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Articles in PresS, published online ahead of print October 10, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00465.2002
Submitted on July 31, 2002
Accepted on October 3, 2002
1 Neurology, University of Vermont, Burlington, VT, USA
2 Surgery, University of Vermont, Burlington, VT, USA
3 Neurology, University of Vermont, Burlington, VT, USA; Surgery, University of Vermont, Burlington, VT, USA
4 Neurology, University of Vermont, Burlington, VT, USA; Anatomy and Neurobiology, University of Vermont, Burlington, VT, USA
* To whom correspondence should be addressed. E-mail: mvizzard{at}zoo.uvm.edu.
The purpose of this study was to determine the role of cyclooxygenase-2 (COX-2) and its metabolites in lower urinary tract function after induction of acute (4 hr), intermediate (48 hr) or chronic (10 day) cyclophosphamide (CYP)-induced cystitis. Bladders were harvested from euthanized, female rats for analyses. Conscious cystometry was used to assess the effects of a COX-2-specific inhibitor, DFU (5 mg/kg; s.c.), a di-substituted furanone, in CYP-induced cystitis. COX-2 mRNA was increased in inflamed bladders after acute (12-fold) and chronic (9-fold) treatment. COX-2 protein expression in inflamed bladders paralleled that of COX-2 mRNA. Prostaglandin D2-methoxime (PGD2-Mox) expression in the bladder was significantly (p 
0.01) increased in acute (3-fold) and chronic (5.5-fold) cystitis. Prostaglandin (PG) E2 was significantly (p 0.01) increased (2-fold) in the bladder with intermediate (1.7-fold) and chronic (2.6-fold) cystitis. COX-2-IR cell profiles were distributed throughout the inflamed bladder and co-expressed histamine-IR. Conscious cystometry in CYP+DFU-treated rats showed increased micturition intervals 4-hr and 48-hr after CYP-treatment and decreased intravesical pressures during filling and micturition compared to CYP+vehicle-treated rats. These studies suggest an involvement of urinary bladder COX-2 and its metabolites in altered micturition reflexes with CYP-induced cystitis.
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