Long-term management of a glaucomatous eye in a dog treated with medical therapy alone.
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An acute open angle glaucoma of the right eye was diagnosed in an 8-year-old male Yorkshire terrier which was presented with anorexia, depression, and trembling. Abnormal findings of the right eye on admission included elevated intraocular pressure (IOP; 40 mmHg), the presence of fibrin and flare in the anterior chamber, and immature cataract. Morphological abnormalities of the iridocorneal angle were not detected, and an open angle was seen in the eye. Although an elevated IOP was observed at one year after admission, lowering IOP (< or = 24 mmHg) was maintained with medical therapy using dichlorphenamide (DCPA) and timolol maleate, DCPA alone, or no-treatment for 1973 days. This case suggests that lower IOP can be maintained with medical therapy alone for a long period in a patient with open angle glaucoma. (+info)
THE RESPIRATORY ACTION OF DICHLORPHENAMIDE.
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The action of dichlorphenamide has been investigated in three healthy subjects. After this drug had been given, ventilation increased while alveolar and oxygenated mixed venous Pco(2) both fell. The magnitude of these changes was closely related to the degree of acidosis produced by the drug. The effect of intravenous acetazolamide, tested in one subject, was qualitatively similar to that of orally administered dichlorphenamide. Respiratory responses to carbon dioxide were studied in two of the subjects and in one of them the metabolic acidosis was sufficient to account for the short-term effect of dichlorphenamide on respiration. (+info)
Acetazolamide prevents vacuolar myopathy in skeletal muscle of K(+) -depleted rats.
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Hyperkalaemia induced by carbonic anhydrase inhibitor.
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An 81-year-old man developed hyperkalaemic and hyperchloraemic metabolic acidosis following treatment with a carbonic anhydrase inhibitor for his glaucoma. He had mild renal failure and selective aldosterone deficiency was confirmed. In this case the treatment did not lead to hypokalaemia because of the limited potassium secretory capacity in the renal tubules from selective aldosterone deficiency; rather, it may have led to hyperkalaemia because metabolic acidosis induced by the carbonic anhydrase inhibitor caused transcellular movement of potassium. (+info)
Emerging role of calcium-activated potassium channel in the regulation of cell viability following potassium ions challenge in HEK293 cells and pharmacological modulation.
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Effect of dichlorphenamide on gas exchange and CSF acid-base state in chronic respiratory failure.
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Dichlorphenamide was administered to 13 patients with chronic respiratory failure, and the effects on gas exchange at rest and during exercise and on the acid-base state of CSF were observed. The ventilation for a given level of CO(2) production was increased both at rest and during exercise, resulting in an increased arterial Po(2) and decreased Pco(2).The ventilatory stimulation paralleled the development of a metabolic acidosis but was not associated with tissue CO(2) accumulation. Indeed, CSF Pco(2) and the oxygenated mixed venous (rebreathing) Pco(2) fell by the same amount as arterial Pco(2). The level of CO(2) elimination after two minutes of exercise was as great for a given work load after dichlorphenamide as before. These findings do not support the view that the drug impairs CO(2) transport from tissues either at rest or during exercise. They are most consistent with the view that the primary locus of action of dichlorphenamide in therapeutic doses is the kidney. The metabolic acidosis which results is likely the basis of the respiratory stimulatin, perhaps by its effects on the CSF H(2)CO(3)-HCO(3) - system. Inhibition of carbonic anhydrase in the red cell and choroid plexus are probably unimportant effects. (+info)
Metabolic acidosis induced by carbonic anhydrase inhibitors and salicylates in patients with normal renal function.
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Two young patients with unimpaired renal and hepatic function were found to have developed metabolic acidosis after treatment for glaucoma and joint pain with a combination of salicylates and carbonic anhydrase inhibitors in normal doses. Carbonic anhydrase inhibitors appear to interact with salicylates to produce serious metabolic acidosis in patients without the predisposing factors generally considered to constitute risks. It is recommended that treatment combining salicylates and carbonic anhydrase inhibitors is either kept to a minimum or avoided. (+info)