Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The unopened eye maintains a relatively stable spherical contour due to the expansile influence of the intraocular pressure. When the eye is opened this expansile pressure is lost and some degree of collapse of the scleral shell ensues. In eyes with a relatively flaccid sclera an anterior segment incision may induce significant reduction in the volume of the posterior segment of the globe. During intracapsular cataract extraction on such eyes, scleral collapse can cause anterior displacement of the lens and iris when the eye is opened and vitreous loss as soon as the lens is extracted. Scleral collapse tends to occur during intraocular surgery on previously aphakic eyes. In this situation it may become difficult to achieve a vitreous-free anterior sement by open sky vitrectomy. Metallic scleral supporters prevent inward collapse of that portion of the sclera to which they are attached. They do not prevent downward collapse of the posterior sclera shell. Upward traction is required to prevent the downward component of scleral collapse. A system for controlled suspension of the globe during intraocular surgery has been devised and used in a variety of surgical procedures. The apparatus is simple and it does help to minimize downward scleral collapse. It does not prevent scleral identation or distortion by external forces and cannot substitute for inadequate anesthesia and akinesia or faulty surgical technique.
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PMID:Suspension of the globe during intraocular surgery. 75 77

Forty patients with severe Parkinson's disease (23 men, 17 women) who had been treated for six years with L-dopa-decarboxylase inhibitor, were part of a placebo-controlled double-blind trial to test the effectiveness of bromocriptin. In all patients the effectiveness of L-dopa had been decreasing, 34 patients had L-dopa-induced dyskinesias, 35 "on-off" symptoms. Bromocriptin dosage was gradually increased to a total dose of 30 - 40 mg daily. This led to a 25% reduction in L-dopa requirements. The symptoms of Parkinson's disease were favourably influenced, with rigor, tremor and also walking disturbances responding better than bradykinesia of the hands. At the same time, there was a marked prolongation of the periods of good mobility ("on" time) from 7 to 10.8 hours without influence on other "on-off" symptoms such as paradoxical akinesia. Two patients had to be excluded from the trial because the treatment caused side effects (orthostatic hypotension, exogenous psychotic symptoms). Other side effects, such as nausea and mild forms of collapse, could be controlled by drugs.
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PMID:[Bromocriptin in the treatment of progressive stages of Parkinson's disease (author's transl)]. 679 66

KW-5092 ([1-[2-[[[5-(piperidinomethyl)-2- furanyl]methyl]amino]ethyl]-2-imidazolidinylidene) propanedinitrile fumarate) is a novel gastroprokinetic agent with acetylcholinesterase (AChE) inhibitory activity and acetylcholine (ACh) release facilitatory activity. The present study examined the effects of KW-5092 on gastrointestinal (GI) motor activity in dogs. In anesthetized dogs, KW-5092 at 0.03 to 1 mg/kg, i.v. dose-dependently enhanced the gastric antral and the colonic motor activity. Neostigmine, an AChE inhibitor, enhanced the motor activity at 0.03 and 0.1 mg/kg, i.v. Ranitidine, a histamine H2-receptor antagonist with AChE inhibitory activity and ACh release facilitatory activity, enhanced the motor activity but decreased blood pressure at 1 to 10 mg/kg, i.v. In conscious dogs, KW-5092 at 0.03 to 1 mg/kg, i.v. or 1 to 10 mg/kg, p.o. dose-dependently enhanced the gastric antral, duodenal, ileal and the colonic motor activities. Neostigmine at 0.1 mg/kg, i.v. or 3 mg/kg, p.o. enhanced the duodenal, ileal and colonic motor activities, but induced excitement, slavering, vomiting and diarrhea. Ranitidine at 3 mg/kg, i.v. enhanced the gastric antral and colonic motor activities, but induced collapse or akinesia. The present results suggest that KW-5092 enhances the GI motor activity in a wide range from the gastric antrum to the colon and does not induce behavioral and cardiovascular side effects. KW-5092 may be a useful drug for the treatment of GI motility dysfunctions.
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PMID:Enhancement by KW-5092, a novel gastroprokinetic agent, of the gastrointestinal motor activity in dogs. 796 26

Inhibitory control of basal ganglia output to thalamocortical projection plays an important role in normal cortical activity in the current model of the basal ganglia motor circuit. Hypokinetic and hyperkinetic movement disorders of basal ganglia origin can be explained by excess or collapse of the basal ganglia output. An abundance of evidence indicates that parkinsonian akinesia results from hyperactivity of the basal ganglia output. Reversal of akinesia by lesions of the internal division of the globus pallidus (GPi) or its excitatory source, the subthalamic nucleus, agrees with this pathological schema. Ballism associated with subthalamic lesions, and dopa-induced dyskinesia are regarded as hyperkinetic disorders resulting from suppressed subthalamopallidal projection. Decreased firing rate in GPi was reported in both disorders. However, pallidotomy has recently been postulated to abolish both ballism and dopa-induced dyskinesia. A possible mechanism for the effect of GPi destruction in these hyperkinetic disorders may be blockade of the generation or conduction of phasic neuronal activities driving choreic movements. Symptomatologically, dystonia has aspects of both hypokinetic and hyperkinetic disorders. Overactivity of the premotor cortices, which receive projections from the basal ganglia via the ventral thalamus, was found both at rest and on movement in idiopathic dystonia. This abnormal cortical activity may arise from underactivity of basal ganglia output; however, the amelioration of dystonia with pallidotomy suggests a complex pathomechanism of the pallidothalamic system in dystonia.
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PMID:[Pathophysiology of involuntary movements in adults]. 914 23

Chylothorax and chylous ascites are very rare clinical entities generally caused by obstruction and disruption of the thoracic duct. A 60-year-old man presented with exertional dyspnea, fatigue, and chest discomfort of 18-month history. Physical examination revealed S4, bilateral pretibial edema, and moderate amount of ascites. Computed tomography and X-ray of the thorax showed left-sided pleural effusion. Abdominal imaging showed normal liver and spleen structure with intraperitoneal effusion and periportal edema. Thoracentesis and paracentesis yielded a milky, lipemic fluid of exudative nature. Biochemical analysis of the fluids showed a high triglyceride content and elevated lymphocyte count, typical of chylous fluid. All laboratory analyses for possible etiologies including neoplasms, tuberculosis, and cirrhosis were negative. Positron-emission tomography did not show any pathological uptake. Transthoracic echocardiographic examination showed bilateral atrial enlargement, left ventricular hypertrophy, anteroseptal hypokinesia and akinesia, and moderate mitral and tricuspid regurgitation, with an ejection fraction of 25%. Coronary arteries were normal on angiography. The patient was diagnosed with severe congestive heart failure accompanied by chylothorax and chylous ascites. Despite appropriate treatment, there was little change in congestion and no change in symptoms. He died during ultrafiltration therapy due to hemodynamic collapse and asystole.
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PMID:Development of chylothorax and chylous ascites in a patient with congestive heart failure. 2191 21