Functional effect of chronic ischemia on the rabbit urinary bladder

Lin, Alex Tong‐Long; Wein, Alan J.; Gill, Harcharan; Levin, Robert M.

doi:10.1002/nau.1930070102

Cited by 55 publications

(24 citation statements)

References 17 publications

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“…With time, the obstructed bladder deteriorates due to alterations in its physiology and structure, and it is known that similar changes can also occur in the hypoxic bladder in experimental models [3]. Consequently, it was postulated that ischaemia has a major role in detrusor dysfunction [4] and this condition is characterized by a shift of metabolism towards anaerobic pathways [5].…”

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical estimation of hypoxia in human obstructed bladder and correlation with clinical variables

Koritsiadis¹,

Stravodimos²,

Koutalellis³

et al. 2008

BJU International

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OBJECTIVETo investigate the tissue distribution of ischaemia in human detrusor in patients with bladder outlet obstruction (BOO) and to correlate the results with clinical variables, as clinical BOO is a common problem in ageing men and ischaemia might be important in detrusor dysfunction.PATIENTS AND METHODSFrom September 2004 to October 2006, 70 patients were recruited, comprising 60 scheduled for surgery to treat benign prostatic hyperplasia (the study group) and 10 as controls. Detrusor tissue was retrieved and stained for hypoxia‐inducible factor (HIF)‐1α, a cellular marker of hypoxia.RESULTSThe mean (sd) total number of cells immunoreactive to HIF‐1α in the study group was 93.3 (48.09), and in the specimens from the control group only few rare cells showed weak immunoreactivity to HIF‐1α (0–2). Positive cells were in different proportions between muscle bundles and submucosa, expressed mainly in stromal cells. The urothelium and detrusor muscle showed no immunoreactivity to HIF‐1α. There was strong immunoreactivity in patients with prolonged BOO (<10 years), declining thereafter, and in those patients with urinary retention.CONCLUSIONSThe urothelium and detrusor seem to be more resistant to hypoxic stress, while stromal cells perceive low oxygen tension. The bladder response to chronic hypoxia through HIF‐1α expression is limited in time and might depend on the functional status of the detrusor.

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Section: Introductionmentioning

confidence: 99%

“…However, reduced bladder wall blood flow during the emptying phase results in further tissue hypoxia [6]. This observation comes from experimental models in animals, where obstruction is artificially induced from days to several weeks [1][2][3][4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical estimation of hypoxia in human obstructed bladder and correlation with clinical variables

Koritsiadis¹,

Stravodimos²,

Koutalellis³

et al. 2008

BJU International

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“…The integrity and function of detrusor smooth muscle is extremely sensitive to hypoxia, overdistension, diabetes, and ischemia [5][6][7][8][9][10][11]. One common factor in these pathologies may be a reduction in blood flow.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 1998

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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 ...

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“…Studies indicate that bladder hypoxia and ischemia may play a role in specific forms of bladder dysfunction [10][11][12][13][14][15][16]. However, little is known about the relative sensitivity of rat and rabbit bladders to hypoxia and ischemia [17,18].…”

Section: Introductionmentioning

confidence: 99%

Rabbit versus Rat Urinary Bladder: Effects of in vitro Hypoxia

Whitbeck

Barreto²,

Horan³

et al. 1999

Pharmacology

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Purpose: Studies indicate that bladder hypoxia may be an etiological factor for lower urinary tract dysfunction. Rat and rabbit are two species of experimental animals used frequently to study lower urinary tract function and dysfunction. The objective of this study was to compare directly effects of in vitro hypoxia on contractile responses of rat and rabbit urinary bladder to different forms of stimulation. Methods: Sexually mature male New Zealand White rabbits and Sprague-Dawley rats were compared. Each bladder was excised while the animal was anesthetized, and longitudinal bladder strips were cut, then mounted in organ baths. A tension of 2 g was placed on all strips. Effects of 1, 2, 3 and 4 h hypoxia followed by 1 h of reoxygenation on contractile responses of bladder strips to field stimulation (FS), carbachol (100 μmol/l), ATP (1 mmol/l) and KCl (120 mmol/l) were determined. Results: Contractility, per unit tissue mass, of rat bladder strips was significantly greater than that of rabbit bladder strips in response to FS (all frequencies), carbachol, KCl and ATP. Hypoxia (followed by reoxygenation) resulted in time-dependent progressive reduction in contractile responses of bladder strips to all stimuli. Rat bladder was significantly more sensitive to hypoxia than rabbit bladder in response to FS and carbachol. Hypoxia induced similar effects on rat and rabbit bladder responses to ATP and KCl. Conclusion: Rat bladder neurogenic and cholinergic responses are significantly more sensitive to hypoxia than are those of rabbit bladder, which may be due to the rat bladder’s greater contractile force generation and previously reported higher Ca²⁺-ATPase activity.

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Functional effect of chronic ischemia on the rabbit urinary bladder

Cited by 55 publications

References 17 publications

Immunohistochemical estimation of hypoxia in human obstructed bladder and correlation with clinical variables

Immunohistochemical estimation of hypoxia in human obstructed bladder and correlation with clinical variables

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

Rabbit versus Rat Urinary Bladder: Effects of in vitro Hypoxia

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