dorzolamide has been researched along with dipivefrin* in 4 studies
1 review(s) available for dorzolamide and dipivefrin
| Article | Year |
|---|---|
Contact dermatitis to topical drugs for glaucoma.
A review of the literature has identified 10 agents causing contact dermatitis among topically administered drugs for glaucoma. These agents include beta-blockers (timolol, befunolol, betaxolol, levobunolol, carteolol, metipranolol), a carbonic anhydrase inhibitor (dorzolamide), a parasympathomimetic (pilocarpine), and sympathomimetics (dipivefrin, apraclonidine). Patch testing has been documented in certain individuals as well as cross sensitization and reactivity. Systemic reactions to these topically applied medications have been briefly noted. Topics: Dermatitis, Allergic Contact; Epinephrine; Glaucoma; Humans; Ophthalmic Solutions; Pilocarpine; Sulfonamides; Thiophenes; Timolol | 2001 |
1 trial(s) available for dorzolamide and dipivefrin
| Article | Year |
|---|---|
The effect of topical glaucoma medications evaluated by perimetry.
Topics: Administration, Topical; Antihypertensive Agents; Betaxolol; Clonidine; Epinephrine; Glaucoma; Humans; Intraocular Pressure; Levobunolol; Prospective Studies; Sulfonamides; Thiophenes; Visual Field Tests | 2003 |
2 other study(ies) available for dorzolamide and dipivefrin
| Article | Year |
|---|---|
Allergic contact dermatitis from timolol and dorzolamide eye drops.
Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Carbonic Anhydrase Inhibitors; Dermatitis, Allergic Contact; Epinephrine; Female; Glaucoma; Humans; Ophthalmic Solutions; Patch Tests; Sulfonamides; Thiophenes; Timolol | 2006 |
Effects of commercial antiglaucoma drugs to glutamate-induced [Ca2+)]i increase in cultured neuroblastoma cells.
Over releasing of glutamate and cellular calcium influx always results in neuronal death. In the present study, we investigated various commercial antiglaucoma drugs including timolol (0.58 microM to 58 microM), betaxolol (1.62 microM to 162 microM), carteolol (6.8 microM to 680 microM), pilocarpine (4.08 microM to 408 microM), latanoprost (0.01 microM to 1.1 microM), dorzolamide (6.16 microM to 616 microM), brinzolamide (2.6 microM to 260 microM), brimonidine (0.68 microM to 68 microM), dipivefrin (0.28 microM to 28 microM) and preservative benzalkonium chloride on their effects to inhibit glutamate-induced intracellular free Ca(2+) ([Ca(2+)](i)) increase in cultured N1E-115 neuroblastoma cells. These drugs were diluted from original concentrations to 1/100, 1/1000 and 1/10000. The [Ca(2+)](i) mobility was studied after loading with fura-2-AM and analyzed by spectrofluorometry. It was found that betaxolol, dipivefrin and brimonidine have remarkable effects not only to inhibit the glutamate-induced [Ca(2+)](i) increase but also to decrease the basal [Ca(2+)](i). In the case of other drugs, only high concentration of timolol (58 microM) exhibited significant effect to completely prevent glutamate-induced [Ca(2+)](i) increase. Moreover, benzalkonium chloride did not exhibit any inhibitive effect. These results indicate that betaxolol, dipivefrin and brimonidine may have neuroprotective effects to inhibit the glutamate-induced over Ca(2+) influx damage. Topics: Animals; Antihypertensive Agents; Betaxolol; Brimonidine Tartrate; Calcium; Carteolol; Cell Death; Dose-Response Relationship, Drug; Epinephrine; Glaucoma; Glutamic Acid; Latanoprost; Mice; Neuroblastoma; Neurons; Neuroprotective Agents; Pilocarpine; Prostaglandins F, Synthetic; Quinoxalines; Sulfonamides; Thiazines; Thiophenes; Timolol; Tumor Cells, Cultured | 2003 |