Abstract:Cystometries were performed in normal rats and in rats with bladder hypertrophy due to infravesical outflow obstruction. Investigations were performed in the presence and absence of anesthesia. pentobarbital anesthesia depressed spontaneous contractile activity in the bladder and the micturition reflex, thereby making measurements of other variables, such as bladder capacity and residual volume, impossible. In conscious animals infravesical outflow obstruction led to development of increased bladder capacity, … Show more
“…The impairment of bladder and its innervation and peri--urethral blood vessel was avoided. Therefore, compared to the previous studies (3,7), the influence of injury on bladder, which might be the etiology of DO, was excluded. 3.…”
Section: Discussionmentioning
confidence: 99%
“…The most common method to create a model of DO rats involved reduction of the urethral diameter by placing a suture around the urethra (7), and significant increases were demonstrated in voiding frequency, voiding pressure and bladder capacity. Moreover, DO rats showed a pronounced "non-voiding contractions" during cystometry, and the categorization of different types of DO in conscious rats has been described (3).…”
Section: Introductionmentioning
confidence: 99%
“…However, many disadvantages presented in the model of DO rats established in the previous studies. For example, DO rats were established by partial obstruction with a method of transabdominal pathway, and the abdomen was opened through a midline incision (7). The architecture of cavitas pelvis was dissected, and the trauma might induce impairment of nerves and deformity of bladder which might influence the function of bladder.…”
ARTICLE INFO
______________________________________________________________ ______________________Objective: To improve the model for establishment and evaluation of detrusor overactivity in female Wistar rats.
Materials and Methods:We ligated the perineal urethra of female Wistar rats and then performed filling cystometry. The probability of detrusor overactivity, bladder capacity, peak voiding pressure and histological changes were investigated.Results: Detrusor overactivity ratio of the obstruction group was 32.4%. Bladder capacity increased from 0.273 ± 0.036mL in control group to 0.89 ± 0.19mL in detrusor overactivity group (P < 0.001), and peak voiding pressure increased from 45.9 ± 4.1 cm.H 2 O to 63.5 ± 17.4cm.H 2 O (P = 0.007). For obstruction group, compared to no detrusor overactivity rats, detrusor overactivity rats had higher bladder capacity (0.89 ± 0.19mL versus 0.43 ± 0.09mL, P < 0.001) and higher peak voiding pressure (63.5 ± 17.4cm.H 2 O versus 44.8 ± 6.2cm.H 2 O, P = 0.005). Detrusor overactivity rats were classified according to peak voiding pressure (49.2 ± 4.2cm.H 2 O versus 80.8 ± 7.1cm.H 2 O, P < 0.001). Moreover, bladder weight increased significantly in detrusor overactivity rats (P = 0.003, P = 0.028) and detrusor histological hypertrophy was observed. Conclusions: Ligating perineal urethra and filling cystometry with intra-urethral cannula approach is a simple and easily reproducible method to establish and evaluate the model of detrusor overactivity in rats.
“…The impairment of bladder and its innervation and peri--urethral blood vessel was avoided. Therefore, compared to the previous studies (3,7), the influence of injury on bladder, which might be the etiology of DO, was excluded. 3.…”
Section: Discussionmentioning
confidence: 99%
“…The most common method to create a model of DO rats involved reduction of the urethral diameter by placing a suture around the urethra (7), and significant increases were demonstrated in voiding frequency, voiding pressure and bladder capacity. Moreover, DO rats showed a pronounced "non-voiding contractions" during cystometry, and the categorization of different types of DO in conscious rats has been described (3).…”
Section: Introductionmentioning
confidence: 99%
“…However, many disadvantages presented in the model of DO rats established in the previous studies. For example, DO rats were established by partial obstruction with a method of transabdominal pathway, and the abdomen was opened through a midline incision (7). The architecture of cavitas pelvis was dissected, and the trauma might induce impairment of nerves and deformity of bladder which might influence the function of bladder.…”
ARTICLE INFO
______________________________________________________________ ______________________Objective: To improve the model for establishment and evaluation of detrusor overactivity in female Wistar rats.
Materials and Methods:We ligated the perineal urethra of female Wistar rats and then performed filling cystometry. The probability of detrusor overactivity, bladder capacity, peak voiding pressure and histological changes were investigated.Results: Detrusor overactivity ratio of the obstruction group was 32.4%. Bladder capacity increased from 0.273 ± 0.036mL in control group to 0.89 ± 0.19mL in detrusor overactivity group (P < 0.001), and peak voiding pressure increased from 45.9 ± 4.1 cm.H 2 O to 63.5 ± 17.4cm.H 2 O (P = 0.007). For obstruction group, compared to no detrusor overactivity rats, detrusor overactivity rats had higher bladder capacity (0.89 ± 0.19mL versus 0.43 ± 0.09mL, P < 0.001) and higher peak voiding pressure (63.5 ± 17.4cm.H 2 O versus 44.8 ± 6.2cm.H 2 O, P = 0.005). Detrusor overactivity rats were classified according to peak voiding pressure (49.2 ± 4.2cm.H 2 O versus 80.8 ± 7.1cm.H 2 O, P < 0.001). Moreover, bladder weight increased significantly in detrusor overactivity rats (P = 0.003, P = 0.028) and detrusor histological hypertrophy was observed. Conclusions: Ligating perineal urethra and filling cystometry with intra-urethral cannula approach is a simple and easily reproducible method to establish and evaluate the model of detrusor overactivity in rats.
“…administration of drugs as described in detail previously (Igawa et al, 1993b). Thereafter, the abdomen was opened through a midline incision, and a polyethylene catheter (Clay-Adams PE-50, NJ, U.S.A.) was implanted into the bladder through the dome as described previously (Malmgren et al, 1987). The catheters were tunnelled subcutaneously and orifices were made on the back of the animal.…”
Section: Surgical Proceduresmentioning
confidence: 99%
“…After each drug administration, recording was continued for at least another 120 min. The following cystometric parameters were investigated (Malmgren et al, 1987): basal pressure (the lowest bladder pressure during filling), threshold pressure (bladder pressure immediately prior to micturition), micturition pressure (the maximum bladder pressure during micturition), bladder capacity (residual volume at the latest previous micturition plus volume of infused saline at the micturition), micturition volume (volume of expelled urine), residual volume (bladder capacity minus micturition volume), and spontaneous contractile activity (mean amplitude and frequency of bladder pressure fluctuations during 2 min prior to micturition). Analysis was performed for a 20 min period before drug administration.…”
1 By means of continuous cystometry in normal, unanaesthetized rats, the effects on micturition of intrathecally (i.t.) administered morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G), the two main metabolites of morphine, were studied and compared with those of i.t. morphine.2 Both M6G (0.01, 0.1, and 0.5 lg) and M3G (5 pg) were found to have significant effects on micturition. Like morphine (0.1, 0.5, and 10pg), M6G was able to inhibit the micturition reflex, and produce urinary retention and dribbling incontinence in a dose-dependent manner. The potency of M6G for inhibiting micturition was approximately 10 times higher than that of morphine, and the duration of its effect was longer. All effects of M6G could be reversed by naloxone.3 M3G (5 jig) facilitated the micturition reflex, resulting in decreases in bladder capacity and micturition volume, and an increase in spontaneous contractile activity. Pretreatment with naloxone (10 fig), which by itself had no effect on micturition, enhanced the facilitatory effects of M3G. In addition, M3G tended to counteract the inhibitory effects of both morphine and M6G on micturition. M3G (5 jg) also produced an excitatory behavioural syndrome. 4 It is concluded that in rats, i.t. M3G has excitatory effects on micturition and behaviour, probably not mediated via opioid receptors. I.t M6G has a potent inhibitory effect on micturition mediated by stimulation of opioid receptors. It may have effects on somatosensory afferent input in lower doses than those required for effects on micturition.
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