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J Urol. 2004 Oct;172(4 Pt 1):1524-8.

A male murine model of partial bladder outlet obstruction reveals changes in detrusor morphology, contractility and Myosin isoform expression.

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  • 1Division of Urology Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.



Mice with gene deletion or targeted over expression are important for understanding the remodeling that follows partial bladder outlet obstruction (PBOO). This condition predominates in males. We produced PBOO in male mice and now report the physiological, histological and molecular consequences.


Male C57bl/6 mice were surgically obstructed or subjected to sham surgery and unoperated mice served as controls. Four weeks later the bladders were excised and their function was assessed with in vitro whole bladder cystometry. The optimum volume for pressure generation was determined and isometric pressures were measured for field stimulation and depolarization with KCl. Bladder hypertrophy was classified as severe-bladder mass greater than 50 mg or mild-bladder mass less than 50 mg. The percent muscle fraction was determined by histological analyses. The expression of C-terminal (SM1 and SM2) and N-terminal (SM-B and SM-A) isoforms of myosin heavy chain was analyzed by reverse transcriptase-polymerase chain reaction.


Severely hypertrophied bladders had larger optimum volume (p >0.001) and generated less pressure in response to field stimulation (p >0.001) and KCl (p >0.01) with a slower rate of pressure generation than controls or sham operated mice. Increased SM1-to-SM2 and SM-A-to-SM-B ratios were noted in severely obstructed bladders relative to controls or sham operated mice (p <0.05). The muscle fraction decreased slightly in the severely hypertrophied group (p not significant).


Our male mouse model of PBOO demonstrates an increase in bladder mass, larger capacity and significantly decreased pressure generation in the in vitro whole bladder model. Obstruction induced increases in the expression of C-terminal (SM1) and N-terminal (SM-A) myosin heavy chain isoforms.

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