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Biomedical subjects

R M Levin

Publications and source records attributed to R M Levin.

At least 19 recordsLinked to original sources
PubMed2007

Effect of short-term outlet obstruction on rat bladder nerve density and contractility.

1 The present study was designed to investigate the relationship between innervation density and contractile responses to field stimulation and exogenous agonists at early time points after induction of bladder outlet obstruction (BOO) in rats. 2 When compared with sham-operated animals, 1, 3 and 7 days of BOO were associated with a 75%, 80% and 90% increase of bladder weight. Field stimulation caused a frequency-dependent increase in force of contraction. The force of contraction was reduced at each frequency in BOO rats with the greatest decrease after 1 day and a gradual but incomplete recovery thereafter. In contrast, contractile responses to ATP, carbachol and KCl were markedly reduced after 1 day of BOO and fully recovered after 7 days. The neurofilament staining was not altered by 1 day of BOO, but gradually decreased with increasing duration of BOO reaching the lowest levels after 7 days. 3 We conclude that impaired cellular contractility seems to underlie the early reductions of field stimulation-induced contraction, possibly reflecting surgical trauma of the tissue. However, at later time points a reduced nerve density, possibly reflecting a partial denervation, appears to be the main reason for impaired contractile response to field stimulation.

Adenosine Triphosphate↗
PubMed2005

Low-dose tadenan protects the rabbit bladder from bilateral ischemia/ reperfusion-induced contractile dysfunction.

Recent studies indicate that focal ischemia/reperfusion (I/R) can cause the contractile dysfunctions induced in animal models of partial bladder outlet obstruction. Tadenan (Pygeum africanum) pretreatment can prevent the rabbit bladder from developing the contractile and biochemical dysfunctions induced by partial outlet obstruction, possibly by protecting the bladder from ischemic injury. The current study was designed to determine whether pre-treating rabbits with a clinically relevant dose of Tadenan could prevent the bladder from developing the contractile dysfunctions that are induced by bilateral ischemia followed by reperfusion. New Zealand White rabbits were separated into two groups. One group was pre-treated by oral gavage for 3 weeks with Tadenan (3.0 mg/kg body wt./ day). The second group was treated with vehicle (peanut oil). Five rabbits from each group were subjected to either bilateral ischemia for 1 or 3 h and than reperfused for either 1 h or 1 week. Five rabbits from each group were subjected to sham surgery and run with each of the experimental groups. The results of the current study show that Tadenan pretreatment at the clinically relevant dose of 3.0 mg/kg body wt./day protected the bladder from the contractile dysfunctions induced by bilateral ischemia followed by reperfusion. These data are consistent with the assertion that Tadenan therapy in both rabbits and humans acts by protecting the bladder smooth muscle against cellular damage caused by ischemia and reperfusion.

Administration, Oral↗
PubMed2004

Effect of vaginal distension on blood flow and hypoxia of urogenital organs of the female rat.

Vaginal delivery of children causes traumatic injury to tissues of the pelvic floor and is correlated with stress urinary incontinence; however, the exact mechanism of organ and tissue injury leading to incontinence development is unknown. The purpose of this project was to test the hypothesis that vaginal distension results in decreased blood flow to, and hypoxia of, the urogenital organs responsible for continence, which would suggest an ischemic and/or reperfusion mechanism of injury. Thirteen female rats underwent vaginal distension for 1 h. Thirteen age-matched rats were sham-distended controls. Blood flow to the bladder, urethra, and vagina were determined using a microsphere technique. Hypoxia of these organs was determined by immunohistochemistry. Blood flow to all three organs was significantly decreased just before release of vaginal distension. Bladder blood flow decreased further immediately after release of vaginal distension and continued to be significantly decreased 15 min after the release. Blood flow to both the urethra and vagina tripled immediately after release, inducing a rapid return to normal values. Vaginal distension resulted in extensive smooth muscle hypoxia of the bladder, as well as extensive hypoxia of the vaginal epithelium and urethral hypoxia. Bladders from sham-distended rats demonstrated urothelial hypoxia as well as focal hypoxic areas of the detrusor muscle. We have clearly demonstrated that vaginal distension results in decreased blood flow to, and hypoxia of, the bladder, urethra, and vagina, supportive of hypoxic injury as a possible mechanism of injury leading to stress urinary incontinence.

Animals↗
PubMed2001

The effect of urine volume and nitric oxide on basal bladder blood flow: response to catheterization and drainage.

Preliminary studies demonstrated that catheterization and drainage of the urinary bladder resulted in a significant increase in blood flow to the bladder. The objectives of this study were to determine 1) the relationship between urine volume and basal blood flow to the bladder smooth muscle and mucosa, 2) the effect of acute catheterization and drainage on bladder mucosal and smooth muscle blood flow, and 3) whether nitric oxide was involved in regulation of basal blood flow or the increase in blood flow observed after catheterization and bladder drainage. Twenty-four rabbits were separated into two groups: group 1 (14 rabbits) and group 2 (10 rabbits) treated with L-NAME (NOS inhibitor) 30 minutes before blood flow measurement. Blood flow was measured in all animals using a fluorescent microsphere technique before and immediately after catheterization and drainage of the bladder. The results demonstrated that 1) blood flow to the muscle and mucosa were independent of urine volume at the time of catheterization and drainage; 2) catheterization and drainage significantly increased blood flow to both the bladder smooth muscle and bladder mucosa, but not to the kidney; 3) L-NAME significantly reduced basal blood flow to the kidney, but not to the bladder smooth muscle or mucosa; and 4) L-NAME completely prevented the catheterization- and drainage-induced increases in blood flow to the bladder body mucosa and muscle. This study demonstrates that basal blood flow to the bladder smooth muscle and mucosa during filling is independent of NO control; although bladder blood flow may be increased significantly by NO synthesis and release during bladder emptying, and thus may be an important regulator of blood flow during and immediately following micturition.

Animals↗
PubMed2001

Increased blood flow after catheterization and drainage in the chronically obstructed rabbit urinary bladder.

OBJECTIVES: To determine the effect of drainage on rabbit bladder blood flow after 4 weeks of partial outlet obstruction. Previous studies have shown that catheterization and drainage of the urinary bladder in control rabbits resulted in a significant nitric oxide-induced increase of blood flow to the bladder. It was also shown that 4 weeks' partial outlet obstruction caused a significant decrease in blood flow to the bladder. METHODS: Male New Zealand White rabbits underwent partial outlet obstruction by standard methods. After 4 weeks, the blood flow to the bladder muscle and mucosa was determined by a microsphere technique. Within 1 to 2 minutes after transurethral catheterization and complete drainage of the bladder, the blood flow was again determined. Unobstructed animals served as controls. Four other control animals underwent a repetitive blood flow study during 10 minutes to determine the time frame of blood flow changes after drainage. Blood flow was also measured in 2 control rabbits after transurethral catheterization without drainage and in 2 control rabbits after drainage by suprapubic puncture. To exclude the possibility that increased intravesical pressure alters the blood flow measurements, the relationship between the intravesical volume and the bladder pressure was examined in the obstructed rabbits. RESULTS: After drainage of the bladder, the blood flow to the bladder muscle increased 4.5-fold in the decompensated obstructed group (bladder weights greater than 15 g) and 2.5-fold in the compensated animals (bladder weights less than 5 g) and control animals. Blood flow to the mucosa followed the same pattern but without reaching significance. Blood flow returned to near baseline values within 5 minutes. Catheterization without drainage did not alter the blood flow. In contrast, drainage by puncture increased the blood flow significantly. Higher intravesical volumes increased the intravesical pressure slightly, but after opening the abdominal fascia, the intravesical pressure did not change with increasing volumes. CONCLUSIONS: Although the previously shown decreased blood flow to the bladder smooth muscle may be an etiologic factor in bladder contractile dysfunction secondary to partial outlet obstruction, the bladder does have the ability to increase the blood flow after drainage. This ability could be a compensatory and possibly protective mechanism after outlet obstruction.

Animals↗
PubMed2001

Aspirin treatment improves bladder function after outlet obstruction in rabbits.

OBJECTIVES: To examine whether bladder smooth muscle dysfunction after outlet obstruction could be altered by treatment with aspirin. Long-term outlet obstruction causes contractile and metabolic dysfunction of the bladder in vivo and in vitro. The evidence is growing that a decrease in bladder perfusion is an important cause of this phenomenon. The platelet aggregation inhibitor, acetylsalicylic acid (aspirin), has been used to improve perfusion of the heart for decades. METHODS: Ten male New Zealand white rabbits were obstructed for 4 weeks. Five rabbits received no further treatment (Obs), and 5 rabbits received 2 mg/kg/day aspirin (Obs+aspirin), administered by an osmotic pump implanted subcutaneously 1 week before the surgical obstruction. The bleeding time was measured to confirm the effectiveness of the aspirin treatment. Three different control groups were created: sham-operated rabbits, unobstructed rabbits with pumps containing DMSO (vehicle), and unobstructed rabbits with pumps containing aspirin. The contractile responses of bladder strips to field stimulation, adenosine triphosphate, carbachol, and KCl were determined. A section of each detrusor tissue was fixed in formalin and used to determine the smooth muscle and collagen (connective tissue) volume fraction. RESULTS: No differences were found in the bladder weights or responses to stimuli in the different control groups, which were therefore combined. Partial bladder outlet obstruction caused significant increases in the bladder weight of the obstructed animals (Obs+aspirin, 10.15 +/- 0.87 g; Obs, 10.17 +/- 0.88 g; and controls, 2.87 +/- 0.21 g). The aspirin treatment increased the bleeding time from 1.7 +/- 0.3 minutes to 3.3 +/- 0.1 minutes. The responses to field stimulation were significantly reduced in all of the obstructed rabbits. However, the responses of the bladder strips from the Obs rabbits to field stimulation were impaired to a significantly greater degree than were those from the Obs+aspirin rabbits. The response to 32-Hz stimulation was reduced by 86% in the Obs group but by only 64% in the Obs+aspirin group. The responses to carbachol were significantly reduced by 62% in the strips from the Obs rabbits, but the responses of the strips from the Obs+aspirin rabbits were similar to the responses of the strips from the controls. The responses to KCl and adenosine triphosphate were reduced, although they just failed to achieve statistical significance using Bonferroni's analysis. The ratio of smooth muscle and connective tissue shifted slightly toward smooth muscle after 4 weeks of obstruction, but no difference was found with or without aspirin treatment. CONCLUSIONS: Low-dose aspirin has a small but significant protective effect on the contractile dysfunction induced by bladder outlet obstruction in rabbits, although the increase in bladder mass was not altered. Bladders of the same weight showed improved responses to all forms of stimulation after pretreatment with aspirin. Already used by millions of patients with heart diseases, aspirin could be a useful protection against contractile dysfunction of the obstructed bladder.

Animals↗
PubMed2001

The effect of partial outlet obstruction on prostaglandin generation in the rabbit urinary bladder.

Partial outlet obstruction of the urinary bladder has been demonstrated to induce specific dysfunctions in cellular and sub-cellular membrane structures within the bladder's smooth muscle and mucosal compartments. Recent studies have linked these membrane dysfunctions to alterations in phospholipid metabolism leading to mobilization of free arachidonic acid, the precursor for synthesis of prostaglandins (PG). The purpose of this study was to determine if partial outlet obstruction of the urinary bladder induces changes in the capacity of bladder smooth muscle and mucosa to generate PG. PG were isolated from control and partially obstructed urinary bladder smooth muscle and mucosa of male New Zealand White (NZW) rabbits. PG concentrations (PGE2, PGF2alpha and PGI2, as its stable metabolite 6-keto-PGF1alpha) were determined after 30 minute incubations using enzyme-linked immunoassay (ELISA) kits. In both control and obstructed rabbit urinary bladders, PG generation was significantly higher in isolated mucosa than muscle tissues. A significantly higher concentration of PGF2alpha, and 6-keto-PGF1alpha was measured in obstructed muscle tissue relative to controls. The concentration of 6-keto-PGF1alpha was also significantly higher than the concentrations measured for PGE2 and PGF2alpha in both control and obstructed smooth muscle samples. The generation of PGE2 was significantly higher in rabbit urinary bladder mucosa than either PGF2alpha or 6-keto-PGF1alpha in both control and obstructed samples. The capacity of obstructed mucosal tissue to generate 6-keto-PGF1alpha was significantly higher than control tissue, while no significant differences in PGE or PGF2alpha generation were noted. These data suggest obstruction of the urinary bladder induce specific elevations in PG in both smooth muscle and mucosal tissues.

6-Ketoprostaglandin F1 alpha↗
PubMed2001

Vascular response of the rabbit bladder to chronic partial outlet obstruction.

Partial outlet obstruction of the rabbit urinary bladder results, initially, in a rapid increase in bladder mass and remodeling of the bladder wall. Previously, it was shown that this response was characterized by serosal growth (thickening) which was apparent after 1 day of obstruction, before any visible vascularization was observed. After 1 week of obstruction, significant microvessel formation was seen in the transition region between the detrusor smooth muscle and the thickening serosa; after 2 weeks the entire serosa was vascularized. In this study we investigated the effect of chronic (4 week) partial outlet obstruction on microvessel density and distribution in the bladder wall immunohistochemically using CD31 as a marker for vascular endothelium. Transverse sections of bladder wall were examined after 4 weeks of no surgery, sham surgery or partial obstruction. The microvessel density of the obstructed rabbit bladder mucosa and detrusor smooth muscle increased relative to augmentation of these compartments while new vessels appeared in the thickening serosa. Although vessel density did not change with obstruction a significant shift in mean vessel circumference to the left occurred indicating a significant increase in the number of microvessels and small vessels consistent with angiogenesis.

Adenosine Triphosphate↗
PubMed2001

Loss of mitochondrial DNA in rabbit bladder smooth muscle following partial outlet obstruction results from lack of organellar DNA replication.

When the rabbit bladder outlet is partially obstructed, the relative amount of mitochondrial (mt) DNA per cell in bladder smooth muscle falls rapidly. In order to assess whether this loss of organellar genome results from attenuation of mt DNA replication, we cloned portions of rabbit genes specifying the single-strand binding (SSB) protein required for initiation of mt DNA replication, and the catalytic subunit of DNA polymerase gamma (pol gamma), the replication enzyme itself. We then designed primer-probe systems for real-time RT-PCR (TaqMan) analyses for each gene. These were used to assess mRNA in preparations from bladder smooth muscle and mucosa from rabbits subjected to surgical obstruction of the bladder outlet for up to 14 days. mRNA from the pol gamma gene remained essentially at control level in smooth muscle and mucosa in all samples. In mucosa, mRNA from the SSB protein gene remained virtually at control levels in all samples, as did mt genome copy number. In smooth muscle, however, levels of this mRNA declined by >95% within 3 days of obstruction and remained at that level through 14 days; this attenuation of SSB protein mRNA paralleled the loss of mt DNA in the same smooth muscle samples. Thus, lack of mt SSB protein, and consequently attenuated mt DNA replication, is a primary factor in the loss of mt genome copies in bladder smooth muscle after outlet obstruction in the rabbit model of benign bladder dysfunction.

Animals↗
PubMed2001

Effect of chronic bladder outlet obstruction on blood flow of the rabbit bladder.

PURPOSE: Previous studies have shown that the initial reaction of the rabbit bladder to partial bladder outlet obstruction is increased blood flow at day 1 and a return to baseline blood flow at 1 week. Mucosal and muscle blood flow followed this pattern but mucosal blood flow was always 4 to 5-fold greater. In this study we examined the effect of 4 weeks of outlet obstruction on bladder blood flow and correlated it with the severity of bladder contractile dysfunction. MATERIALS AND METHODS: A total of 14 male New Zealand White rabbits underwent partial outlet obstruction creation by standard methods. After 4 weeks the rabbits were anesthetized, and blood flow to the muscle and mucosa was determined by standard fluorescent microsphere technique. A section of each detrusor was used for in vitro contractility studies. Contractile responses to field stimulation, carbachol and potassium chloride were determined. A section of each detrusor tissue was fixed in formalin and used to determine the smooth muscle volume fraction. RESULTS: Four weeks of partial bladder outlet obstruction caused a significant and variable increase in bladder weight and a decrease in blood flow to bladder muscle without changes in the blood flow to mucosa. There was a clear correlation between the severity of contractile dysfunction, bladder weight and the magnitude of the decrease in blood flow in muscle. The smooth muscle volume fraction remained stable at approximately 40%. CONCLUSIONS: Bladder decompensation was associated with decreased blood flow to bladder smooth muscle. Because compensated obstructed bladders with relatively normal contractile function are also hypertrophied but have normal blood flow, decreased blood flow in decompensated bladders is not simply a response to bladder hypertrophy. From this study we hypothesize that decreased blood flow to bladder smooth muscle is an etiological factor in bladder contractile dysfunction (bladder decompensation) secondary to partial outlet obstruction.

Animals↗
PubMed2001

Urethra is more sensitive to ischemia than bladder: evidence from an in vitro rat study.

PURPOSE: Experimental studies have demonstrated that ischemia may induce significant bladder dysfunction. Because multiple causes leading to bladder ischemia also decrease urethral perfusion, we assessed the effect of in vitro ischemia on the contractile responses of the rat bladder and urethra. We evaluated the hypothesis that neurogenic dysfunction in urethral ischemic injury occurs before myogenic dysfunction is present. We also compared contractile responses of the rat bladder and urethra to in vitro ischemia followed by reoxygenation. MATERIALS AND METHODS: Isolated strips of rat bladder detrusor muscle and prostatic urethra were incubated in normal physiological medium and stimulated electrically and chemically. In vitro ischemia was produced by incubating tissue in ischemic medium for 30 or 60 minutes. The maximal tension and maximal rate of tension generated were analyzed digitally before ischemia and after ischemia followed by reoxygenation. RESULTS: We demonstrated that after 30 minutes of ischemia followed by reperfusion the maximal rate of tension generated decreased significantly only in the urethra and only in response to field stimulation. After 60 minutes of ischemia the decrease in urethral contractile responses was greater than the decrease in bladder contractile responses. Ischemia 60 minutes in duration caused a significant decrease in the maximal rate of tension generated as well as maximal tension in the urethra and bladder but only in response to field stimulation. CONCLUSIONS: This experiment demonstrates that the urethra is more sensitive to ischemic injury than the bladder. Our finding may explain the development and symptoms of urinary incontinence secondary to sphincteric damage before bladder dysfunction is present. We also demonstrated that in the bladder and urethra the response to field (neurogenic) stimulation is the most sensitive form of stimulation to ischemia.

Animals↗
PubMed2001

Protective effect of vitamin E on the response of the rabbit bladder to partial outlet obstruction.

PURPOSE: There is increasing evidence that ischemia/reperfusion is a major etiological factor in the progression of bladder dysfunction after partial outlet obstruction. If this evidence is correct, treatment with an antioxidant should be beneficial in rabbits subjected to partial outlet obstruction. We designed the current study to determine if diets high in alpha-tocopherol protected the rabbit bladder against dysfunction induced by partial outlet obstruction. MATERIALS AND METHODS: A total of 32 rabbits were separated into 4 groups of 8. Groups 1 and 2 were placed on a diet enriched with 1,000 IU/kg. alpha-tocopherol, and groups 3 and 4 were fed a regular diet containing 44 IU/kg. alpha-tocopherol. After 4 weeks partial outlet obstruction was created in groups 1 and 3, while groups 2 and 4 underwent sham operation. After 4 weeks of obstruction the rabbits were anesthetized and the bladders were rapidly excised. Four longitudinal strips obtained from the bladder body were used for contractility studies. The balance of the bladder body was separated between muscle and mucosa. Each section was frozen and stored at -70C for analysis of malondialdehyde as a measure of peroxidation and for alpha-tocopherol concentrations. RESULTS: Feeding rabbits a diet high in alpha-tocopherol resulted in significant protection against the development of contractile dysfunction after partial outlet obstruction. The protective effect of alpha-tocopherol was related to significantly decreased malondialdehyde and significantly increased tissue concentrations of alpha-tocopherol. CONCLUSIONS: These data indicate that a major etiology of bladder dysfunction secondary to partial outlet obstruction is related to free radical generation and resultant membrane lipid peroxidation.

Analysis of Variance↗
PubMed2001

The response of fetal sheep bladder tissue to partial outlet obstruction.

PURPOSE: We characterized the response of fetal ovine bladder strips to stimulated contraction and relaxation, and compared this response to that of strips from the pregnant mother and those obtained after a short duration of fetal bladder outlet obstruction. MATERIALS AND METHODS: Sham surgery or bladder obstruction was performed in fetal sheep at 90 days of gestation (term 147 days). Bladder tissue was obtained 3 and 5 days later. Isolated strips of full-thickness bladders from fetuses and pregnant females were mounted individually in Tyrode's solution containing glucose. The strips were subjected to electrical field stimulation. Alternate strips were stimulated by adding carbachol, adenosine triphosphate and KCl. Each strip stimulated by carbachol also underwent field stimulation in the presence of carbachol. Relaxation was also tested using isoproterenol and nitroprusside. RESULTS: The response of isolated strips to field stimulation showed phasic contraction or biphasic response, consisting of initial phasic contraction followed by phasic relaxation and a return to control tension after the end of stimulation. In fetal bladder strips field stimulation at all frequencies after carbachol stimulation produced phasic relaxation or a biphasic response with an initial relaxation phase followed by phasic contraction. This field stimulated relaxant response was not present in adult female bladder strips. In addition, field stimulation stimulated relaxation was completely eliminated by pretreatment with N-nitro-L-arginine-methyl ester, indicating that relaxation was nitric oxide mediated. The fetal responses to all forms of stimulation and relaxation were significantly greater than those of pregnant females. After 5 days or greater of obstruction the responses to field stimulation were reduced significantly. In contrast, there were no significant differences in contractile responses to adenosine triphosphate, carbachol or KCl, or the relaxant response to field stimulation after obstruction. However, there was a significant reduction in relaxant responses to isoproterenol and nitroprusside. CONCLUSIONS: In mid gestation sheep fetus contractile responses to field stimulation, adenosine triphosphate, carbachol and isoproterenol are well developed. The fetal ovine bladder shows a strong neuronal nitric oxide response that is not present in the pregnant mother and is maintained after short-term obstruction.

Animals↗
PubMed2000

Absorption of oxybutynin from vaginal inserts: drug blood levels and the response of the rabbit bladder.

OBJECTIVES: Oxybutynin has been used for treatment of urge urinary incontinence for more than 20 years. However, one of the major problems with its use is uncomfortable anticholinergic side effects that can lead to discontinuation of treatment. Alternative forms of drug administration may reduce side effects and thus improve patient compliance. METHODS: A cylinder-shaped, curved silicone elastomer insert containing oxybutynin was anchored in the vagina of female rabbits. The inserts were designed to release oxybutynin at rates of 0.5, 1.0, and 5.0 mg/day, respectively. Blood drug and metabolite levels were monitored for 1 to 7 days and cystometry was carried out after 7 days of treatment. RESULTS: There was a consistent dose-dependent absorption of the oxybutynin resulting in stable plasma concentrations by 3 days. Levels of N-desethyloxybutynin, the active metabolite that is thought to be responsible for side effects, were less than 1.0 ng/mL in all groups. The cystometrograms showed a decrease in the detrusor pressures for the higher oxybutynin groups and a dose-dependent decrease in micturition pressure. The vaginal wall in contact with the insert showed no irritation. CONCLUSIONS: The inserts produced stable blood levels and released sufficient amounts of oxybutynin to have measurable effects on the bladder. There was no irritating effect of the insert on the vaginal wall after a 1-week treatment. Vaginal inserts containing oxybutynin may be an interesting alternative method for the chronic delivery of oxybutynin.

Absorption↗
PubMed2000

Acute increase in blood flow to the rat bladder subsequent to partial bladder outlet obstruction.

Partial obstruction of the rat bladder outlet initiates a multi-step process during which the bladder progressively loses its functional ability. The first step in this progression is bladder hypertrophy; the organ dramatically increases in size and weight to compensate for the effects of obstruction. Unoperated female rats, age-matched, sham-obstructed rats, and rats that received a partial bladder outlet obstruction were studied. During the first 24 hours after partial bladder outlet obstruction, relative bladder blood flow was measured using a fluorescent microsphere infusion technique and laser Doppler imaging. Nitric oxide synthase (NOS) activities of control and obstructed rat bladder tissues were determined using an enzymatic assay that measures the conversion of (3)H-L-arginine to (3)H-L-citrulline. Using the microsphere infusion technique, a significant increase in blood flow to the obstructed rat bladder was observed during the first 24 hours after partial bladder outlet obstruction. Relative bladder blood flow increased approximately sixfold at 4 and 6 hours post-obstruction and remained elevated through 24 hours of obstruction. Sham operations (evaluated after 6 hours after surgery) resulted in a minor increase in blood flow that did not reach statistical significance. Relative blood flow to the spleen, measured in the same rats, was not significantly changed. Laser Doppler measurements also identified a significant increase in rat bladder blood flow after outlet obstruction and showed that increased blood flow could be detected as early as 1 hour post-obstruction. Interestingly, despite the significant differences in bladder blood flow between control and early post-obstructed rat bladders, NOS activities of control and obstructed rat bladders were comparable. The increase in bladder blood flow precedes the urothelial, fibroblast and smooth muscle cell hyperplasia, and the smooth muscle hypertrophy that occurs after obstruction. We propose that, in response to surgical induction of partial outlet obstruction, acute up-regulation of bladder blood flow may be an initiating factor for subsequent bladder cell proliferation and smooth muscle hypertrophy. Neurourol. Urodynam. 19:195-208, 2000.

Animals↗