History
The condition of bronchitis has been recognised for many centuries, in several different cultures including the Ancient Greek, Chinese, and Indian, with the presence of excess phlegm and cough noted in recognition of the same condition. Early treatments of chronic bronchitis included garlic, cinnamon and ipecac, among others. Modern treatments were developed during the second half of the 20th century.In Britain in 1808, a physician Charles Badham was the first person to describe the condition and name the acute form as acute bronchitis. This was written of in a book entitled Inflammatory conditions of the bronchia. In this book Badham distinguished three forms of bronchitis including acute and chronic. A second edition of this book was renamed An Essay on Bronchitis and published in 1814. Bradham used the term catarrh to refer to the cardinal symptoms of chronic cough and mucus hypersecretion of chronic bronchitis, and described chronic bronchitis as a disabling disorder.In 1901 an article was published on the treatment of chronic bronchitis in the elderly. The symptoms described have remained unchanged. The cause was thought to be brought on by dampness, cold weather, and foggy conditions, and treatments were aimed towards various cough mixtures, respiratory stimulants, and tonics. It was noted that something other than the weather was thought to be at play. Exacerbations of the condition were also described at this time. Another physician Harry Campbell was referred to who had written in the British Medical Journal a week before.
Normally, carbonic anhydrase converts carbonic acid (H2CO3) into bicarbonate (HCO3), releasing a proton (H+) into solution. The H+ is then exchanged for  sodium (Na+) ions, which facilitates the production of aqueous humor. By blocking the function of carbonic anhydrase, the Na+/H+ exchange is unable to occur, which leads to a decrease in Na+ in the cell and prevents aqueous humor production. History
This drug, developed by Merck, was the first drug in human therapy (market introduction 1995) that resulted from structure-based drug design. It was developed to circumvent the systemic side effects of acetazolamide which has to be taken orally. References
Further reading
Kubinyi H (1999). "Chance favors the prepared mind--from serendipity to rational drug design". J Recept Signal Transduct Res. 19 (1–4): 15–39. doi:10.3109/10799899909036635. PMID 10071748. Plummer C, MacKay E, Gelatt K (2006). "Comparison of the effects of topical administration of a fixed combination of dorzolamide-timolol to monotherapy with timolol or dorzolamide on IOP, pupil size, and heart rate in glaucomatous dogs". Veterinary Ophthalmology. 9 (4): 245–9. doi:10.1111/j.1463-5224.2006.00469.x. PMID 16771760. Grover S, Apushkin M, Fishman G (2006). "Topical dorzolamide for the treatment of cystoid macular edema in patients with retinitis pigmentosa". Am J Ophthalmol. 141 (5): 850–8. doi:10.1016/j.ajo.2005.12.030. PMID 16546110. Almeida G, Faria e Souza S (2006). "Effect of topical dorzolamide on rabbit central corneal thickness". Braz J Med Biol Res. 39 (2): 277–81. doi:10.1590/S0100-879X2006000200015. PMID 16470316.