Response Of Rabbit Urinary Bladder Research Articles

Effects of Coenzyme Q10 on Bladder Dysfunction Induced by Chronic Bladder Ischemia in a Rat Model

We investigated the protective effects of coenzyme Q10 on bladder dysfunction in a rat model of atherosclerosis induced chronic bladder ischemia. A total of 24 male Sprague-Dawley® rats at age 16 weeks were divided into 4 groups of 6 each, including group 1--untreated, sham operated rats, group 2--coenzyme Q10 treated, sham operated rats, group 3--untreated rats with chronic bladder ischemia and group 4--coenzyme Q10 treated rats with chronic bladder ischemia. Groups 3 and 4 received an endothelial injury to the iliac arteries and were fed a 2% cholesterol diet for 8 weeks. Groups 2 and 4 were treated with coenzyme Q10 and the others were treated with vehicle for 4 weeks. Eight weeks postoperatively we performed continuous in vivo cystometry, an in vitro detrusor muscle strip study and a malondialdehyde assay. Histological examination of the bladder walls and iliac arteries was also done. In vivo cystometry revealed that coenzyme Q10 administration after the induction of chronic bladder ischemia prolonged micturition frequency and the intercontraction interval, and increased bladder capacity compared to those in untreated rats with chronic bladder ischemia. In the detrusor muscle strip study coenzyme Q10 administration after the induction of chronic bladder ischemia increased contractile responses compared to those in untreated rats with chronic bladder ischemia. Rats with chronic bladder ischemia also showed higher malondialdehyde in bladder tissue and serum than the other groups. Chronic bladder ischemia induced submucosal fibrosis of the bladder walls and a degenerative change in the blood vessel tunical media, as shown on histological examination. Our study suggests that coenzyme Q10 acts as an antioxidant to protect bladder function in this chronic bladder ischemia model.

Effect of Co-enzyme Q10 and Alpha-Lipoic Acid on Response of Rabbit Urinary Bladder to Repetitive Stimulation and In Vitro Ischemia

To determine the efficacy of coenzyme Q10 (CoQ10) and alpha-lipoic acid (alpha-LA), either alone or in combination, to protect the contractile responses of the rabbit urinary bladder from damage caused by repetitive stimulation in the presence or absence of in vitro ischemia. Four groups of New Zealand white rabbits (4 per group) were treated with vehicle (group 1), CoQ10 (group 2), alpha-LA (group 3), or CoQ10 plus alpha-LA (group 4) for 2 weeks. At the end of the treatment period, eight longitudinal strips from each rabbit bladder body were placed in oxygenated Tyrode's solution with glucose (normal physiologic medium). The strips were stimulated by field stimulation, carbachol, and KCl, and the responses were recorded. One half of the strips were switched for 1 hour to Tyrode's solution with no glucose equilibrated with nitrogen (ischemia medium). Simultaneously, all strips were subjected to 1 h of repetitive field stimulation followed by 1 hour of recovery in normal physiologic medium, and the responses to all stimuli were recorded again. CoQ10 showed no protective effect. Alpha-LA resulted in increased contractile responses of the control bladder and showed a moderate protective effect for all forms of stimulation. The combination, however, showed a significantly greater increase in the contraction of the control bladder and a greater protective effect than alpha-LA alone. The combination of alpha-LA and CoQ10 treatment enhanced the contractile response in normal medium and diminished the contractile dysfunction induced by repetitive field stimulation and ischemia.

URETHRA IS MORE SENSITIVE TO ISCHEMIA THAN BLADDER: EVIDENCE FROM AN IN VITRO RAT STUDY

URETHRA IS MORE SENSITIVE TO ISCHEMIA THAN BLADDER: EVIDENCE FROM AN IN VITRO RAT STUDY

Effect of Repetitive Stimulation on the Contractile Response of Rabbit Urinary Bladder Subjected to in vitro Hypoxia or in vitro Ischemia Followed by Reoxygenation

Purpose: We studied the effects of hypoxia followed by reoxygenation and an in vitro model of ischemia (hypoxia + substrate [glucose] deprivation) followed by reperfusion (reoxygenation + substrate replacement) on the contractile response of rabbit urinary bladder strips to nonrepetitive and repetitive field stimulation (FS), and correlated the results with the rate of lipid peroxidation. We view repetitive FS as a model for hyperreflexia. Methods: The effects of repetitive and nonrepetitive FS on the contractile responses of isolated strips of rabbit bladder to FS, carbachol, and KCl were determined in the presence of 3 different incubation media: O₂ + glucose (normal physiological medium); N₂ + glucose (in vitro hypoxia), and N₂ – glucose (in vitro ischemia). Then, all strips were incubated for 1 h in normal physiological medium (‘reperfusion’) followed by a final stimulation; the resultant contractile responses were correlated with the level of lipid peroxidation as determined by malonedialdehyde (MDA) concentration. Results: Repetitive stimulation, a model of hyperreflexia, significantly increased the rate of development of contractile dysfunction in bladder tissue strips incubated in all 3 media as compared to nonrepetitive stimulation, which caused no degradation of the contractile response in normal physiological medium. The rate of development of contractile dysfunction was significantly greater in bladder tissue strips incubated in the in vitro ischemia medium (N₂ – glucose) than in strips incubated in the hypoxia medium (N₂ + glucose); which, in turn, was significantly greater than in those incubated in the normal physiological medium (O₂ + glucose). Repetitive stimulation (‘hyperreflexia’) during all 3 incubation conditions resulted in increased [MDA] after reoxygenation or ‘reperfusion’. Incubation in in vitro ischemia buffer (N₂ – glucose) followed by 1 h reoxygenation + substrate replacement stimulated lipid peroxidation to a significantly greater extent than did incubation in hypoxia buffer (N₂ + glucose) followed by 1 h of reoxygenation; the level of lipid peroxidation, [MDA], paralleled the magnitude of the contractile dysfunctions present. Independent of the incubation medium, the magnitude of FS-induced contractile dysfunction after reoxygenation or ‘reperfusion’ was significantly greater than the magnitude of dysfunction in response to carbachol or KCl. Conclusions: The results demonstrate that the rate of contractile failure induced by in vitro ischemia is greater than that induced by in vitro hypoxia, and that the contractile response to FS is significantly more sensitive to both hypoxia and in vitro ischemia than is the contractile response to either carbachol or KCl. Repetitive stimulation (‘hyperreflexia’) increases the rate of contractile failure under all conditions tested, and the magnitude of the contractile failure may be due, in part, to the generation of free radicals and subsequent stimulation of lipid peroxidation upon reoxygenation or ‘reperfusion’.

ATP is released from rabbit urinary bladder epithelial cells by hydrostatic pressure changes--a possible sensory mechanism?

1. The responses of rabbit urinary bladder to hydrostatic pressure changes and to electrical stimulation have been investigated using both the Ussing chamber and a superfusion apparatus. These experiments enabled us to monitor changes in both ionic transport across the tissue and cellular ATP release from it. 2. The urinary bladder of the rabbit maintains an electrical potential difference across its wall as a result largely of active sodium transport from the urinary (mucosal) to the serosal surface. 3. Small hydrostatic pressure differences produced by removal of bathing fluid from one side of the tissue caused reproducible changes in both potential difference and short-circuit current. The magnitude of these changes increases as the volume of fluid removed increases. 3. Amiloride on the mucosal (urinary), but not the serosal, surface of the membrane reduces the transepithelial potential difference and short-circuit current with an IC50 of 300 nM. Amiloride reduces the size of, but does not abolish, transepithelial potential changes caused by alterations in hydrostatic pressure. 4. Field electrical stimulation of strips of bladder tissue produces a reproducible release of ATP. Such release was demonstrated to occur largely from urothelial cells and is apparently non-vesicular as it increases in the absence of calcium and is not abolished by tetrodotoxin. 5. It is proposed that ATP is released from the urothelium as a sensory mediator for the degree of distension of the rabbit urinary bladder and other sensory modalities.

Developmental factors in the contractile response of rabbit urinary bladder: effect of anoxia and extracellular acidosis.

Previous studies have demonstrated that the mechanism of excitation contraction coupling changes with normal development in rabbit urinary bladder smooth muscle. The present study was designed to determine whether there were any differences in the effects of anoxia and extracellular acidosis in response to field stimulation, bethanechol and KCl between mature (8 weeks) and neonatal (3 days) rabbit bladder smooth muscle. Bladder smooth muscle strips from mature and neonatal New Zealand White rabbits were mounted in organ baths and bathed in oxygenated Tyrode's solution. Anoxia was produced by changing the gas mixture to 95% nitrogen/5% CO2 and the effects on contractility were determined at different times after initiation of anoxia. The extracellular acidosis was produced by decreasing the buffer's NaHCO3 concentration. We conclude that bladder smooth muscle does not exhibit an age-specific ability to counteract the effects of anoxia or acidosis as is seen in the developing rabbit myocardium. Instead it appears that the purinergic mechanisms of contraction are much more sensitive to the effects of anoxia or acidosis. Neonatal bladder smooth muscle exhibits a greater drop in contractility with anoxia or acidosis at low frequency (2 Hz) field stimulation; we attribute this to the fact that neonatal bladder smooth muscle has a greater purinergic component in its response to field stimulation. These differences in the responses to anoxia and pH reflect alternate mechanisms of pharmacologic activation, and not inherent differences in the biochemistry of the maturing smooth muscle.

Effect of ryanodine on the contractile response of the normal and hypertrophied rabbit urinary bladder to field stimulation.

Bladder contraction, similar to most smooth muscle contraction, is dependent on both the translocation of extracellular calcium across the cell membrane, and the calcium-stimulated release of intracellular bound calcium. Partial outlet obstruction of the urinary bladder induces a marked increase in bladder mass which results in part from a substantial hypertrophy of the smooth muscle elements. In addition, the increase in bladder mass is associated with specific contractile dysfunctions. It is not known if the contractile dysfunction induced by partial outlet obstruction is related to alterations in calcium metabolism. Ryanodine is a pharmacological tool which can be utilized to study the role of intracellular calcium in mediating contractile events. Ryanodine stimulates the loss of intracellular calcium (bound in the sarcoplasmic reticulum) and reduces the participation of intracellular calcium in the contractile response to specific forms of stimulation. The current study investigates the effect of partial outlet obstruction on the ryanodine inhibition of the contractile response of rabbit urinary bladder to field stimulation. New Zealand White rabbits were anesthetized and catheterized with an 8-french Foley catheter. A 00 silk suture was surgically placed around the catheterized urethra, the incision closed, and the catheter removed. After 1, 3, 5 and 7 days of partial outlet obstruction, the bladder was rapidly removed and utilized immediately for contractile studies. The effect of ryanodine (0-80 microM) on the peak response to 2-, 8- and 16-Hz field stimulation at 0.6, 1.8 and 5.4 mM calcium was determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Pharmacological Responses of Rabbit Urinary Bladder after Subtotal Cystectomy

Partial cystectomy is used clinically in specific circumstances. There have been some reports indicating that the bladder following subtotal cystectomy can regenerate to a certain degree. The present study investigates the physiology and pharmacology of bladder regeneration at eight weeks after resection of a major part of the bladder body in rabbits. The following studies were performed on control and cystectomy bladders: 1) in vivo cystometry (prior to and four weeks after the operation, and before the sacrifice at eight weeks); 2) sequential muscle strip study (the strips were obtained by dividing bladder transversely into upper body, lower body, mid-bladder, upper base and lower base); and 3) in vitro whole bladder studies. The results can be summarized as follows: 1) grossly there was no regeneration of the bladder body; the cystometric capacity was increased slowly after the operation primarily due to increased size and capacity of the bladder base. 2) The contractile response of the subtotal cystectomized bladder body to field stimulation and bethanechol stimulation was less than the response of normal bladder body. 3) The contractile response to epinephrine showed that the ratio of alpha/beta adrenergic response was much greater in the cystectomy bladder than in the normal bladder. 4) In the whole bladder study, the intravesical pressure response to field stimulation was about the same in both groups, the response to bethanechol was less for cystectomized bladder, and the response to methoxamine was greater for the cystectomized bladder. 5) The ability of cystectomy bladder to empty in response to both field stimulation and bethanechol was impaired whereas the control bladder fully emptied to both field stimulation and bethanechol.In conclusion, over the eight week period following subtotal cystectomy the capacity increased via distention (and hypertrophy) of the bladder base area as opposed to regeneration of the bladder body. (J. Urol., 142: 409-412, 1989)

Contribution of prostaglandins to the adenosine triphosphate-induced contraction of rabbit urinary bladder.

1 Adenosine 5'-triphosphate (ATP) produced an initial rapid, phasic contraction and a later, slowly developing tonic contraction in the isolated detrusor of the rabbit but mainly a rapid, phasic response in the guinea-pig bladder. 2 Electrical field stimulation elicited only a rapid, phasic contraction in both rabbit and guinea-pig bladders. 3 Prostaglandin synthesis inhibition by means of indomethacin and suprofen abolished the tonic response to ATP in the rabbit detrusor, leaving the phasic part of the contraction almost unaffected. The ATP-induced contraction in guinea-pig bladder was not influenced by indomethacin. 4 The contractile response of rabbit urinary bladder to prostaglandins F2 alpha and E2 and to carbachol were not significantly influenced by indomethacin. The contractions induced by the prostaglandins were similar to the tonic response to ATP. 5 Tetrodotoxin, atropine, phentolamine, and theophylline did not alter the ATP-induced contraction. However, the calcium antagonists, nifedipine and nimodipine, abolished the phasic ATP response and greatly reduced the tonic part of the contraction. 6 Tachyphylaxis occurred on repeated addition of ATP; the response to field stimulation was progressively reduced only after indomethacin pretreatment. 7 ATP and prostaglandins may contribute to the non-adrenergic, non-cholinergic component of the excitation of rabbit and guinea-pig bladder.

Expansion Mechanisms of the Partially Cystectomized Bladder: 1 an Experimental Study in Rabbits

No AccessJournal of Urology1 Sep 1970Expansion Mechanisms of the Partially Cystectomized Bladder: 1 an Experimental Study in Rabbits A.M.B. Goldstein, V. Gualtieri, and P.L. Getzoff A.M.B. GoldsteinA.M.B. Goldstein More articles by this author , V. GualtieriV. Gualtieri More articles by this author , and P.L. GetzoffP.L. Getzoff More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)61749-XAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail © 1970 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited byKropp B, Rippy M, Badylak S, Adams M, Keating M, Rink R and Thor K (2018) Regenerative Urinary Bladder Augmentation Using Small Intestinal Submucosa: Urodynamic and Histopathologic Assessment in Long-term Canine Bladder augmentationsJournal of Urology, VOL. 155, NO. 6, (2098-2104), Online publication date: 1-Jun-1996.Tong-Long Lin A, Kato K, Monson F, Wein A and Levin R (2018) Pharmacological Responses of Rabbit Urinary Bladder after Subtotal CystectomyJournal of Urology, VOL. 142, NO. 2 Part 1, (409-412), Online publication date: 1-Aug-1989. Volume 104Issue 3September 1970Page: 413-417 Advertisement Copyright & Permissions© 1970 by The American Urological Association Education and Research, Inc.MetricsAuthor Information A.M.B. Goldstein More articles by this author V. Gualtieri More articles by this author P.L. Getzoff More articles by this author Expand All Advertisement PDF downloadLoading ...