Effects of urethane on reflex activity of lower urinary tract in decerebrate unanesthetized rats

Abstract

Effects of urethane on lower urinary tract function were examined in decerebrate unanesthetized rats. During single slow infusion (0.04 ml/min) cystometrograms (CMGs), urethane (0.3 g/kg) increased micturition pressure threshold (PT) by 73%, postvoid residual volume (RV) by 425%, and decreased voiding efficiency (VE) by 57%, but did not change maximal voiding pressure (MVP), closing peak pressure (CPP), bladder compliance, bladder contraction duration (BCD), or volume threshold (VT) for inducing micturition. Lower doses (0.01-0.1 g/kg) did not alter any parameter. During continuous fast infusion (0.21 ml/min) CMGs, urethane at doses of 0.6-1.2 g/kg (iv) markedly decreased CPP by 69-85%, whereas only the largest dose (1.2 g/kg iv) decreased MVP and external urethral sphincter electromyogram activity by 42 and by 80%, respectively. Doses of 0.001-0.6 g/kg did not alter the intercontraction interval and BCD. Taken together, these results suggest that urethral activity, which is essential for efficient voiding, is more sensitive to the suppressive effect of urethane than afferent or efferent mechanisms controlling the bladder. The threshold dose of MK-801 (0.3 mg/kg), an NMDA antagonist, required to decrease MVP and increase VT in urethane (1.2 g/kg)-anesthetized rats, only increased VT in rats treated with a subanesthetic dose of urethane (0.3 g/kg), suggesting a higher sensitivity of the afferent vs. efferent limb of the micturition reflex pathway to urethane-MK-801 interactions. Because effects of urethane persisted after removal of the forebrain, they must be mediated by actions on the brain stem, spinal cord, or peripheral nervous system.

Functional roles of TRPV1 and TRPV4 in control of lower urinary tract activity: dual analysis of behavior and reflex during the micturition cycle

“…This suggests that in the former mice, the awake forebrain was the site likely responsible for the decreased volume threshold, since it has an excitatory input as well as an inhibitory input into the brain stem, which contains the switching mechanism for micturition initiation (11). In general, neurally intact conscious mice under normal circumstances are known to have a larger bladder capacity than decerebrate (unanesthetized) mice (42,49).…”

“…Moreover, a recent study by Sorge et al (33) revealed that the pain response in conscious rodents is remarkably influenced by olfactory stimuli from male experimenters, strongly suggesting that data analysis would be confounded when in vivo experiments are performed in awake animals. On the other hand, anesthetics are known to interfere with both reflex micturition (23,49) and the pharmacological effects of drugs such as glutamatergic antagonists (47,48,50). As an alternative, animals under decerebrate unanesthetized conditions whose forebrains were previously removed under inhalation anesthesia can be used to examine reflex responses during cystometry (43,45).…”

Dopamine is produced in the rat spinal cord and regulates micturition reflex after spinal cord injury

“…(Yoshiyama et al, 2013) and placed in a restraining cage (KN-326, Natsume). The bladder catheter was connected to a pressure transducer (Transbridge, WPI) and a microinjection pump (SP2001, WPI).…”

Combination of bladder ultrasonography and novel cystometry method in mice reveals rapid decrease in bladder capacity and compliance in LPS-induced cystitis

“…However, these cystometric VVs are remarkably small compared with mouse spontaneous VVs estimated from voided spots on paper (ranging from 200 to 520 l) (12,16,22). It has been suggested that the low VV as measured by mouse cystometry can be attributed to the inhibition of bladder function caused by anesthesia (25), laparotomy, and bladder catheter placement. Because bladder catheter placement will affect bladder wall movement in cystometry, the catheter position in the mouse bladder is one of the most important factors.…”