Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nervous control of gastrointestinal motility is extremely complex, is regulated by the enteric system, the "brain of the gut", and modulated by extrinsic nerves. This system with its multiplicity of transmitters and receptors does not always allow a clear interpretation of experimental data, especially with compounds lacking specificity. In this review the complex situation is described particularly in relation to receptor populations (cholinergic, adrenergic, dopamine, histamine, 5-hydroxytryptamine, opioid, gamma-aminobutyric acid (GABA), prostanoid and dihydropyridine receptors), therapeutic aspects of drugs and their usefulness in children. Newer principles with known drugs and promising new compounds with a more appropriate kinetic or fewer side-effects, deriving from distinct pharmacological groups, as candidates for the treatment of gastrointestinal disorders are considered e.g. anticholinergics (prifinium or actilonium bromide), adrenergic alpha 2-agonists (clonidine, lidamidine) for diarrhoea in diabetic neuropathy, adrenergic beta-blockers for shortening postoperative ileus (propranolol), dopamine receptor antagonists (metoclopramide, domperidone, alizapride) and another prokinetic substance (cisapride) which may be useful for a number of applications as gastro-oesophageal reflux, gastro-paresis, intestinal pseudo-obstruction, cystic fibrosis and constipation, morphine derivatives (e.g. loperamide) for intractable diarrhoea and calcium antagonists (e.g. nifedipine) for achalasia. Increasing experience in digestive tract pharmacology and reliable clinical studies will furthermore be the basis for a more specific and better tolerated therapy of gastrointestinal motility disorders in adults and children.
 ...
PMID:Rational pharmacotherapy of gastrointestinal motility disorders. 266 4

We examined 32 patients with cystic fibrosis, paying special attention to optic nerve performance and pupillary function. Decreased visual acuity occurred in nine of 64 eyes. Three of 17 patients (18%) who used chloramphenicol had bilaterally delayed P100 waves of the visual-evoked response of greater than 3 standard deviations. This was not found in patients who did not use chloramphenicol. Contrast sensitivity in patients with cystic fibrosis was decreased at every spatial frequency when compared to healthy controls. This decrease was noted in patients who did and did not use chloramphenicol, suggesting that chloramphenicol is not the only cause of decreased contrast sensitivity in cystic fibrosis. With pharmacologic pupil testing we determined that patients with cystic fibrosis display a preganglionic oculosympathetic paresis that corresponded to the disease severity, as measured by the Shwachman score.
 ...
PMID:Ocular findings in cystic fibrosis. 349 18