A RAT MODEL FOR INVESTIGATION OF SPINAL MECHANISMS IN DETRUSOR INSTABILITY ASSOCIATED WITH INFRAVESICAL OUTFLOW OBSTRUCTION

A rat model of infravesical outflow obstruction was modified to allow cystometric investigation in conscious, free-moving animals after intr athecal drug administration. The catheter position and extent of drug distribution were controlled by injection of dye and dissection of the spinal canal. Continuous cystometries were performed in awake normal rats as well as rats with bladder hypertrophy and hyperactivity follow ing infravesical outflow obstruction. In some animals of each group, c ystometry was performed with simultaneous recording of intra-abdominal pressure. The possible effects of the presence of the intrathecal cat heter were studied, as well as the effects of saline, local anesthetic s, morphine and naloxone administered through the catheter. Neither th e presence of the intrathecal catheter nor injection of saline affecte d the cystometric pattern. Bupivacaine (50 mug) produced paralysis of both lower extremities and a complete, though reversible, suppression of micturition in normal rats. In rats with hypertrophy, intrathecal b upivacaine in doses of 50 mug and 100 mug produced decreases in mictur ition pressure, increases in bladder capacity and dribbling incontinen ce. However, the amplitude of spontaneous contractile activity increas ed after the administration. The inhibitory.effects of morphine (0.5-1 0 mug) on micturition in normal rats, which were rapidly reversed by n aloxone, were in accordance with results obtained in previous studies in anesthetized animals. Rats with bladder hypertrophy showed a simila r response to morphine and naloxone. However, the bladder hyperactivit y-was not inhibited by morphine. We conclude that the present model se ems reliable for the study of spinal mechanisms in the development of detrusor instability associated with infravesical outflow obstruction.