Diamox is an FDA-approved medication used to treat certain types of glaucoma, congestive heart failure, certain types of seizures. Diamox also prevents altitude sickness.
Other names for this medication:
Also known as: Acetazolamide.
Diamox contains an active ingredient Acetazolamide, which belongs to class of drugs called carbonic anhydrase inhibitors.
Diamox effectively treats certain types of glaucoma (excessive pressure in the eyes) by reducing the amount of fluid in the eye, and thereby decreases pressure inside the eye.
Acetazolamide acts also as a diuretic ("water pill") and inhibits the protein in the body called carbonic anhydrase. This leads to reducing the build-up of certain fluids in the body, significantly alleviating the symptoms of congestive heart failure.
Acetazolamide is also used to treat certain types of seizures, and to treat or prevent altitude sickness.
Diamox is available in tablets.
The dosage depends on the disease and its prescribed treatmen.
250 mg to 1 gram per 24 hours in 2 or more smaller doses.
In secondary glaucoma and before surgery in acute congestive (closed-angle) glaucoma, the usual dosage is 250 mg every 4 hours or, in some cases, 250 mg twice a day.
The daily dosage is 8 to 30 mg per 2.2 pounds of body weight in 2 or more doses. Typical dosage may range from 375 to 1,000 mg per day.
Congestive Heart Failure treatment:
The usual dosage is 250 mg to 375 mg per day or 5 mg per 2.2 pounds of body weight, taken in the morning.
Diamox can be used by children.
If you want to achieve most effective results do not stop taking Diamox suddenly.
If you overdose Diamox and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Diamox are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Diamox if you are allergic to Diamox components.
Be careful with Diamox if you're pregnant or you plan to have a baby, or you are a nursing mother.
Do not take Diamox if your sodium or potassium levels are low.
Do not take Diamox if you have kidney or liver disease, including cirrhosis.
Be careful with Diamox if you suffer from or have a history of emphysema or other breathing disorders.
Be careful with Diamox if you take high doses of aspirin.
Be careful with Diamox if you are taking Amitriptyline, Cyclosporine, Lithium, Methenamine, oral diabetes drugs such as Glyburide, Quinidine.
Do not use potassium supplements or salt substitutes.
If you want to achieve most effective results without any side effects it is better to avoid alcohol.
Do not stop taking Diamox suddenly.
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Because the secretion of endolymph has been localized in the ampullar part of the frog semicircular canal, we attempted to determine by cytochemical methods the ultrastructural localization of two enzymes that are assumed to play a role in endolymph secretion: carbonic anhydrase and adenylate cyclase. Functionally, the epithelium of the frog semicircular canal can be schematically divided into three areas: sensory (crista ampullaris), secretory (dark cells), and non-sensory and nonsecretory (transitional and undifferentiated cells) areas. Carbonic anhydrase activity was widely distributed in dark cells. Dark cell labeling disappeared in the presence of acetazolamide. The other cells of the canal did not show any carbonic anhydrase labeling except for the supporting cells of the sensory cells. Adenylate cyclase activity was found on the basolateral and apical membranes of dark cells, and on the apical membrane of sensory cells; weak labeling was also observed in the other epithelial cells. In the apical membrane of the dark cells, adenylate cyclase labeling was dependent on the presence of vasotocin, the frog antidiuretic hormone. The dark cells of the frog semicircular canal thus possess the enzyme equipment needed for the secretion of endolymph and its possible hormonal regulation.
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To evaluate MRI methods for estimating cerebrovascular reserve, we computed changes in the R2* and R2 transverse relaxation rate and apparent diffusion coefficient (ADC) at 2.0 Tesla in five rats after administration of 30 mg of acetazolamide and in four rats during inhalation of 20% carbon dioxide gas. Significant decreases in R2*, corresponding to increases in gradient echo MRI signals, occurred in both the acetazolamide (average change -8.3%, P = 0.005) and the carbon dioxide (-2.7%, P = 0.009) treated animals. The computed values for R2 and ADC were unchanged. The magnitude of the gradient echo MRI changes observed should permit anatomic mapping of blood flow reactivity patterns in normal human subjects and in patients at risk for cerebrovascular disease.
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CADASIL patients (n=16) were treated with ACZ (250 mg) daily for 24 weeks. The mean blood flow velocity (MFV) of the middle cerebral artery (MCA) and CO(2)-induced cerebrovascular reactivity (CVR) were tested using transcranial Doppler sonography (TCD) before and after treatment.
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Blinded, randomized, controlled trial.
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In human medicine, the carbonic anhydrase (CA) inhibitor acetazolamide is used to treat irregular breathing disorders. Previously, we demonstrated in the rabbit that this substance stabilized closed-loop gain properties of the respiratory control system, but concomitantly weakened respiratory muscles. Among others, the highly diffusible CA-inhibitor methazolamide differs from acetazolamide in that it fails to activate Ca(2+)-dependent potassium channels in skeletal muscles. Therefore, we aimed to find out, whether or not methazolamide may exert attenuating adverse effects on respiratory muscle performance as acetazolamide. In anesthetized spontaneously breathing rabbits (n = 7), we measured simultaneously the CO(2) responses of tidal phrenic nerve activity, tidal transpulmonary pressure changes, and tidal volume before and after intravenous application of methazolamide at two mean (+/- SE) cumulative doses of 3.5 +/- 0.1 and 20.8 +/- 0.4 mg/kg. Similar to acetazolamide, low- and high-dose methazolamide enhanced baseline ventilation by 52 +/- 10% and 166 +/- 30%, respectively (P < 0.01) and lowered the base excess in a dose-dependent manner by up to 8.3 +/- 0.9 mmol/l (P < 0.001). The transmission of a CO(2)-induced rise in phrenic nerve activity into volume and/or pressure and, hence, respiratory work performance was 0.27 +/- 0.05 ml x kg(-1) x kPa x unit(-1) under control conditions, but remained unchanged upon low- or high-dose methazolamide, at 0.30 +/- 0.06 and 0.28 +/- 0.07 ml x kg(-1) x kPa x unit(-1), respectively. We conclude that methazolamide does not cause respiratory muscle weakening at elevated levels of ventilatory drive. This substance (so far not used for medication of respiratory diseases) may thus exert stabilizing influences on breathing control without adverse effects on respiratory muscle function.
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A 53-year-old man presented in 1985 with bilateral middle ear infections requiring myringotomies. During the next 18 months, he went on to develop a left Bell's palsy. The patient then began to develop recurrent occipital headaches along with left sixth and seventh nerve palsies and a green nasal discharge requiring hospitalization. Workup included magnetic resonance imaging showing pronounced enhancement of the tentorium and meninges in the occipital region with normal ventricle size. An x-ray of the chest showed multiple pulmonary nodules. A regimen of prednisone and cyclophosphamide was initiated. The patient did well for 2 years until he again developed middle ear infections and headache. Serial lumbar punctures showed increased pressures. A circulating antineutrophil cytoplasmic antibody was positive. Cyclophosphamide was administered, with acetazolamide added for treatment of the elevated intracranial pressure. The patient stabilized for another 2 years but then presented in 1994 with recurrent headache, bilateral papilledema, and mild left arm and right leg weakness. A lumbar puncture was performed with an opening pressure of 52 cm H2O. Computed tomography of the head revealed moderate enlargement of the lateral third and fourth ventricles, consistent with communicating hydrocephalus.
The EC-IC bypass surgery can maintain CBO immediately after surgery or gradually within 1 year when the preoperative rCBF is below 24.5 to 25 ml/100 g/min. Furthermore, bypass flow plays a critical role in maintaining an adequate CBO when preoperative rCBF is below 22.2 to 24 ml/100 g/min.
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Sudden infant death syndrome is the leading cause of death in infants in the United States. The laryngeal chemoreflex (LCR) is thought to contribute to its pathogenesis. In adult animals, increasing levels of intralaryngeal CO2 result in a decrease in ventilatory activity. Intravenous acetazolamide (AZ) abolishes this response. The purpose of this study was to determine the effects of intralaryngeal CO2 and AZ on the LCR and respiratory physiology of piglets under normoxic and hypoxic conditions. We applied 0% or 10% CO2 in a randomized order to the larynx of 26 piglets. Intubation via tracheotomy prevented inhalation of the gas mixtures. Laryngeal stimulation was performed under normoxic conditions (PaO2 of >70 mm Hg) in 15 animals and under hypoxic conditions (PaO2 of 50 to 65 mm Hg) in 11 animals both with and without intravenous AZ (5 mg/kg). Respiratory and cardiovascular response data were recorded. Ten percent intralaryngeal CO2 has no significant effect on mean baseline respiratory rate, systemic PaCO2 or PaO2 levels, or apnea duration (p > .05). The use of AZ (versus no AZ) resulted in significantly higher baseline respiratory rates (64 versus 51 breaths per minute; p = .016), a decreased baseline systemic PaCO2 level (38.8 versus 45.9 mm Hg; p < .001), a higher baseline PaO2 level (97.9 versus 82.8 mm Hg; p < .001), shorter mean apnea durations (15.5 versus 24.8 seconds; p = .001), a higher lowest O2 saturation level after the stimulus (78.0% versus 68.4%; p = .003), and fewer profound apneas (10 of 90 versus 41 of 90 trials; p < .001). We conclude that 10% intralaryngeal CO2 does not decrease ventilatory activity in piglets and has no significant effect on the LCR. Acetazolamide, however, appears to have a protective effect against the LCR, resulting in shorter and less severe apneas. The protective effect of AZ against the LCR appears to be related to its ability to stimulate the respiratory drive and increase oxygenation at baseline.
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Patients with steno-occlusion in the internal carotid artery or middle cerebral artery (MCA) at our institution between 2007 and 2013 were retrospectively studied. Intracranial flows were obtained using QMRA, and flow change with Diamox (QMRAΔd) was calculated as follows: ([flow after Diamox-flow before Diamox]/[flow before Diamox])×100%. Poor LMC was defined as grade 1 or 2, and robust LMC was defined as grade 3 or 4 based on the ASITN/SIR (American Society of Interventional and Therapeutic Neuroradiology/Society of Interventional Radiology) grading system on digital subtraction angiography.
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Trichinellosis is a globally distributed helminthic infection. There is a considerable interest in developing new anti-helminthic drugs affecting all the developmental stages of Trichinella. Acetazolamide (carbonic anhydrase (CA) inhibitor) involves a novel mechanism of action by inhibiting such an essential enzyme for parasite metabolism. This work aimed to study the effect of acetazolamide against different stages of T. spiralis in experimental animals. Mice were divided into three groups: group I: infected and treated with acetazolamide on day 2 post infection (P.I.), group II: infected and treated with acetazolamide on day 12 P.I., and group III: infected non-treated. From each group, small intestine and muscles were removed for histopathological and immunohistochemical studies. Also, total adult and muscle larval count were estimated. We found that acetazolamide was effective in reduction of both adult and muscle larval counts. When given early, the effect was more pronounced on the adults (62.7 %). However, the efficacy of the drug against muscle larvae was increased when given late (63 %). Improvement of the intestinal histopathological changes was observed in all the treated groups. Degeneration of encysted larvae with minimal pathologic changes of infected skeletal muscle was observed in the treated groups. Expression of matrix metalloproteinase-9 showed a statistically significant decrease in the intestinal and muscle tissues in all treated groups as compared to the control group. In conclusion, the present study revealed that acetazolamide, carbonic anhydrase inhibitor, could be a promising drug against both adults and larvae of T. spiralis.
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A stopped-flow pH electrode apparatus was used to investigate the mechanisms underlying slow changes in plasma pH (pHO) after blood leaves the pulmonary capillaries in carbonic anhydrase-inhibited animals. After acetazolamide was administered to an anesthetized dog or cat, arterial blood was withdrawn through the electrode apparatus into a syringe. Syringe movement was then suddenly stopped. Temperature and pHO of the blood in the electrode chamber were monitored both before and after blood withdrawal ceased. After stopping flow, pHO of the blood in the electrode chamber a) rose 0.02 after a dose of about 1 mg/kg acetazolamide; b) did not change after a dose of about 2 mg/kg acetazolamide; and c) fell 0.10 after a dose greater than about 5 mg/kg acetazolamide. With reasonable red cell and plasma carbonic anhydrase activities assumed for each dose level of acetazolamide, a computer model of the reaction and transport processes occurring in blood after gas exchange in the lung yielded predicted time courses of pHo that were in good agreement with the experimental results. The observed slow pHo changes are largely a result of disequilibrium of [H+] between red blood cells and plasma as blood leaves the pulmonary capillaries.
Intraocular pressures 1 and 3 hours after laser therapy were recorded.
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Retrospective chart review was conducted on all patients with retinitis pigmentosa or X-linked retinoschisis who were either currently on treatment or had been treated with carbonic anhydrase inhibitors for cystic macular lesions. A total of three patients were included in the study.
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1. The intracellular (I.C.) concentrations of Na, K and Cl in mammary cells from lactating guinea-pigs have been calculated from the analysis of fresh tissue and the measurement of the extracellular (E.C.) space with [(14)C]sucrose and the milk content with [(14)C]lactose.2. Assuming that alveolar milk has the same concentration as teat milk, the intracellular concentrations were calculated to be K 115, Na 42 and Cl 66 m-equiv. l(-1) intracellular water.3. Intracellular concentrations were also calculated in slices incubated in Krebs-bicarbonate medium plus glucose. There was a large increase in the sucrose (E.C.) space and a rise in total tissue [Na] and [Cl]. On the assumption that the medium had equilibrated with the milk space as well as the E.C. space, the calculated I.C. concentrations of Na (43 m-equiv. l(-1)), and Cl (62) were very similar while [K] was somewhat higher (143 m-equiv. l(-1)I.C. water).4. The calculated I.C. concentrations of all three ions are all higher than in milk but the ratios between them are almost identical.5. Similar figures for the I.C. concentrations of Na, K and Cl have been obtained in the goat, cow and sheep mammary tissue incubated in vitro.6. Moderate changes in the concentrations of Na, K and Cl in the external medium had no effect on cell composition but during incubation without ions [(14)C]sucrose became distributed throughout the total tissue water indicating that sucrose had entered the I.C. compartment.7. Acetazolamide (10(-2)M), aldosterone (1.4 x 10(-6)M) and, in some experiments, lack of glucose lowered I.C. [Cl(-)], but oxytocin, vasopressin and low doses of insulin had no effect.8. The data are difficult to reconcile with the hypothesis of Zaks, Natochin, Sokolova, Tanasiichuk & Tverskoi (1965) that freshly secreted milk has the ionic composition of plasma.9. Comparison of I.C. ion concentrations and the membrane potential between the cells and milk suggests that Na(+) and K(+) are passively distributed across the apical membrane but that Cl(-) must be actively held in the cells. Across the basal membrane the data are consistent with the presence of a Na(+) pump and with Kinura's (1969) detection of a Na:K ATPase on the basal and lateral membranes. In addition another inward-facing Cl(-) pump may exist at this site.
The perfusion SPECT with acetazolamide improves the diagnostic capacity of the baseline perfusion (99m)Tc-HMPAO SPECT, and makes it possible to classify the abnormalities as metabolic or vascular, with a preference for the post-acetazolamide CBS imaging analysis.
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Telemetric ICP monitoring is useful in patients with complicated CSF dynamic disturbances who would otherwise require repeated invasive pressure monitoring. It seems to be a feasible method to guide adjustment of programmable valve settings and to identify patients with chronic or repeated shunt problems.
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Spinal carbonic anhydrase contributes to nociceptive hyperreflexia induced by pentobarbital and midazolam and to a lesser extent with propofol. These findings are consistent with a role for carbonic anhydrase in nociceptive signal enhancement by these drugs.
These results suggest that the body water regulation and inflammation are key factors in AMS development when all other factors such as the level of physical exertion during ascent, the rate and magnitude of ascent and the use of acetazolamide are controlled.
Many investigations have indicated a functional role for carbonic anhydrase in the mediation of hormone-stimulated bone resorption. These studies depend heavily on the use of heterocyclic sulfonamide inhibitors of carbonic anhydrase. These drugs have effects on many tissues other than bone, and some of these effects confound the interpretation of studies of the role of carbonic acid in bone metabolism. A novel, "bone-targeted" sulfonamide has been produced to obviate these extraosseous effects. This compound (designated WP-1) is the combination of tetracycline and acetazolamide, such that the acetazolamide is not an active inhibitor. Hydrolysis of WP-1 yields an active carbonic anhydrase inhibitor. WP-1 has a marked affinity for bone mineral, allowing deposition of the drug in bone. At a concentration of 10(-5) M, WP-1 attenuates parathyroid hormone stimulated net release of calcium from neonatal rat calvaria in culture. WP-1 is the first member of a class of drugs which may prove useful as pharmacological probes in the study of bone metabolism.
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To examine a possible effect of 7-methylxanthine, theobromine, acetazolamide, or L-ornithine on the ultrastructure and biochemical composition of rabbit sclera.
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Isc changes (Ussing-type chamber) induced either by the NO donors SNP or SIN-1, or by the cGMP analogue 8-pCPT-cGMP were assessed. The effect of inhibitors of guanylate cyclase (10 microM ODQ, 100 microM LY83583), protein kinase G (30 microM Rp-8-pCPT-cGMP, 3 microM KT 5823), protein kinase A (1 microM KT 5720), or protein kinase C (1 microM Go6983) on SNP- or 8-pCPT-cGMP-induced Isc changes were investigated. The effect of inhibitors of anion channel (100 microM niflumic acid, 1 mM DIDS, and 1 mM 9-AC), K+-channel (10 mM TEA, 10 mM BaCl2), Na+-channel blockers (1 mM amiloride), Na+-K+-2Cl- cotransporter inhibitor (0.5 mM bumetanide), or carbonic anhydrase inhibitor (1 mM acetazolamide) was studied. In Cl(-)- or HCO3(-)-free Krebs-Ringer solution, the effect of SNP- or 8-pCPT-cGMP-induced Isc changes was accessed.
In order to evaluate hemodynamic features of ophthalmic arteries in patients with severe carotid artery stenosis, we assessed and compared vasomotor reactivity in the middle cerebral and ophthalmic arteries.
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Information was abstracted from the findings of individual case reports and clinical trials.
Chemical sympathectomy with 6-hydroxydopamine combined with subsequent topical epinephrine therapy was evaluated with regard to intraocular pressure effects in primary open-angle glaucoma. After chemical sympathectomy intraocular pressure was maintained below 20 mm Hg with 1.0% epinephrine three times daily in 29 of 36 eyes of 25 patients for two to 29 weeks. Chemical sympathectomy combined with epinephrine therapy was most effective in patients whose intraocular pressure had been well controlled with pilocarpine and epinephrine and was less effective in patients whose intraocular pressure had not been controllable with maximum medical therapy prior to the administration of 6-hydroxydopamine. The results of this study suggest that chemical sympathectomy combined with topical epinephrine therapy has considerable clinical value in the medical management of primary open-angle glaucoma.
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We report a case of acute generalized exanthematic pustulosis induced by 2 different drugs, cefaclor and acetazolamide. The diagnosis was confirmed by challenge tests, and these 2 drugs respectively were proven to be responsible for the patient's pustular eruptions.
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