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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Recently, much knowledge of the molecular mechanism of diuretic actions has been accumulated. Molecular cloning of carbonic anhydrase revealed a difference in isozymes and the localization of each isozymes was also identified. Carbonic anhydrase VI, located in brush border of the proximal tubules, is inhibited by acetazolamide. Loop diuretics, furosemide, bumetanide, piretanide and ethacrynic acid, inhibit Na(+)-K(+)-Cl(-)-cotransport system in the thick ascending limb of the Henle's loop. The histochemical localization and biological characterization were investigated by using [3H]-bumetanide. Loop diuretics cotransport protein and inhibit Na+ and Cl- reabsorption. Spironolactone inhibits the binding of aldosterone and cytosol mineralocorticoid receptor in the cortical connecting tubule competitively.
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To investigate possible mechanisms of increased urinary calcium excretion and increased prevalence of urolithiasis in 16- to 20-year-old children, oral calcium loading and diuretic tests were performed in 120 normal children in three age groups (7-8, 12-13, and 17-18 years of age). Urinary calcium/creatinine ratios and 24-h urinary calcium excretion were significantly increased following the oral calcium loading test in 17- to 18-year-olds compared with the two younger age groups. Oral furosemide resulted in increased urinary calcium excretion in the 17- to 18-year age group, while hydrochlorothiazide was less effective in reducing urinary calcium excretion in this age group. These results suggest that increased intestinal calcium absorption and decreased renal tubular reabsorption of calcium in 17- to 18-year-olds may be contributing factors in the increased prevalence of nephrolithiasis in older Taiwanese children.
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The familial periodic hypokalemic paralysis is an infrequent disease characterized by paralytic attacks of sudden appearance affecting the muscles of the trunk and limbs. There is a marked hypokalemia during the paralytic episodes of the disease, and a family history in 80 percent of the cases. The differential diagnosis includes hyperthyroidism with periodic paralysis, congenital paramyotony and adynamia episodica hereditaria. Two typical cases of hypokalemic periodic paralysis are presented, with biological, electrophysiological, clinical, and ultrastructural pictures characteristics of the disease. The clinical manifestations of both patients are discussed, stressing the diagnostic importance of the electrophysiological study during the insulin test, and the interest of the histologic and ultrastructural studies. The spectacular response during the acute episodes to the intravenous perfusion of potassium salts, and the usefulness of the acetazolamide administration to prevent the paralytic episodes are emphasized.
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For consideration of the determinants of access of diuretics to their site of action to be meaningful, one must understand molecular modes of action of diuretics and the anatomic site of effect along the nephron in addition to determinants of the renal handling of diuretics. Although the molecular mode of action is known for a number of drugs, such as the inhibition of carbonic anhydrase by acetazolamide, that for loop diuretics remains obscure. Sites of diuretic action along the nephron have been well delineated through collation of results from in vitro and in vivo techniques in a variety of species. Loop diuretics clearly block chloride reabsorption throughout the thick ascending limb of the loop of Henle. Access of diuretics to their renal tubular sites of action varies among drugs. Important determinants are plasma protein binding, active tubular secretion, nonionic diffusion, and intrarenal metabolism.
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Follow-up periods varied between 6 and 8 months (mean 6.8 months); all patients completed 6 months of follow-up. After intravitreal triamcinolone acetonide injection all patients showed good anatomic response. The baseline median central macular thickness was 418 microm (range 376-626 microm). At 1 month, the median central macular thickness had decreased to 224 microm (range 214-326 microm). At 3 and 6 months, the median central macular thicknesses were 275 microm (range 215-584 microm) and 312 microm (range 239-521 microm), respectively. Recurrent CMO was found in one patient at the 3-month follow-up and in two patients at the 6-month follow-up. Retreatment was performed in these patients. At the 1-month follow-up, no patient was found to have lost vision and two patients showed improvement. At the 3- and 6-month follow-ups, no patient had lost vision from baseline but no patient had maintained their improved visual acuity (VA).
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Catastrophic hyperemic states are known complications after the treatment of certain types of intracranial arteriovenous malformations (AVMs). A case is presented in which a large AVM was preoperatively embolized and later resected. There was clear intra- and postoperative evidence of edema and hemorrhage, which resulted in a fatal outcome. Regional cerebral blood flow (rCBF) data from this patient obtained with single photon emission computed tomography (SPECT) both before and after embolization were compared with data from four patients with similar size supratentorial AVMs treated and studied in a similar protocol who did not develop perfusion breakthrough. Pretreatment hemispheric rCBF was significantly reduced in this patient's ipsilateral hemisphere (50 ml/100 g/min) compared to the control group mean (83 +/- 9.5 ml/100 g/min). A similar relative depression was found in the contralateral hemisphere. After therapeutic embolization, the ipsilateral rCBF increased by 33 ml/100 g/min and the contralateral hemispheric rCBF increased by 30 ml/100 g/min; this embolization-induced increase in rCBF was significantly higher than in the control group. Acetazolamide, known to increase rCBF in normal tissue by 35 +/- 3%, resulted in a 56% augmentation of ipsilateral hemispheric flow before embolization in the reported patient vs. a 22 +/- 10% increase for the control group. Postembolization, this hyperresponsiveness to acetazolamide remained unchanged. It is possible that these hemodynamic derangements may indicate a dissociation between the vasoconstrictive and vasodilatory reactivity in chronically hypoperfused territories adjacent to AVMs such that pharmacological or metabolic stimuli may induce further vasodilation, but sudden redistribution of large volumes of flow will not promote protective vasoconstriction.
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The clinical manifestations of hemolytic glaucoma in five patients showed that the glaucoma began after a large intraocular hemorrhage. Gonioscopy revealed open angles in the anterior chamber and reddish-brown pigment covering the trabecular meshwork. Numerous red-tinted blood cells were floating in the aqueous humor; some of these were macrophages found by cytologic examination to contain golden-brown pigment granules. The presumed cause of hemolytic glaucoma is obstruction of the trabecular meshwork by fragments of hemolyzed red blood cells and hemoglobin-laden macrophages. Two patients, whose intraocular pressures were not decreased with medication, improved remarkably after irrigation of hemolytic debris from the anterior chamber.
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The purpose of this work is to evaluate if the asymmetry of venous outflow between the two hemispheres is a reliable criterion of impairment of the cerebral vascular reserve among symptomatic patients harbouring a spontaneous atherosclerotic occlusion of internal carotid artery.
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This study evaluates aqueous humor dynamics in rhesus monkeys from the University of Florida inbred colony with ocular normotension and naturally occurring ocular hypertension. Eight monkeys with untreated intraocular pressures (IOPs) of less than 18 mmHg in one eye (ONT group) and seven with untreated IOPs of greater than or equal to 18 mmHg in one eye (OHT group) were included in the study. Assessments included central cornea thickness by ultrasound pachymetry, IOP by tonometry, aqueous flow and outflow facility by fluorophotometry, and uveoscleral outflow by mathematical calculation. Animals were sedated with ketamine for all measurements. Values from the two eyes of each animal were averaged, with the exception of one animal that had only one good eye. Comparisons between groups were made by Student's two-tailed unpaired t-tests. Compared to the ONT group, the OHT group had higher IOPs at all times measured (4:00 PM the day before the study, 21.2 ± 6.5 versus 14.4 ± 1.5 mmHg, p = 0.01; 9:00 AM the day of the study, 20.7 ± 6.6 versus 14.8 ± 1.2 mmHg, p = 0.03; 11:00 AM the day of the study, 16.0 ± 1.6 versus 13.3 ± 2.9 mmHg, p = 0.05) and lower aqueous flow (2.12 ± 0.40 versus 4.54 ± 1.11 μl/min, p = 0.0001), outflow facility (0.17 ± 0.10 versus 0.33 ± 0.07 μl/min/mmHg, p = 0.01) and uveoscleral outflow (p < 0.05). The elevated IOP in inbred Florida rhesus monkeys is a result of significantly reduced outflow facility and uveoscleral outflow. These animals also have slower aqueous flow than the ONT animals which does not contribute to the higher IOP.
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We studied the effect of the carbonic anhydrase inhibitor acetazolamide on 24 patients with essential tremor by patient self-evaluation of functional disability, rating of motor task function, and clinical rating of tremor severity. Acetazolamide significantly reduced tremor severity, but there was no statistically significant change in patient self-assessment of function or motor task rating. Although side effects were common, over half the patients elected to remain on the drug.
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Hyperkalemia is commonly encountered in patients who receive a renal transplant and the immunosuppressive drug, cyclosporine. There is also a high incidence of hypertension (which is thought to be due to expansion of the extracellular fluid volume) and hyperchloremic metabolic acidosis in this group of patients. This constellation of findings led to the suspicion of the possibility that their basis might be type II hypoaldosteronism. To test this hypothesis, 12 patients with hyperkalemia (plasma K+, 5.1 +/- 0.2 mmol/L at the time of study) while receiving cyclosporine were studied. Patients who had diabetes mellitus, those receiving drugs known to cause hyperkalemia (e.g., beta blockers, angiotensin-converting enzyme inhibitors, K(+)-sparing diuretics), or those with a serum creatinine greater than 200 mumol/L were excluded. The renal response to hyperkalemia was inappropriate because the transtubular K+ concentration gradient (TTKG) was only 4.3 +/- 0.4 compared with a TTKG of 13 +/- 1, 2 h after 50 mmol of KCl was given to normal subjects. The TTKG, after administration of 200 micrograms of fludrocortisone, was still very low (5.6 +/- 0.6) in the patients compared with that of controls (12 +/- 1). After administration of 250 to 500 mg of acetazolamide to increase the delivery of bicarbonate to the distal nephron, the TTKG rose significantly to 11 +/- 1 in patients on cyclosporine, compared with 17 +/- 1 in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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The most common afflictions among climbers were cough, diarrhea, nausea, and vomiting, and the most common medications used were acetazolamide, aspirin, and antibiotics. Average postacclimatization, presummit "rest" altitude was 4571 m, and average weight carried 10.7 kg. Average body mass loss during expedition, regardless of success, was 7%.
Acetazolamide is a thiazide derivative clinically used in skeletal muscle disorders related to altered K+ homeostasis such as the periodic paralyses. The mechanism of action responsible for the therapeutic effects of the drug is still unknown, however. In the present work, we investigated the mechanism of action of acetazolamide in the K-deficient diet rat, an animal model of human hypokalemic periodic paralysis (hypoPP). The in vivo administration of 2.8- and 5.6-mg/kg(-1)/day(-1) concentrations of acetazolamide to K-deficient diet rats prevented paralysis and depolarization of the fibers induced by insulin. In the acetazolamide-treated animals, intense sarcolemma Ca2+-activated K+ channel (KCa2+) activity was recorded. Acetazolamide also restored the serum K+ levels to control values. The concentrations of acetazolamide needed to enhance the KCa2+ current by 50% in vitro were 6.17 and 4.01x10(-6) M at -60 and +30 mV of membrane potentials, respectively. In normokalemic animals, the thiazide derivative enhanced the KCa2+ current with similar efficacy. Our data demonstrate that the therapeutic effects of acetazolamide in the K-deficient diet rats and possibly in human hypokalemic periodic paralysis patients can be mediated by activation of the KCa2+ channel.
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Mouse strain differences exist in post-hypoxic ventilatory behavior, specifically, the C57BL/6 J (B6) mouse exhibits irregular breathing including apnea during re-oxygenation after acute hypoxic exposure, while A/J mouse does not. This phenomenon of the B6 mouse responding to the hypoxia-reoxygenation cycle which is a mimic of human sleep apnea syndrome let us consider the B6 mouse as an animal model of sleep apnea. Moreover, the B6 mouse tends to show spontaneous apnea and post-sigh apnea compared to the A/J mouse. In this brief review, we present evidence that pharmacologic approaches as well as genetic modification can improve irregular breathing including apnea in the B6, suggesting that these pharmacologic treatment might be effective for the patients with sleep apnea who cannot tolerate nCPAP. Moreover our findings regarding genetic difference and modification should be helpful to explore the pathogenesis of sleep apnea.
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Blood was collected and DNA isolated from 66 subjects (19 affected individuals) in two multigenerational families. The microsatellite markers used in the analysis either flanked or were tightly linked to the disease gene regions. Two-point and multipoint linkage analyses were performed to define the limits of exclusion.
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Scleritis can be the initial clinical manifestation of graft-versus-host disease after allogenic bone marrow transplantation.
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Exposure of vascular smooth muscle cells (VSMCs) to excessive cyclic stretch such as in hypertension causes a shift in their phenotype. The focal adhesion protein zyxin can transduce such biomechanical stimuli to the nucleus of both endothelial cells and VSMCs, albeit with different thresholds and kinetics. However, there is no distinct vascular phenotype in young zyxin-deficient mice, possibly due to functional redundancy among other gene products belonging to the zyxin family. Analyzing zyxin function in VSMCs at the cellular level might thus offer a better mechanistic insight. We aimed to characterize zyxin-dependent changes in gene expression in VSMCs exposed to biomechanical stretch and define the functional role of zyxin in controlling the resultant VSMC phenotype.
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Periodic vestibulocerebellar ataxia is an autosomal dominant disorder characterized by defective smooth pursuit, gaze-evoked nystagmus, ataxia, and vertigo. The age of onset ranges from the third to the sixth decade. To date, all patients have originated from North Carolina, suggesting a single common founder.
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Idiopathic intracranial hypertension (IIH) is uncommon in the paediatric population. Papilloedema is the hallmark sign and patients can suffer permanent vision loss as a consequence. We describe the role of optical coherence tomography (OCT) in the follow-up of two paediatric patients with newly diagnosed IIH. Patient A presented with vomiting and examination showed ophthalmoplaegia and papilloedema. She was treated with acetazolamide, furosemide and therapeutic lumbar punctures. Patient B presented with incidental papilloedema and was treated with acetazolamide and she reported intermittent headache during follow-up. Fundoscopic examinations for both patients showed persistent blurred disc margins but OCT examinations documented improvement of average retinal nerve fibre layers. OCT may be of value in monitoring for recurrence in paediatric IIH.
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Sequential, 5-min SPECT scans were performed. We estimated the time-dependent change in the brain using the change in slopes of two linear equations derived from the first three SPECT counts. For the one-day method, ACZ was administered 15 min or 20 min after IMP administration. The second IMP was administered 10 min after ACZ administration.
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It appeared possible to reduce re-uptake of 111In-DTPA-octreotide in the rat kidney in vivo. The most pronounced effects were seen after administration of sodium maleate or lysine but, because of the described toxic effects of maleate, we will study further only the effects of lysine in a clinical setting.
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Both the US National Library of Medicine and the Cochrane Database of Systematic Reviews were queried using MeSH headings and key words relevant to PHH. Two hundred thirteen abstracts were reviewed, after which 98 full-text publications that met inclusion criteria that had been determined a priori were selected and reviewed.
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A madrepore fragment implanted into Dog's long bone diaphysis is quickly vascularized and then progressively resorbed; this is due to an osteoclasic action. At the same time, in replacement of resorbed coral, cancellous bone grows which progressively let the place to compact bone. Injections of diamox given to formerly implanted Dogs, slacken the resorption of coral implants which seems to be the work of carbonic anhydrase contained in osteoclasts.
To investigate whether or not MDCK cells may be used as a model for beta-intercalated cells, we studied: (1) The effect of luminal [Cl-]0 changes on pHi measured by video-imaging micro-fluorometry, (2) the influence of the inhibitor 4,4'-diisothiocyano-2,2'-disulfonic stilbene (DIDS) on anion-exchange activity, and (3) the effect of acetazolamide on intracellular pH-indicator (c-SNAFL-2) accumulation and anion-exchange activity. At least three different modes of fluorescence accumulation were found in confluent monolayers: cells with high, low or undetectable fluorescence. Highly fluorescent cells responded to a rise of [Cl-]0 (30-140 mM) with a proportional decrease of pHi (7.6-6.4). Acetazolamide (10(-4) M) completely blocked the acidifying effects of the increased [Cl-]0, indicating that HCO3- is the intracellular ion exchanged for extra-cellular Cl-. Acetazolamide caused a reduction of SNAFL-2 fluorescence suggesting that carbonic anhydrase activity contributes to indicator accumulation. The high DIDS concentration (50 microM) required to prevent intracellular acidification suggests that the exchanger involved is identical to that present in beta-intercalated cells. All cells of non-confluent monolayers were highly fluorescent and expressed Cl-/ HCO3(-)-exchanger activity. In conclusion, highly fluorescent MDCK cells in confluent monolayers have a luminal DIDS inhibitable, carbonic anhydrase dependent Cl-/HCO3(-)-exchanger, and may therefore be used as a model for beta-intercalated cells.
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A decrease in extracellular pH is well known to inhibit vasopressin stimulated water flow in the toad bladder. It remains unclear whether this inhibition is the result of the effect of extracellular pH per se or the consequence of altered intracellular pH. In the present study we evaluated the effect of several maneuvers capable of altering intracellular pH on vasopressin or cyclic AMP stimulated water flow in the toad bladder in the absence of alterations of extracellular pH. In the presence of a normal extracellular pH, bladders subjected to a high partial pressure of CO2 or bladders from acidotic toads had a significant decrease in vasopressin or cyclic AMP stimulated water flow as compared to controls. We also examined the effect of maneuvers capable of increasing intracellular pH on vasopressin and cyclic AMP stimulated water flow. Intracellular alkalosis was induced by exposing the bladders in vitro to NH4Cl at pH 8 or to acetazolamide. Both maneuvers resulted in a significant decrease in vasopressin, but not in cyclic AMP stimulated water flow. Bladders removed from alkalotic toads, incubated in a normal extracellular pH also showed a decrease in AVP stimulated water flow. Intracellular muscle pH assessed with phosphorus nuclear magnetic resonance, was not different among bladders from control, acidotic and alkalotic toads. It is concluded that alterations of intracellular pH, in the absence of alterations of extracellular pH, are important in regulation of water transport in the toad bladder in response to vasopressin or cyclic AMP. In addition, metabolic acidosis or alkalosis alters AVP or cyclic AMP stimulated water flow by a mechanism independent of the intracellular pH.
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Studies in intact animals have shown that intestinal solute absorption is enhanced with increasing flow rates; the mechanism of this phenomenon has not been explored in detail. We used single pass perfusions of rat ileum to study the effect of higher flow rate on electrolyte absorption. Augmenting perfusion rate from 0.5 to 5.0 ml/min resulted in increased rates of sodium (11.0 +/- 0.9 vs. 23.5 +/- 2.7 mueq/min X g) and chloride (12.1 +/- 0.8 vs. 25.0 +/- 2.2 mueq/min X g) absorption, reduction in the estimated unstirred layer thickness (668 +/- 31 vs. 433 +/- 28 micron), minimal changes in intraluminal pressure and transmural potential difference, and a small, though significant, increase in intraluminal volume (19.4 +/- 8.4%). Removal of sodium from the perfusion medium abolished the effect of increased flow rate on chloride absorption as did removal of chloride on sodium absorption; addition of furosemide or acetazolamide to Ringer's solution also inhibited this effect. In separate experiments, stepwise increases in intraluminal volume were induced by elevating the outflow tubing; no effect on electrolyte transport was observed. These studies demonstrate that neutral sodium chloride absorption is enhanced in rat ileum at higher flow rates, perhaps as a result of a decrease in the thickness of unstirred layers.
Recurrent ataxia was reported in 21 patients. Their age range was between 6 and 32.75 years (males=12). The crude period prevalence rate for the 18-year study period was 7.44/100,000. Eight patients had episodic ataxia and seven had inflammatory and metabolic disorders. In the rest the etiology was unknown. Many patients presented with ataxia, dizziness, and vertigo. The frequency and duration of the ataxic episodes varied from several per day to one every few months. Other clinical features included developmental delay and seizures. Neuroimaging in episodic ataxia was normal and abnormal in inflammatory or metabolic disorders. Acetazolamide provided symptomatic relief in patients with episodic ataxia, while steroids were beneficial in patients with an inflammatory etiology. One child with a metabolic disorder died.
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Hagfish are unusual among vertebrates in having red cells that almost completely lack the anion-exchanger membrane protein band III and hemoglobins that are highly sensitive to CO2 but only weakly affected by protons. This suggests a different linkage between oxygen and CO2 transport from that of the majority of vertebrates, which is characterized by oxygen-linked proton binding to hemoglobin and chloride-bicarbonate exchange across band III protein. We here report that the hemoglobin of the hagfish Myxtne glutinosa shows oxygen-linked binding of bicarbonate, which decreases the oxygen affinity and thereby enhances oxygen unloading to the tissues. Bicarbonate binding to the hemoglobin moreover facilitates the hydration of CO2 and its transport as intraerythrocytic bicarbonate, and may compensate at least in part for the virtual absence of band III protein. This represents a unique linkage between oxygen and CO2 transport among vertebrates, where the physiological role of protons in the Bohr and Haldane effects is played by bicarbonate ions.
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