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At least 307 records · Page 17Linked to original sources
PubMed2006

Epinephrine promotes hemostasis in rats with cyclophosphamide-induced hemorrhagic cystitis.

OBJECTIVES: To evaluate the hypothesis that intravesical instillation of epinephrine would attenuate bladder hemorrhage in a rat model of cyclophosphamide (CYP)-induced hemorrhagic cystitis. METHODS: Female Sprague-Dawley rats were divided into seven treatment groups: positive control (CYP, 150 mg/kg), negative control (epinephrine, 10 microg/mL), intravesical instillation of normal saline (vehicle) and epinephrine (2.5, 5, and 10 microg/mL), and intraperitoneal administration of mesna (50 mg/kg). Rats were killed on days 1, 2, and 3, and the urinary bladders were removed, weighed, and evaluated by gross and histologic analysis. Vesical vascular permeability was determined by wet bladder weight and Evan's blue dye absorbance. RESULTS: Cyclophosphamide administration induced severe hemorrhagic cystitis with marked edema, hemorrhage, and inflammation. All three epinephrine-treated groups had marked attenuation of hemorrhagic cystitis compared with the positive and negative control and mesna-treated groups. Epinephrine was also associated with significant inhibition of tissue edema, indicating decreased vesical vascular permeability. CONCLUSIONS: In this rat model of CYP-induced hemorrhagic cystitis, intravesical instillation of epinephrine inhibited edema, hemorrhage, and inflammation.

Administration, Intravesical↗
PubMedDate not supplied

The importance of re-evaluation in patients with cystitis glandularis associated with pelvic lipomatosis: a case report.

Pelvic lipomatosis is a rare, proliferative disease involving an overgrowth of normal fat in the pelvic retroperitoneal space. Cystitis glandularis, cystitis cystica, or cystitis follicularis can be observed in 75% of patients with pelvic lipomatosis. We describe a 58-yr-old man with pelvic lipomatosis in whom adenocarcinoma of the bladder was diagnosed in the second transurethral resection of the bladder 1 month after the first operation. This proliferative disease can cause obstruction of the bladder drainage leading to a proliferative cystitis because of an altered environment rich in protein fluid. Because the association of this proliferative disease with adenocarcinoma of the bladder is frequent, we recommend close follow-up of these patients to detect the associated adenocarcinoma of the bladder.

Adenocarcinoma↗
PubMed2000

Neurokinin-1 (NK-1) receptor is required in antigen-induced cystitis.

Interstitial cystitis (IC) is a debilitating disease that has been adversely affecting the quality of women's lives for many years. The trigger in IC is not entirely known, and a role for the sensory nerves in its pathogenesis has been suggested. In addition to inflammation, increased mast cell numbers in the detrusor muscle have been reported in a subset of IC patients. Experimentally, several lines of evidence support a central role for substance P and neurokinin-1 (NK-1) receptors in cystitis. The availability of mice genetically deficient in neurokinin-1 receptor (NK-1R(-/-)) allows us to directly evaluate the importance of substance P in cystitis. An unexpected finding of this investigation is that NK-1R(-/-) mice present increased numbers of mast cells in the bladder when compared with wild-type control mice. Despite the increase in mast cell numbers, no concomitant inflammation was observed. In addition, bladder instillation of wild-type mice with a sensitizing antigen induces activation of mast cells and an acute inflammatory response characterized by plasma extravasation, edema, and migration of neutrophils. Antigen-sensitized NK-1R(-/-) mice also exhibit bladder mast cell degranulation in response to antigen challenge. However, NK-1R(-/-) mice are protected from inflammation, failing to present bladder inflammatory cell infiltrate or edema in response to antigen challenge. This work presents the first evidence of participation of NK-1 receptors in cystitis and a mandatory participation of these receptors on the chain of events linking mast cell degranulation and inflammation.

Animals↗
PubMed1997

Molecular marker for development of interstitial cystitis in rat model: isoactin gene expression.

PURPOSE: To determine whether the differential expression of bladder smooth muscle isoactin can be used as a molecular marker for the development of interstitial cystitis (IC). METHODS: Three groups of five female Sprague-Dawley rats each underwent urethral catheterization and intravesical instillation of 0.5 ml. of 0.4N HCl. One group was sacrificed one, two and four weeks after the application of HCl, and their bladders harvested for histologic examination and evaluation using Northern blot analysis of bladder smooth muscle isoactins. Five control animals were sacrificed and their bladders harvested to establish isoactin gene expression of bladder smooth muscle in the normal state. The bladders of the rats in each group were excised, immediately frozen in liquid nitrogen, pooled, then stored -70 degrees C until needed for RNA isolation. Isoactin cDNA probes have been developed, therefore isoactin specific cDNA insert fragments were isolated and insert DNA was purified by gel electrophoresis. Total cellular RNA was isolated from 1.0 gm. of bladder smooth muscle from each group. After spectrophotometric quantification, Northern Blot analysis was performed using 2% agarose-formaldehyde gels and Biotrans nylon membranes. Two complete Northern Blot series were run on a single gel and blotted to a single membrane to eliminate gel and blotting discrepancies. RESULTS: Microscopic histologic analysis revealed detrusor mastocystosis and eosinophilia as has been noted in humans with chronic interstitial cystitis. Two weeks after the intravesical application of hydrochloric acid, the relative expression of gamma-smooth muscle isoactin was noted to increase by 1.7-fold, while alpha-smooth muscle isoactin expression increased by a factor of 9. These effects were seen to stabilize four weeks after acid application. CONCLUSIONS: The intravesical application of dilute HCl in rats results in a histologic appearance which mimics that seen in humans with interstitial cystitis. The appearance of detrusor mastocytosis and eosinophilia was accompanied by a relative decrease in the expression of gamma- and a relative increase in alpha-smooth muscle isoactin gene expression. This pattern of smooth muscle isoactin expression is consistent with a more immature and possibly synthetic smooth muscle phenotype, which may be responsible for the clinical presentation of those with IC. Northern blot analysis of bladder smooth muscle cells may serve as an effective marker for the development of interstitial cystitis in humans.

Actins↗
PubMed1995

Fluorescein angiography of the bladder: technique and relevance to bladder cancer and interstitial cystitis patients.

PURPOSE: Fluorescein angiography has been used in the study of bleeding vessels, neovascularity, tumors and ischemic tissues in a variety of disorders. This pilot study was designed to evaluate the feasibility, safety and relevance of this interesting technology for the evaluation of bladder wall vessels in patients with interstitial cystitis and bladder cancer. MATERIALS AND METHODS: Five patients with National Institutes of Health defined interstitial cystitis symptoms and 10 with bladder cancer were studied during cytoscopy while they were under general anesthesia. A yellow-green barrier filter (520 nm.) was placed over the cystoscope eyepiece and a blue exciter filter (465 nm.) was attached to the light source. Patients received a 5 ml. bolus of 10% fluorescein intravenously. RESULTS: After hydrodistension, glomerulations in interstitial cystitis patients were more prominent with fluorescein angiography and occurred in the venule phase. Areas of papillary transitional cell tumor and carcinoma in situ developed a brilliant yellow-green fluorescence. Adjacent normal urothelium was nonfluorescent and provided a contrasting dark background facilitating the detection of all lesions. No allergic reaction or other adverse effect related to the fluorescein injection was observed. CONCLUSIONS: These unique observations in a limited number of patients suggest that fluorescein angiography of the bladder is a safe and simple procedure. This preliminary report underscores the relevance of fluorescein angiography in the detection of bladder tumor and offers a new approach to the evaluation of bladder wall vessels in interstitial cystitis patients.

Arterioles↗
PubMed2003

Coping strategies in patients with interstitial cystitis: relationships with quality of life and depression.

PURPOSE: Previous research has demonstrated that interstitial cystitis patients experience depressive symptoms and decrements to quality of life. However, to our knowledge the extent to which patients may be able to influence quality of life and depressive symptoms through coping strategies has not been investigated in this population. In a number of other chronic conditions specific coping strategies have been associated with the degree of impairment beyond disease severity. Therefore, the association of coping strategies with depressive symptoms, quality of life and self-reports of pain was assessed in patients with interstitial cystitis. MATERIALS AND METHODS: A total of 64 females with interstitial cystitis were recruited from a urology clinic at a tertiary medical center. Questionnaires assessing depression, quality of life, coping and symptom severity were completed and returned at a clinic appointment. Depression was also measured through a standardized semi-structured interview (Hamilton Rating Scale for Depression). All analyses controlled for age. RESULTS: Patients coping by greater catastrophizing reported greater impairments in various domains, including depressive symptoms, general mental health, social functioning, vitality and pain. Greater venting was associated with greater depressive symptoms and poorer mental health. Seeking instrumental social support was associated with fewer depressive symptoms. CONCLUSIONS: These findings suggest that maladaptive coping strategies are associated with higher levels of depressive symptoms and quality of life decrements in patients with this condition. Psychosocial interventions aimed at increasing adaptive coping may positively impact the female experience with interstitial cystitis.

Adaptation, Psychological↗
PubMed1994

Activation of urinary kallikrein in patients with interstitial cystitis.

A potential pathophysiological role for the urinary kallikrein-kinin system is suggested by the prominent symptoms of bladder pain and urinary frequency in interstitial cystitis. Kallikrein activity in the urine of 84 patients with interstitial cystitis and 33 normal volunteers was determined by cleavage of the synthetic substrate Val-Leu-Arg-pNA. Interstitial cystitis patients had significantly higher levels of kallikrein activity than did the normal volunteers. Kallikrein activity was correlated with symptoms of bladder pain and voiding frequency. The percentage of total urinary kallikrein in the active form correlated with active kallikrein levels and was also increased in interstitial cystitis patients, particularly those with higher levels of pain. Patients who underwent hydrodistention and subsequently experienced relief from the bladder symptoms had a decrease in urinary kallikrein levels, whereas patients who failed to improve following hydrodistention did not.

Adult↗
PubMed1994

The in vitro cytotoxicity of urine from patients with interstitial cystitis.

Urine from patients with interstitial cystitis has been reported to be more cytotoxic than urine from healthy subjects when tested in vitro against cells from a normal urothelial cell line. The purpose of the present study was to develop a method to measure urinary cytotoxicity and so make it possible to estimate the toxicity of urine from interstitial cystitis patients. The study included 10 women with interstitial cystitis and 10 healthy controls. Urine specimens were obtained from both groups and urine cytotoxicity was measured by a modified 51Cr-release assay: A range of urine dilutions was added to suspensions of target cells with intracellular bound 51Cr, and cellular death was recorded by measuring the 51Cr-release from the target cells. The transitional cell bladder cell lines T24 and Hu609 and the erythroleukemia K562 cell line were used as target cells. There was no difference in urine cytotoxicity between interstitial cystitis patients and healthy controls. Urine cytotoxicity was increased by dilution in both groups.

Adult↗
PubMed1993

Urinary glycosaminoglycan excretion as a laboratory marker in the diagnosis of interstitial cystitis.

Urinary macromolecular uronate and glycosaminoglycan uronate concentrations were determined in 209 urine specimens obtained from 192 interstitial cystitis patients, 47 asymptomatic normal individuals and 32 spinal cord injury patients. As a group the concentration of macromolecular uronate or glycosaminoglycan uronate was significantly less in the interstitial cystitis patients than in the normal controls. Some interstitial cystitis patients showed low values of macromolecular uronate and glycosaminoglycan uronate. Analysis of the population distributions suggested that macromolecular uronate may have significant value in diagnosis of interstitial cystitis.

Adult↗
PubMed1993

Hyperbaric oxygen treatment for experimental cyclophosphamide-induced hemorrhagic cystitis.

Acrolein is a toxic metabolite of cyclophosphamide that causes hemorrhagic cystitis in 2 to 40% of treated patients. Hyperbaric oxygen (HBO) is used to treat poorly healing wounds in conditions such as Fournier's gangrene and radiation-induced cystitis. The present study was designed to evaluate the effects of HBO on acute acrolein-induced hemorrhagic cystitis in a rat model. Rats were divided into 4 groups. Group I served as a control and received only HBO prior to sacrifice. Group II received acrolein only, while groups III and IV received acrolein as well as HBO therapy. Hyperbaric oxygen (100% oxygen, 2.8 atmospheres, 90 minutes) was delivered twice a day for 4 days, with group III receiving a fifth HBO treatment just before acrolein and group IV receiving the fifth HBO treatment just after acrolein. After therapy, the amount of urothelial injury was determined morphometrically. Group II untreated rat bladders had only 33% of the urothelium intact after acrolein injury, whereas groups III and IV rat bladders had 93% (p < 0.01) and 55% (p < 0.01) intact urothelium, respectively, after treatment with HBO. The timing of the HBO treatment appeared to be a critical factor, with less injury occurring if the fifth HBO treatment immediately preceded acrolein. These results suggest that HBO may be useful as prophylaxis and treatment of cyclophosphamide-induced hemorrhagic cystitis.

Acrolein↗
PubMed1992

Emphysematous cystitis: a review of the spectrum of disease.

Emphysematous cystitis is an uncommon condition in which pockets of gas are formed in and around the bladder wall by gas-forming organisms. Persons with diabetes, neurogenic bladder and chronic urinary infection are predisposed to the disease. Severity of illness ranges from an asymptomatic condition to life-threatening cystitis. We present 2 cases of emphysematous cystitis. One case was an incidental finding on evaluation of abdominal discomfort with resolution upon removal of predisposing factors. The other patient presented with an acute abdomen that progressed to severe necrotizing cystitis ultimately requiring cystectomy. The initial involvement of the urologist as a consultant is emphasized. A complete review of the literature describes the incidence, various presentations, associated diseases and organisms, pathogenesis, and available methods for diagnosis and treatment reported for this disease. Successful management depends on early diagnosis with correction of underlying causes, administration of appropriate antibiotics, establishment of adequate bladder drainage and surgical excision of involved tissue when required. Early detection and prompt treatment are encouraged.

Cystitis↗
PubMed1992

Lymphocyte function in patients with interstitial cystitis.

To determine whether there is a primary immunological disorder involved in the etiology of interstitial cystitis, we compared the in vitro function of peripheral blood lymphocytes from 10 patients with interstitial cystitis to those from 10 healthy female controls. The lymphocytes were isolated and incubated in either cell culture medium alone, cell culture medium supplemented with the mitogen phytohemagglutinin or cell culture medium with autologous sterile filtered urine, the latter to detect any immunogenic potential of urine in this disease. We studied the relative proliferation of the phenotypes CD2, CD4, CD8, CD19, CD14 and CD56 by immunofluorescence and flow cytometry. To detect activation of T lymphocytes we also studied expression of HLA-Dr and interleukin-2 receptors. There was no difference in the rate of proliferation of the various lymphocyte phenotypes between the 2 groups in any of the culture media. Similarly, there was no difference between the 2 groups in the degree of lymphocytic activation after incubation. Furthermore, incubation in the presence of autologous urine caused no increase in activation above that seen in control cultures. We also assessed the production of the lymphokines interleukin-1, interleukin-2 and interferon-gamma in the supernatant fluid of the cell cultures. There was no difference in the production of these immunoregulatory cytokines between the control and patient groups, and again urine did not act as a mitogen in either group. We conclude from this study that there is no primary immunological disorder evident in patients with interstitial cystitis, and that the urine does not act as a stimulant to the immune system. This finding casts severe doubt on any theory suggesting that interstitial cystitis is an autoimmune disease or that urine contains an autoantigen causing the disease.

Adult↗
PubMed1992

Urinary neutrophil chemotactic factors in interstitial cystitis patients and a rabbit model of bladder inflammation.

The present study investigates a possible source of inflammatory mediators involved in the pathogenesis of bladder inflammation characteristics of interstitial cystitis disease. Our tested hypothesis is that in response to injury, tissues of the urinary bladder participate in the initiation of bladder inflammation by releasing inflammatory mediators such as neutrophil chemotactic factors. Bladders of anesthetized rabbits (n = 7) were instilled with an acidic solution (pH 4.5) for 15 minutes, then washed with saline and instilled with sterile phosphate buffered saline (PBS) (pH 7.2) for an additional 45 minutes prior to sacrificing the rabbits. Control rabbits (n = 7) were instilled with sterile PBS (pH 7.2) for 15 minutes, then 45 minutes. The levels of neutrophil chemotactic factors were measured using modified Boyden chambers and rabbit peritoneal neutrophils as indicator cells. Results indicated the release of high levels of neutrophil chemotactic factors (via a checkerboard analysis) from acid-treated bladders after 15 minutes (70 +/- 4% of standard) and 45 minutes (80 +/- 7%). Electron microscopy analysis of these acid-treated bladders revealed the infiltration of a large number of neutrophils, which correlates with the recovery of neutrophil chemotactic factors. Control rabbits, on the other hand, showed low levels of chemotactic activity (less than 10 percent) and exhibited normal bladder morphology with absence of neutrophils. The glycosaminoglycan (GAG) layer was intact in both acid-treated and control bladders. High levels of neutrophil chemotactic factors were also detected in urine samples from eleven patients with interstitial cystitis (113 +/- 25%) (not due to interleukin-1 or leukotriene B4) which were not detected in urine samples from healthy volunteers (n = 9) or from thirteen control patients with bladder diseases other than interstitial cystitis. These preliminary studies indicate the capability of injured bladder tissues to release neutrophil chemotactic factors which contribute to the initiation of bladder inflammation. The presence of neutrophil chemotactic factors in urine samples of interstitial cystitis patients suggests a possible role of these mediators in the pathogenesis of the disease.

Animals↗
PubMed1991

Tamm-Horsfall autoantibodies in interstitial cystitis.

Interstitial cystitis presents a diagnostic and therapeutic challenge. Although many etiologies, including autoimmunity, have been proposed its pathogenesis remains obscure. Tamm-Horsfall protein has been identified in the superficial urothelium of patients with interstitial cystitis demonstrating abnormal urothelial permeability. Eight patients with a clinical diagnosis of interstitial cystitis underwent cystoscopy and bladder biopsy. Characteristic cystoscopic findings were present, and each patient had chronic inflammation and mast cells by histopathological analysis. Preoperative anti-Tamm-Horsfall protein serum antibody (IgG) titers were determined by enzyme-linked immunosorbent assay (range 500 to 8,000, mean 2,750). A control group of 8 patients with a negative urological history also had titers of 0 to 500 (p = 0.02). The humoral response to Tamm-Horsfall protein in these patients suggests a role for Tamm-Horsfall protein in interstitial cystitis. Measurement of serum Tamm-Horsfall protein antibody may prove to be useful as a noninvasive diagnostic test in patients with this disease.

Adult↗
PubMed1991

Pelvic lipomatosis associated with cystitis glandularis and adenocarcinoma of the bladder.

Pelvic lipomatosis is a rare condition characterized by an overgrowth of normal fat in the perivesical and perirectal spaces. Cystitis glandularis, cystica or follicularis has been observed in 75% of the patients with pelvic lipomatosis. Although cystitis glandularis is widely regarded as premalignant few reports have documented its transition to adenocarcinoma. We describe a 41-year-old man with pelvic lipomatosis in whom primary adenocarcinoma of the bladder developed 6 years after a histological diagnosis of cystitis cystica and glandularis was established. To our knowledge this is the second case reported of pelvic lipomatosis associated with proliferative cystitis and adenocarcinoma of the bladder, indicating that intestinal metaplasia of the urothelium may be a precursor of malignancy in these patients.

Adenocarcinoma↗
PubMed1990

Decreased urinary uronic acid levels in individuals with interstitial cystitis.

The pathogenesis of interstitial cystitis currently is unknown. A possible etiology is that the transitional epithelium is defective, leading to molecular leaks that initiate the disease complex. An important surface defense mechanism is the glycosaminoglycans or polysaccharides that line the bladder epithelium and act as a nonspecific antiadherence factor blocking access of bacteria, microcrystals, proteins and ions to the underlying transitional cells. We examined the excretion of urinary macromolecular uronic acid and glycosaminoglycans in normal individuals and those with interstitial cystitis. A total of 37 controls had a mean macromolecular uronic acid level of 56 nmol. per mg. creatinine, compared to 40.2 nmol. per mg. creatinine in 43 patients with active disease (differences were significant, p equals 0.03). The median excretions of glycosaminoglycan uronate for controls and patients were 15.1 and 11.1 nmol. per mg. creatinine, respectively. (There was an over-all tendency to decrease excretion in patients with a p value of 0.06.) Specimens obtained at cystoscopy from patients with active interstitial cystitis had ureteral macromolecular uronic acid levels of 40.5 nmol. uronate per mg. creatinine compared to 43.6 nmol. uronate per mg. creatinine from the bladder. Interstitial cystitis patients had 16.0 nmol. glycosaminoglycan uronate per mg. creatinine compared to 14.6 nmol. per mg. creatinine in normal controls. Neither of these differences was statistically significant. It would appear that there is a tendency to lower macromolecular uronic acid and polysaccharide excretion in individuals afflicted with this syndrome.

Creatinine↗
PubMed1987

Increased mast cells of the bladder in suspected cases of interstitial cystitis: a possible disease marker.

Mast cells reportedly have been increased in the detrusor muscle bundles of the bladder in patients with interstitial cystitis. In 30 patients with suspected interstitial cystitis quantification of mast cells within the muscularis and submucosa was done. The results were compared to those obtained from a variety of normal bladder specimens removed surgically (16 specimens) and at autopsy (15), and from bladders with a variety of miscellaneous inflammatory conditions (20). In patients with suspected interstitial cystitis the number of mast cells was increased significantly (p less than 0.001) compared to the 3 control groups. This finding suggests that quantification of mast cells in the muscularis may be a useful marker in the histopathological evaluation of bladder biopsies in patients with suspected interstitial cystitis.

Adult↗
PubMed1986

Electron microscopic investigation of the bladder urothelium and glycocalyx in patients with interstitial cystitis.

The electron microscopic appearance of the bladder urothelium and glycocalyx was investigated in ten patients with well defined interstitial cystitis and compared to the findings in ten control patients with stress incontinence as the only symptom. Ruthenium red, a polycationic dye which binds specifically to cell surface acid polysaccharides, was used to demonstrate the glycocalyx. In cases of interstitial cystitis two types of luminal cell were observed, each possessing a distinct surface glycocalyx. One type of cell possessed numerous plaques of asymmetric unit membrane associated with a relatively thin glycocalyx. The second type of cell was characterised by numerous microvilli and a relatively thick glycocalyx. In control material each type of cell and its associated glycocalyx was identified with similar frequency. Our study concludes that there are no differences in the morphologic appearances of the glycocalyx and of urothelial cells in patients with interstitial cystitis when compared with controls. Hence, the hypothesis that an important pathogenic factor in interstitial cystitis is a defective glycocalyx associated with a permeable urothelium, has not been supported.

Adult↗