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)

A 24-year-old white man had a history of "epilepsy" since the age of eight years. Prolapse of the mitral valve was documented by auscultation and echocardiographic and left ventriculographic studies. At 120 hours after stopping therapy with phenobarbital and diphenylhydantoin (Dilantin) sodium, continuous electrocardiographic monitoring (Holter monitor) revealed episodes of complete atrioventricular block lasting up to 23 seconds. The results of hemodynamic studies were normal. The patients' symptoms were all totally corrected by implantation of an epicardial demand pacemaker. This report raises the possibility that sudden death in association with the mitral valve prolapse syndrome may be due to intermittent severe disturbances in conduction, in addition to ventricular arrhythmias.
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PMID:Intermittent complete atrioventricular block masquerading as epilepsy in the mitral valve prolapse syndrome. 89 Dec 92

In order to evaluate the importance of the contraction of the perineal muscular system in causing the symptomatology following a hemorrhoidal prolapse operation, a drug, dantrolene sodium which has a known myorelaxant action due to a partial inhibition of the release of calcium ions from the sarcoplasmic reticulum in the muscular cell was used. The double-blind study involved 40 patients, of whom 20 were treated with sodium dantrolene in doses of 25 mg, twice a day, for seven days; the remaining 20 with a placebo. Symptoms, consumption of pain-killers and need for catheters, were monitored daily, while hemochemical parameters were checked before the start, and at the end of the study. The results obtained showed a similar post-operative trend in the patients receiving dantrolene and in the controls. This is interpreted as an indirect demonstration that the mechanism of pain is primarily due to the inflammatory factors rather than due to contraction of the perineal muscles.
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PMID:[Evaluation of the mechanism determining the painful symptomatology after proctological interventions]. 338 Mar 12

Using a scoring system designed to assess the severity of neurologic deficit in gerbils during and after temporary unilateral carotid occlusion, the effects of large doses of methylprednisolone sodium succinate (MPSS: Solu-Medrol sterile powder) on experimental stroke have been examined. By scoring gerbils hourly for torso curvature, circling, inability to walk, ptosis, barrel rolling, opisthotonus, generalized seizures, and loss of righting reflex, their level of neurologic deficit can be easily, quantitatively, and reproducibly evaluated. Approximately 37% of gerbils subjects to a 3-hour unilateral carotid occlusion attained average scores of 4.0-4.5 during the first hour. There was a slight, though not significant, worsening (increase) of scores over the 3-hour occlusion period that was not altered by pretreatment of gerbils with 60 mg/kg of MPSS 10 minutes before occlusion. Following removal of occlusion at 3 hours, gerbils recovered only minimally during the ensuing 4-hour period, with deficit scores remaining around 3.2 +/- 0.3. Pretreatment of gerbils with 60 mg/kg of MPSS, however, resulted in a striking improvement in their deficit scores to 1.6 +/- 0.2 (p less than 0.05) by 2 hours after occlusion removal. Treatment of gerbils with lower (30 mg/kg) or higher (100 mg/kg) doses of MPSS was not as effective in promoting improvement. The survival of 3-hour occluded gerbils was significantly enhanced by pretreatment with 60 mg/kg of MPSS. Vehicle-treated gerbils had survival rates of 41.7%, 16.7%, and 16.7% at 24 hours, 48 hours, and 7 days, respectively, compared with 90.9%, 72.7%, and 45.4%, respectively, for MPSS-treated gerbils.
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PMID:The effects of large doses of methylprednisolone on neurologic recovery and survival in the Mongolian gerbil following three hours of unilateral carotid occlusion. 376 81

This study describes the surgical treatment and eventual outcome of 15 cases of anterior-segment penetrating ocular trauma that would be classically considered as having a poor prognosis. Signs of poor prognosis included: corneal lacerations, complicated by signs of infection ranging from infiltration to necrotic digestion; large scleral lacerations, with ciliary body or choroidal prolapse; and an exaggerated inflammatory response to the trauma. Treatment included careful microsurgical techniques, vitrectomy (when necessary), use of antibiotics and anti-inflammatory agents, and the liberal use of sodium hyaluronate to break fibrin adhesions and maintain the chamber at the close of surgery. Such treatment resulted in no enucleations, an average best corrected visual acuity of 20/80, an average normal angle of 314 degrees, and 13 cases of normal intraocular pressure without medication.
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PMID:Use of sodium hyaluronate in severe penetrating ocular trauma. 395 2

1. Ouabain given by intracerebroventricular injection to mice in small doses (0.1-0.4 mug) produced a dose related depression of central nervous activity, characterized by a reduction in spontaneous locomotor activity, hypothermia, catalepsy and ptosis, lowered body posture and lack of response to external stimuli. Doses above 0.4 mug were excitatory, convulsant and lethal.2. The depressant effects could be antagonized by (+)-amphetamine, desmethylimipramine, dibutyryl cyclic 3'5'-adenosine monophosphate and caffeine.3. The MAO inhibitor nialamide produced only a small antagonism of ouabain, resulting in a greater rate of recovery from the depressant effects of ouabain.4. The depressant effects were associated with a marked elevation of whole-brain dopamine levels with little change in noradrenaline or 5-hydroxytryptamine.5. The dopamine-beta-hydroxylase inhibitor sodium diethyldithiocarbamate, administered by intracerebroventricular injection, produced effects qualitatively similar to those seen after ouabain.6. An interference with central transmitter function is postulated as a possible mode of action of intracerebroventricularly injected ouabain.
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PMID:Pharmacological properties of centrally administered ouabain and their modification by other drugs. 432 23

1. Centrally administered sodium diethyldithiocarbamate (DDC) produced hypothermia, central nervous depression and potentiation of the antinociceptive effect of morphine. These effects resemble those seen with centrally administered ouabain. Furthermore, the interactions of (+)-amphetamine, desmethylimipramine and nialamide with DDC and ouabain were similar.2. 6-Hydroxydopamine by the same route also produced central nervous depressant effects including hypothermia, decreased locomotor activity and catalepsy but not ptosis.3. Both ouabain and chlorpromazine produced similar effects on behaviour and body temperature including selective abolition of a conditioned avoidance response.4. Although centrally administered tetrabenazine produced ptosis, decreased locomotor activity and catalepsy, it had no significant effect on body temperature. However, the hypothermia produced by peripherally administered reserpine was reversed by centrally administered dibutyryl cyclic 3',5'-adenosine monophosphate.5. Centrally administered cocaine and desmethylimipramine produced no depressant effects but an increased excitability and responsiveness were apparent in both cases.6. Although the observed behavioural depression and hypothermia can occur independently both seem to involve an interference with dopaminergic systems.
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PMID:Pharmacological properties of centrally-administered agents which interfere with neurotransmitter function: a comparison with the central depressant effects of ouabain. 435 86

Male Wistar rats, 35-days-old, maintained on a thiamine deficient diet for 30 days showed marked growth inhibition and a heart rate less than 70% of that of control rats. We examined the effect of thiamine deficiency on the action of drugs effecting the central nervous system at this period. In thiamine deficient rats treated with chloral hydrate 200 mg/kg, ketamine 100 mg/kg sodium pentobarbital 50 mg/kg, and hexobarbital 100 mg/kg, the sleeping time increased. Pretreatment with 15 mg/kg of the metabolic enzymes inhibitor, SKF-525A, 30 min prior to the hexobarbital administration resulted in prolongation of sleeping time in all groups. The thiamine deficient rats slept almost 3.5 times longer than did the control group. Pretreatment with 100 mg/kg of the metabolic enzyme inducer, sodium phenobarbital, 48 hours prior to hexobarbital treatment resulted in decreased sleeping time in all groups, as compared with only hexobarbital treatment. In the thiamine deficient rats the catalepsy and ptosis induced by the i.p. administration of tetrabenazine 50 mg/kg was reduced even when the control and pair-fed groups responded to this drug at the drug peak time. The spontaneous neuronal activity of lateral hypothalamus was most sensitive to the administration of 5-hydroxytryptophan in thiamine deficient rats.
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PMID:[The effect of thiamine deficiency on the actions of drugs affecting the central nervous system in rats (author's transl)]. 696 42

Antidepressant-like activity, as evidenced by marked inhibition of tetrabenazine-induced ptosis, was previously reported for (+/-)-4,5-dihydro-4-phenyl-3H-1,3-benzodiazepine derivatives. Since optimal antitetrabenazine activity was associated with (+/-)-4,5-dihydro-2,3-dimethyl-4-phenyl-3H-1,3-benzodiazepine (9k, HRP 543) and the 2-ethyl-3-methyl analogue (10k), the synthesis and evaluation of nuclear-substituted derivatives of these two compounds was also investigated. The initial synthesis involved Friedel-Crafts acylation of substituted benzenes with 2-nitrophenylacetyl chloride to afford 1-aryl-2-(2-nitrophenyl)ethanones 2, which were converted in five steps to (+/-)-alpha-aryl-N-methyl-2-nitrobenzeneethanamines 7. Greater flexibility with respect to the introduction of nuclear substituents was achieved by conversion of 2-nitrotoluene derivatives to 2 via acylation of intermediate beta-(dimethylamino)-2-nitrostyrenes with various aroyl chlorides and hydrolysis. Reductive amination of 2 with methylamine and sodium cyanoborohydride afforded 7 directly and significantly reduced the number of synthetic steps. Reduction of 7a-j to diamines 8a-j and cyclization with appropriate ortho esters gave nuclear-substituted analogues of 9k and 10k. Marked antitetrabenazine activity was associated with many of these compounds. Significant enhancement of activity with respect to the unsubstituted analogues 9k and 10k was not observed, with the exception of 9c which appeared to be slightly more potent than 9k.
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PMID:(+/-)-4-Aryl-4,5-dihydro-3H-1,3-benzodiazepines. 2. Nuclear-substituted analogues of (+/-)-4,5-dihydro-2,3-dimethyl-4-phenyl-3H-1,3-benzodiazepine and (+/-)-4,5-dihydro-2-ethyl-3-methyl-4-phenyl-3H-1,3-benzodiazepine as potential antidepressant agents. 706 12

Malignant hyperthermia, a relatively recently described entity, is a little-understood disease process usually manifesting as operative or postoperative hyperpyrexia in association with a hypermetabolic state. Specific therapy with procaine (Novocaine) and more recently with a muscle relaxant, dantrolene sodium (Dantrium), has shown itself to be life-saving, and currently diagnosis can be made by muscle biopsy in patients from affected pedigrees. Malignant hyperthermia is a risk in all general anesthetic procedures, particularly squint and ptosis repair, and may even be a consideration with local anesthesia.
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PMID:Malignant hyperthermia. Considerations for the ophthalmologist. 724 23

Malignant hyperthermia is an autosomal dominant disorder with variable expressivity that is caused by a membrane defect in the sarcolemma of myofibrils. A patient with strabismus (esotropia) had tachycardia and masseter muscle rigidity on exposure to succinylcholine chloride and halothane, but because of rapid recognition of the condition and discontinuation of the procedure, the potentially lethal complications of malignant hyperthermia did not develop. A serum creatine phosphokinase level showed a substantial increase above normal. Two weeks later, the patient underwent successful correction of the strabismus under general anesthesia, using morphine sulfate and thiopental sodium without complication. This condition is of interest to ophthalmologists because it occurs with increasing frequency in patients with strabismus and ptosis, and it may be triggered by certain local anesthetic agents often used by ophthalmologists.
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PMID:Suspected malignant hyperthermia in a strabismus patient. A case report. 725 98


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