Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied 9 patients with clinical evidence of spinal cord ischemia or infarction who had altered vesicourethral function. Of the patients 6 had some preservation of bladder and lower extremity sensation, a clinical pattern consistent with the anterior spinal artery syndrome. A total of 3 patients had a clinical picture more consistent with complete transverse myelopathy, since they had no preservation of bladder or lower extremity sensation. Despite sensory levels well above the sacral spinal cord segments, 6 patients had detrusor areflexia (4 with bethanechol supersensitivity and 4 with neuropathic changes in the perineal electromyograph) indicating longitudinal spinal cord involvement. Three patients had detrusor hyperreflexia with vesicosphincter dyssynergia, indicating some preservation of the sacral spinal cord. In 6 patients appreciation of pinprick in the lower extremities was absent or decreased but light touch or position sense was preserved. Bladder sensation was dissociated in 4 of these 6 patients, since they had perception of bladder distention but loss of urge to void. These findings indicate that bladder distention is a sensory modality probably mediated via the posterior spinal cord, while the sense of urgency is probably conveyed by the anterior spinal cord.
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PMID:Effect of spinal cord ischemia on vesicourethral function. 140 39

Since 1978, six boys with prostatic rhabdomyosarcoma have been treated at our institution. Three had localized disease and were managed by initial biopsy, vincristine, actinomycin-D, and cyclophosphamide (VAC) chemotherapy, and bladder-sparing surgery with or without irradiation. Further combination chemotherapy ("pulse" VAC, Adriamycin, VP-16, cisplatin, and ifosfamide) was continued for 20 to 22 months following the induction course. Two boys had microscopic residual disease undetected by frozen section and unresponsive to radiotherapy. Subsequent total cystectomy 4 and 7 months later resulted in eradication of disease. In one patient, preservation of the bladder was achieved at the age of 3 months for 8 years. Artificial sphincter inserted to cure his urinary incontinence failed because of ischemia secondary to cuff compression and scar tissue. He is alive today with a modified Koch pouch urinary diversion. Of the 50% who had metastatic disease at presentation, two were dead within 12 months despite aggressive chemotherapy and irradiation. The third is currently on treatment. Although chemotherapy has markedly improved the prognosis, surgery is still necessary in most cases for cure. Bladder salvage is a desirable goal; however, residual microscopic disease, difficulty with frozen-section disease detection, and poor tissue vascularization for subsequent sphincter replacement remain significant obstacles.
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PMID:Rhabdomyosarcoma of the prostate in childhood: current challenges. 280 70

Ischemia of vital organs causes various degrees of impairment. We studied the in vitro effects of ischemia on the function of the rat bladder. Ischemia was induced by ligation of the bilateral (bilateral ischemia) or right (unilateral ischemia) internal iliac arteries. Bladder weight increased significantly following 1 week of bilateral and unilateral ischemia. Passive tension was significantly higher in ischemic bladders than in control bladders at an increase in length between 6 and 12 mm. In both control and ischemic bladders, active tension was highest at a 16-mm increase in length. Bladders subjected to unilateral or bilateral ischemia for 1 or 2 weeks demonstrated impaired contractile responses to field stimulation, bethanechol, ATP and KCl. There were no differences in contractile strength between muscle specimens obtained from the ipsilateral or contralateral sides of unilateral ischemic bladders. Our findings showed that unilateral and bilateral ischemia inhibited the in vitro contractile strength of the detrusor muscle in response to intramural and pharmacologic stimulation.
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PMID:Effects of Ischemia on the function of the isolated rat detrusor muscle. 871 84

Ischemia induced by atherosclerosis is a common cause of organ failure in the elderly. We investigated the effects of in vivo ischemia created by ligation of the internal iliac arteries on the parameters of in vivo infusion cystometry under urethane anesthesia and on in vitro whole bladder contractility of the rat. Bladder weight significantly increased after ischemia for 14 days. Infusion cystometry demonstrated that in the ischemic bladders the capacity increased, the voiding pressure decreased, and the volume of residual urine increased, which resulted in deteriorated voiding efficacy. The in vitro whole bladder contractility to field stimulation, bethanechol, ATP, and KCl was reduced by ischemia. The passive pressure increased as the bladder volume enlarged and the bladder compliance once decreased by ischemia on the 7th day, but increased on the 14th day. In an active volume-pressure relationship study the peak response was decreased by ischemia. The volume at which response reached a peak value shifted to a larger volume 14 days after surgery. In conclusion, ischemia impaired in vivo rat detrusor power to empty. Since detrusor contractility in vitro decreased in response to various kinds of stimulation, this deteriorated bladder function was supposed to be caused by muscle degeneration.
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PMID:Effects of in vivo Ischemia on the infusion cystometry and in vitro whole bladder contractility of the rat. 871 85

We investigated the effects of ischemia induced by ligation of the bilateral internal iliac arteries following partial outlet obstruction on changes in detrusor function in rat. Rats were divided into three groups: sham-operated control rats, rats with partial outlet obstruction, and rats with obstruction+ischemia. Bladder function was studied by the in vitro organ bath technique 7 days after surgery. The weight of the bladder was significantly increased in both the obstruction and obstruction+ischemia groups. The obstruction+ischemia group exhibited a greater increase in weight. The passive length-tension relationship of detrusor muscle strips showed that tissue elasticity was decreased and the active length-tension relationship demonstrated that the peak response was observed at a shorter tissue length in the obstruction+ischemia group compared with the other two groups. There was no difference in the passive and active length-tension relationships between the control group and the obstruction group. The contractile response to various kinds of stimulation (field stimulation, bethanechol, ATP, and KCl) increased in the obstruction group and decreased in the obstruction+ischemia group. These findings suggest that partial outflow obstruction alone increased bladder contractility in response to stimuli. However, ischemia reduced the contractility and elasticity of the bladder wall.
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PMID:Effect of ischemia and partial outflow obstruction on rat bladder function. 922 74

Ischaemia induced by atherosclerosis is a common cause of disorders in the elderly, including impairment of bladder function. To evaluate experimentally the effects of ischaemia on detrusor function, we performed infusion cystometry and evaluated the morphologic findings in the bladder of the rat. Blood flow to the bladder of the rat was evaluated with a Doppler flowmeter before and after the unilateral or bilateral ligation of the internal iliac arteries. Reevaluation was done at one and two weeks after surgery. Bladder function was studied by infusion cystometry performed in vivo under urethane anaesthesia. Finally, histological examination was performed. Blood flow at mid-dorsal wall of the control bladder was inversely related to intravesical volume. Unilateral or bilateral ligation of the internal iliac arteries decreased blood flow to the bladder, which showed a complete recovery two weeks postoperatively. Infusion cystometry of the ischaemic bladder with bilateral ligation of the internal iliac arteries demonstrated a decrease in voiding pressure, an increase in bladder capacity, and an increase in pressure at which micturition was initiated vs. the control. The bladder with unilateral ligation of the artery showed a decrease in voiding pressure, with no change in the other parameters. Histological examination indicated that the bilateral ischaemia and ischaemic side of unilateral ischaemia led to a degeneration of the mucosa, and severe oedema in submucosal and muscle layers one week postoperatively. Degeneration of smooth muscle was predominant at 2 weeks. Contralateral side of the unilaterally ischaemic bladder showed oedema and congestion of the submucosa and smooth muscle. Ligation of the internal iliac artery decreased blood flow to the bladder significantly, which resulted in smooth muscle degeneration. Consequently, in vivo voiding pressure was impaired in the ischaemic bladder.
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PMID:Effects of ligation of the internal iliac artery on blood flow to the bladder and detrusor function in rat. 969 34

Ischemia, induced by atherosclerosis, is a common cause of disorders in the elderly. Bladder dysfunction in older people may be caused by detrusor ischemia. We compared blood flow to the bladder and detrusor function in vivo and in vitro in young (6-month-old) and aged (24-month-old) male Sprague-Dawley rats. In both young and old rats, blood flow to the bladder measured by a laser Doppler flowmeter decreased as intravesical volume increased and was smaller in old rats than in young rats. Cystometrograms performed under anesthesia showed that old rats had smaller voiding pressure and larger bladder capacity than young rats. In isolated bladders, the pressure increase in response to bethanechol and low frequency field stimulation were impaired by aging. Volume-pressure studies showed that in isolated bladders of old rats compliance was greater and peak response to field stimulation was observed at a larger capacity. These findings indicate that bladders of older rats have a larger capacity with good compliance, but less contractility. Aging changes correlate with a decrease in blood flow to the bladder.
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PMID:Effect of ageing on blood flow to the bladder and bladder function. 1046 Nov 10

We attempted in the present study to clarify the preventive effects of cyclohexenonic long-chain fatty alcohol on ischemia-reperfusion injury in the rat bladder. Rat bladders were exposed to 30 min of ischemia and a subsequent 30 min of reperfusion with or without several doses of cyclohexenonic long-chain fatty alcohol (0.5, 2, 8 mg/kg). Muscle-bath studies were performed, and malonaldehyde concentrations were measured in the bladder. Bladder dysfunction and lipid peroxidation caused by ischemia-reperfusion were prevented by cyclohexenonic long-chain fatty alcohol in a dose-dependent manner. Our data indicate that cyclohexenonic long-chain fatty alcohol can prevent the production of free radicals and ischemia-reperfusion injury in the bladder.
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PMID:Preventive effect of long-chain fatty alcohol on ischemia--reperfusion injury in the rat bladder. 1240 8

Reactive oxygen metabolites play important roles in ischemia/reperfusion (I/R) injury in several systems. The aim of this study was to investigate the role of melatonin against I/R injury of the rat urinary bladder. The abdominal aorta was clamped to induce ischemia for 30 min, then the animals were subjected to 60 min of reperfusion. Melatonin (10 mg/kg, i.p.) or the vehicle (control 1% alcohol i.p.) was administered before I/R. After decapitation, the bladder was removed and the tissue was either used for functional studies or stored for measurement of products of lipid peroxidation (LP), glutathione (GSH) levels and myeloperoxidase activity (MPO). Bladder strips were suspended in oxygenated Tyrode's buffer at 37 degrees C and isometric contractions to carbachol (CCh; 10(-8)-10(-4) m) were recorded. In the I/R group, the contractile responses of the bladder strips were lower than those of the control group (P < 0.01-0.001) and were reversed by treatment with melatonin (P < 0.05-0.001). LP which was higher in I/R group compared with control (27.68 +/- 1.69 and 10.59 +/- 1.27 nmol/g, respectively; P < 0.001) was partially reversed by melatonin (19.01 +/- 1.85 nmol/g; P < 0.01). Similarly, GSH showed a decrease in the I/R group compared with controls (0.27 +/- 0.03 and 0.43 +/- 0.04 micromol/g, respectively; P < 0.05) and melatonin prevented this effect completely (0.45 +/- 0.04 micromol/g; P < 0.05). MPO activity in the I/R group (4.19 +/- 0.08 U/g) was significantly higher than that of the control group (1.41 +/- 0.08 U/g; P < 0.001) and melatonin treatment reduced MPO levels compared with I/R alone (3.16 +/- 0.07; P < 0.001). Melatonin almost completely reversed the low contractile responses of rat urinary bladder strips to CCh and prevented oxidative tissue damage following I/R.
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PMID:Melatonin treatment protects against ischemia/reperfusion-induced functional and biochemical changes in rat urinary bladder. 1261 83

Partial bladder outlet obstruction (PBOO) results in cellular damage due to ischemia and reperfusion injury. Our study seeks to establish how early this damage can occur and the role that nitric oxide may play in its pathophysiology. Surgical PBOO (1, 3, and 7 days) were performed on male New Zealand White rabbits. Half of the animals were premedicated for 3 days with N(G)-nitro-l-arginine methyl ester(l-NAME), an inhibitor of nitric oxide synthase before obstruction. Bladder weight increased with duration of PBOO but was significantly lower at 3 and 7 days in animals treated with l-NAME compared with their untreated counterparts. Contractile function decreased progressively with PBOO duration. At 1 day postobstruction, bladder contractility was significantly lower in the l-NAME rabbits than in the untreated rabbits. At 3 and 7 days, contractility of the l-NAME bladders was equal or higher than the untreated bladders. The level of hypoxia at 1 day after obstruction was significantly higher in the l-NAME-treated animals than in the untreated controls but equal at 3 and 7 days obstruction. Increased nitrotyrosine was seen by Western blot in all obstructed animals. However, the amount was significantly less in the l-NAME-treated animals at 3 and especially at 7 days. Nerve density decreased progressively after obstruction; however, it decreased to a significantly lesser degree in the l-NAME-treated bladders than in the untreated groups. These results suggest that l-NAME pretreatment enhanced ischemic damage at 1 day after obstruction but protected the bladder from nitric oxide-generated free radical damage at the later time periods by inhibiting the generation of nitrotyrosine.
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PMID:L-NAME, a nitric oxide synthase inhibitor, diminishes oxidative damage in urinary bladder partial outlet obstruction. 1617 66


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