and Harada’s partial ligation approach. 4 , 5 , 6 However, the models mentioned above had their disadvantages. Most models could not achieve the goal of accurate quantification of occlusion, and some required a second operation on the same spot for occlusion relief, which is technically challenging and hard for tissue recovery.…”

“…Most models could not achieve the goal of accurate quantification of occlusion, and some required a second operation on the same spot for occlusion relief, which is technically challenging and hard for tissue recovery. 3 , 4 , 5 , 6 …”

Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos

“…Enquanto o modelo de obstrução completa é mais fácil de ser reproduzido a partir de ligadura completa do ureter, diversos modelos de obstrução ureteral parcial foram criados com o objetivo de simular esse tipo de obstrução, mais comum na prática clínica. Muitas espécies animais foram utilizadas em modelos de obstrução ureteral completa e parcial incluindo o rato (Chevalier et al, 1998;Yeh et al, 2011;Morsing et al, 1987;Guerin et al, 2008), coelho (Cheng et al, 1993), porco (Dissing et al, 2001;Eskild-Jensen., 2002), cão (Shokeir et al, 1995;Matsui et al, 1986;Harada et al, 1992;Ryan et al, 1987), ovelha e macaco (Wen et al, 2002), entre outros. A maioria desses modelos foi induzida após o nascimento, porém alguns modelos com uropatias obstrutivas congênitas foram utilizados (Miller et al, 2004;Ingraham et al, 2010).…”