TY - JOUR
T1 - Physiologic sequelae of partial infravesical obstruction in the mouse
T2 - Role of inducible nitric oxide synthase
AU - Lemack, Gary E.
AU - Burkhard, Fiona
AU - Zimmern, Philippe E.
AU - Mcconnell, John D.
AU - Lin, Victor K.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1999/3
Y1 - 1999/3
N2 - Purpose: To develop a mouse model for partial infravesical obstruction, and determine the resultant changes in bladder function, with particular emphasis on the role of inducible nitric oxide synthase (iNOS) in the bladder response. Materials and Methods: Wild type mice were subjected to no intervention, sham operation, and varying durations of partial outlet obstruction (1, 3, and 5 weeks). They then underwent cystometric evaluation, bladder strip stimulation studies using carbachol, and relaxation studies using l-arginine, sodium nitroprusside, and 8-bromoguanosine 3'-5' cyclic guanosine monophosphate. Bladder tissue was subjected to RT-PCR and Western analysis for iNOS. Bladders were also studied histologically using morphometric analysis. Results: Bladders from mice obstructed for 5 weeks were heavier (weight increased by 110%), larger (capacity increased by 73%), and had a higher frequency of abnormal appearing cystometric curves than normal bladders. Tissue bath studies demonstrated decreased contractility in response to cholinergic stimulation at 5 weeks of obstruction (decreased by 55% at maximal stimulation). RT-PCR demonstrated iNOS in approximately 70% of bladders obstructed for 1 and 3 weeks, while the iNOS protein was apparent in 50% of the bladders from the same groups. Conclusions: This new animal model of infravesical obstruction is reliable and reproducible. Moreover, the physiologic changes noted are comparable to other models, but an added advantage is the relevance of this model with regard to studying new transgenic or knockout mice. Enhanced expression of iNOS seen early after obstruction may serve to improve oxygenation during obstruction-induced ischemia.
AB - Purpose: To develop a mouse model for partial infravesical obstruction, and determine the resultant changes in bladder function, with particular emphasis on the role of inducible nitric oxide synthase (iNOS) in the bladder response. Materials and Methods: Wild type mice were subjected to no intervention, sham operation, and varying durations of partial outlet obstruction (1, 3, and 5 weeks). They then underwent cystometric evaluation, bladder strip stimulation studies using carbachol, and relaxation studies using l-arginine, sodium nitroprusside, and 8-bromoguanosine 3'-5' cyclic guanosine monophosphate. Bladder tissue was subjected to RT-PCR and Western analysis for iNOS. Bladders were also studied histologically using morphometric analysis. Results: Bladders from mice obstructed for 5 weeks were heavier (weight increased by 110%), larger (capacity increased by 73%), and had a higher frequency of abnormal appearing cystometric curves than normal bladders. Tissue bath studies demonstrated decreased contractility in response to cholinergic stimulation at 5 weeks of obstruction (decreased by 55% at maximal stimulation). RT-PCR demonstrated iNOS in approximately 70% of bladders obstructed for 1 and 3 weeks, while the iNOS protein was apparent in 50% of the bladders from the same groups. Conclusions: This new animal model of infravesical obstruction is reliable and reproducible. Moreover, the physiologic changes noted are comparable to other models, but an added advantage is the relevance of this model with regard to studying new transgenic or knockout mice. Enhanced expression of iNOS seen early after obstruction may serve to improve oxygenation during obstruction-induced ischemia.
KW - Bladder outlet obstruction
KW - Mouse
KW - Nitric oxide
UR - http://www.scopus.com/inward/record.url?scp=0032846026&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032846026&partnerID=8YFLogxK
U2 - 10.1016/S0022-5347(01)61838-X
DO - 10.1016/S0022-5347(01)61838-X
M3 - Article
C2 - 10022743
AN - SCOPUS:0032846026
SN - 0022-5347
VL - 161
SP - 1015
EP - 1022
JO - Journal of Urology
JF - Journal of Urology
IS - 3
ER -