Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty percent of our patients who have had colostomy use irrigation to regulate the bowels. This decision is made by the patient himself after careful deliberation. By means of an irrigation set the large intestine is irrigated with approximately 1-1.5 l of water at body temperature. Subsequently there is a stool-free period of 24-28 h and a reduction of flatulence. The duration of irrigation is 45-60 min. Side effects are occasionally pressure sensation and mild convulsive symptoms, but there are no significant complications. Irrigation can begin after complete healing of the stoma, but is absolutely contraindicated in inflammatory intestinal diseases and relatively contraindicated in prolapse, hernia, stenosis, and intestinal damage by radiation.
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PMID:[The value of irrigation]. 257 30

There are two muscular mechanisms of fecal continence. The anal sphincter squeezes the anal canal, thus lengthening it and increasing its resistance. The puborectalis kinks the distal rectum, preventing the transmission of intra-abdominal pressures into the anal canal. Balloon sphincterography simultaneously records the shape of the anal canal and distal rectum and measures the strength of the puborectalis and anal sphincter muscles. This allows the physician to evaluate the function of these important muscles in patients with symptomatic defecation disorders such as constipation, incontinence, and rectal prolapse. A cylindrical balloon is connected by a hose to a fluid reservoir filled with liquid barium. The deflated balloon is placed into the anal canal and inflated by raising the fluid reservoir in increments. Fluoroscopy visualizes the balloon's shape and video records the results. Quantitative sphincterogram measurements in patients with defecation disorders include (the three measurements in each category refer respectively to incontinent patients [N = 87], prolapse patients without incontinence [N = 26], and constipated patients [N = 65]); anorectal angle (degrees + S.D.): 114 + 28, 103 + 18, 95 + 19; anal canal length (mm + S.D.): 33 + 11, 38 + 10, 39 + 10; squeeze pressure (cm H2O + S.D.): 68 + 23, 80 + 16, 91 + 22, and opening pressure (cm H2O + S.D.): 52 + 25, 67 + 22, 81 + 24. The method is useful in identifying specific defects, such as paradoxic puborectalis contractions, that can cause constipation, and injuries to the sphincters that can cause incontinence. In over 280 patients with a wide variety of defecation disorders, sphincterography has yielded information not available by standard manometric techniques. It augments the findings of defecography.
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PMID:Balloon sphincterography. Clinical findings after 200 patients. 336 32

Eleven continent women with severe degrees of uterovaginal prolapse underwent a complete urodynamic evaluation that included passive and dynamic urethral pressure profilometry with and without careful barrier reduction of their prolapse. The aim of barrier placement was to reduce, but not overcorrect, the prolapse and to restrict stress-induced mobility of the viscera posterior and superior to the urethra. Each of the women had very high pressure transmission ratios in each quarter of the urethra (means of 257, 187, 170, and 166% from internal to external quarters) that were significantly reduced with barrier placement (means of 78, 84, 85, and 101%). Eight of 11 subjects had pressure transmission ratios less than 90% in the proximal three-quarters of the urethra with the barrier in place, a finding in nearly all subjects with genuine stress urinary incontinence. Maximum urethral closure pressure on passive urethral pressure profilometry also decreased significantly from a mean of 75 to 45 cm H2O with the barrier in place. We conclude that the stress continence mechanism in women with severe prolapse results from posterior-superior visceral descent with stress, causing mechanical obstruction of the less mobile urethra. The evaluation methods described may be useful in predicting which of these patients may require concurrent urethropexy at the time of prolapse reduction surgery to prevent postoperative stress urinary incontinence.
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PMID:The mechanism of urinary continence in women with severe uterovaginal prolapse: results of barrier studies. 340 46

The diagnosis of myasthenia gravis (MG) can usually be made on the basis of the characteristic clinical history and signs, improvement by the use of anticholinesterase drugs, decremental responses in repetitive nerve stimulations, and assay of anti-acetylcholine receptor (AchR) antibody titers. We, however, have difficulty to make diagnosis of ocular MG patients with mild symptoms because muscular weakness is minimal and ancillary tests are negative. In the present communication, we report clinical usefulness of a hot test to provoke ptosis by warming the eyelid in ocular MG patients with minimal fatigability. Patient 1, a 27-year-old housewife, developed drooping of the right upper eyelid in May 1985. The ptosis was absent in the morning, but became apparent and worsened later. Neurological examination carried out 3 months after the onset revealed mild right ptosis, but fatigability of the levator palpebrae superioris could not be elicited by the provocative procedures such as sustained upward gaze or repeated opening and closing of eyelids. Both Tensilon and cold tests yielded negative responses. Repetitive nerve stimulations produced no decremental responses. Titers of anti-AChR antibody and antistriational antibody were within normal limits. In order to find a possible neuro-muscular blockade, we warmed the right upper eyelid by applying hot water of about 45 degrees C in a vinyl bag for 3 minutes. The hot test worsened the right ptosis and induced mild left ptosis. Tensilon administration reversed the eyelids to the previous position. Patient 2 was a 12-year-old boy with a typical history and clinical signs of ocular MG. His symptoms remitted spontaneously without any medication 3 weeks after the onset.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnostic usefulness of a hot test in patients with mild ocular myasthenia gravis]. 342 58

The reproductive toxicity of a single oral dose/mouse (15-50 mg/kg) of cyclopiazonic acid (CPA) in the early phase of pregnancy (day 2-8) was investigated. Male mice used in this study were untreated. A limited number of pregnant mice were treated with 66 mg/kg ergonovine maleate (po, sc) to compare its effect with that of an equivalent dose of CPA (50 mg/kg). Among control sperm-positive mice treated with po NaHCO3 solution, 97.5% were gravid on necropsy day (pregnancy day 12). A single dose of CPA (15-50 mg/kg, po) given on days 2 to 8, decreased the pregnancy rates significantly. In groups treated with a single dose of CPA on pregnancy day 4 to 8, vaginal hemorrhage was observed 1 to 7 days after treatment, and it usually resulted in termination of pregnancy (abortion). Fetal resorption rates were higher than the control rate only in the groups treated with 30 mg/kg CPA po on day 4 or 8. CPA decreased body weight gains and the weights of uteri with fetuses. The ovary weights were generally not changed. Ergonovine maleate (66 mg/kg, sc, po) had no significant effect on all of the parameters examined. The estrous cycle returned without any delay in sperm-positive mice in which nidation of fertilized eggs had been inhibited by CPA, and also in nonpregnant mice (used for the LD50 determination) surviving near lethal doses of CPA (50-70 mg/kg, po). The oral LD50 value for CPA in nonpregnant mice was 64 +/- 4.4 mg/kg, and the toxicity signs were ptosis, hypokinesia, hypothermia, action tremor, cessation of food and water intake and resulting cachexia. The duration and intensity of these toxic signs were dose dependent.
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PMID:Toxic effects of cyclopiazonic acid in the early phase of pregnancy in mice. 357 73

An acute administration of MCI-2016 at the doses of 30, 100 and 300 mg/kg (p.o.), and 10, 20 and 30 mg/kg (i.p.) produced a slight CNS depression in rats, such as, sedation, ptosis, decrease in motor activity and systemic muscle relaxation. In a direct physical dependence test, rats were fed the MCI-2016-admixed food together with drinking water ad libitum for 24 hours daily for 51-71 days (mean MCI-2016 intake 29.9-210.7 mg/kg/day), on the gradedly increased dosage schedule with a dosage level of 0.25 and 0.5 mg/g food to 4 mg/g food. In a natural withdrawal following administration of MCI-2016, no significant withdrawal signs were observed in any group. In a naloxone-precipitation test the rats that were treated with MCI-2016-admixed food did not show any withdrawal signs. In a substitution test in either morphine or barbital dependent rats, no suppression of withdrawal signs or maintenance of dependence were observed by cross-administration of MCI-2016. In conclusion, MCI-2016 was considered to have no physical dependence potential.
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PMID:[Physical dependence liability test of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (MCI-2016) in rats]. 362 10

Effects of single and repeated administration of reserpine on time-limited drinking of a hypertonic (1.5% w/w) NaCl solution were investigated in rats to assess whether this drug possesses anxiolytic action. Rats adapted to a 23-hr water-deprivation schedule with a free-feeding regimen were allowed a daily 1-hr water rehydration session. In the single-administration experiment, reserpine (0.1, 0.2 and 0.4 mg/kg, IP) was administered to rats at 15 min or 23 hr before a drinking session, where the fluid available was 1.5% NaCl solution. Drug was administered every 7th day. In the repeated-administration experiment, reserpine (0.1 mg/kg/day) was injected daily for 10 days 15 min before each drinking session. The fluid available was water on the first 9 days and NaCl solution on the 10th day. Reserpine suppressed NaCl solution intake when it was singly administered at 15 min before the rehydration, whereas no significant change in the fluid intake occurred when it was administered 23 hr before drinking, even though rats showed ptosis in response to 0.2 and 0.4 mg/kg doses. Tolerance developed to the suppressing effect of repeated administration of reserpine on fluid intake, although ptosis and sedation continued and body weights decreased. Tolerance was almost complete after 11 days. The results suggest that reserpine does not have an anxiolytic effect.
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PMID:Characteristics of reserpine-induced suppression of NaCl solution intake in rats. 368 56

The liver of Syrian hamsters was studied after exposure to dimethylnitrosamine (DMN) in drinking water for, respectively, 8, 12 and 16 weeks. One additional group of animals was offered DMN for 8 weeks, but maintained for further 8 weeks after removal of the compound. The changes consisted of a narrowing portal venopathy, probably arising, initially, from toxic pylephlebitis, being followed by widespread subendothelial prolapse of hepatocytes encroaching upon the lumen of terminal hepatic veins, which generally were free of inflammatory fibrosing lesions. The venous lesions were unrelated to malignant processes in the biliary duct system, which occurred after 16 weeks. Dilatation of sinusoids and small venules was associated with the presence of prolapsed hepatocytes around their openings into involved larger veins. At the end of 12 and 16 weeks of continuous ingestion of DMN, but also where the agent was withdrawn already at 8 weeks, phlebectasis and transitional stages in the formation of teleangiactatic type of peliosis were demonstrated, probably resulting from progressively impeded blood flow due to partial occlusion by prolapsed hepatocytes in terminal veins. The mechanism enabling hepatocytes to penetrate the venous wall was not clarified. There was no indication of invasive malignancy. Hepatocyte prolapse appeared more likely to result from some unknown mechanism of benign infiltration, promoted by regenerative stimulation. This may have been initiated by mild persistent ischemia due to the demonstrated portal venopathy. No endothelial hyperplasia was seen at any stage of the experiments thus eliminating the probability of peliosis being a source of vascular neoplasia, which has previously been described following more prolonged exposure to DMN. Certain parallelisms of the experimental results with hepatic vascular lesions in man subjected to drug therapy are discussed.
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PMID:Venoocclusive disease of the liver and phlebectatic peliosis in the golden hamster exposed to dimethylnitrosamine. 373 74

The decapeptide from the frog Hyla caerulea, caerulein (caerulein diethylammonium hydrate, ceruletide, CER) is chemically closely related to the C-terminal octapeptide of cholecystokinin (CCK-8). Like CCK-8, CER and some of its analogues produce many behavioural effects in mammals: inhibition of intake of food and water; antinociception; sedation; catalepsy; ptosis, antistereotypic, anticonvulsive and tremorolytic effects; inhibition of self-stimulation. Effects of CER in man comprise sedation, satiety, changes in mood, analgesia and antipsychotic effects. A modulation of central dopaminergic functions appears to be one possible mechanism of CER and its analogues. A common denominator for all effects of CER is, at present, not evident.
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PMID:Caerulein and its analogues: neuropharmacological properties. 391 10

Cyclopiazonic acid (CPA) was found to have many pharmacological properties in common with the antipsychotic drugs chlorpromazine and reserpine. Thus, in mice CPA at ip doses of 5-14 mg/kg body weight produced hypokinesia, hypothermia, catalepsy, ptosis, sedation without loss of righting reflex, tremor, gait disturbance, dyspnoea, opisthotonus, atypical convulsion and prolonged barbiturate-induced sleep. The ip LD50 of CPA was found to be 13 +/- 0.05 mg/kg. The tremors induced by near-lethal doses of CPA were associated with voluntary or forced movements (action tremors); they worsened during the days following treatment, but they were weak compared with the exhausting and continuous tremors of the whole body caused by 20 mg tremorine/kg (used for comparison). When death occurred only 24-259 min after administration of CPA (11-14 mg/kg), it was preceded by dypsnoea, cyanosis, opisthotonus and clonic leg movements and tonic extension of hind legs (convulsions). When death was delayed (2-6 days after CPA administration), it was preceded by prostration, ptosis, hypothermia, tremor and cessation of food and water intake resulting in cachexia; convulsions were not seen in this group of mice. CPA did not affect the rate of convulsion or death caused by either maximal electroshock or metrazol administration but it did delay the onset of metrazol-induced seizures. In rabbits, 10 mg CPA/kg body weight initially produced tachycardia, tachypnoea and sedation with an activated electroencephalogram. Of three rabbits given 10 mg CPA/kg one died, and in this rabbit slow delta waves were seen just before and during a brief period with clonic leg movements. In this animal death was accompanied by tonic extension of the hind legs, respiratory arrest and cardiac fibrillation; and epileptiform EEG was not seen at any time. The unexpected EEG activation with sedation in rabbits treated with CPA was similar to the effect of reserpine on EEG.
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PMID:Toxicity and neuropharmacology of cyclopiazonic acid. 404 83


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