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PubMed1982

Effects of sympathetic stimulation on cerebral and ocular blood flow. Modification by hypertension, hypercapnia, acetazolamide, PGI2 and papaverine.

The effect of unilateral, electrical stimulation of the cervical sympathetic chain in rabbits anesthetized with pentobarbital sodium and vasodilated by hypercapnia, acetazolamide, papaverine or PGI2 was investigated to determine to what extent the sympathetic nerves to the brain and the eye cause vasoconstriction and prevent overperfusion in previously vasodilated animals. Evans blue was given as a tracer for protein leakage. Blood flow determinations were made with the labelled microsphere method during normotension and acute arterial hypertension. Hypertension was induced by ligation of the thoracic aorta and in some animals metaraminol or angiotensin was also used. Acetazolamide caused a two to threefold increase in cerebral blood flow (CBF) and hypercapnia resulted in a fivefold increase. CBF was not markedly affected by papaverine or PGI2. In the choroid plexus, the ciliary body and choroid, papaverine and hypercapnia caused significant blood flow increases on the control side. Sympathetic stimulation induced a 12% blood flow reduction in the brain in normotensive, hypercapnic animals. Marked effects of sympathetic stimulation at normotension were obtained under all conditions in the eye. In the hypertensive state the CBF reduction during sympathetic stimulation was moderate, but highly significant in hypercapnic or papaverine-treated animals as well as in controls. Leakage of Evans blue was more frequently seen on the nonstimulated side of the brain. In the eye there was leakage only on the control side except in PGI2-treated animals where 2 rabbits had bilateral leakage. The effect of sympathetic stimulation on the blood flow in the cerebrum and cerebellum in vasodilated animals seems to be small or absent if the blood pressure is normal. In the eye pronounced vasoconstriction occurs under these conditions. In acute arterial hypertension sympathetic stimulation protects both the cerebral and ocular barriers even under conditions of marked vasodilation.

Acetazolamide↗
PubMed1980

Timolol versus pilocarpine separately or combined with acetazolamide-effects on intraocular pressure.

Fifty-eight patients with intraocular hypertension or primary open angle glaucoma participated in a double masked randomized study. Timolol in concentrations 0.25% and 0.5% was compared with 1, 2, or 4% pilocarpine Acetazolamide (250 mg x 3) was added if intraocular pressure (IOP) was uncontrolled with the highest concentrations tested. No statistical difference was found in hypotensive effect between pilocarpine and timolol neither on ocular hypertensions nor glaucomas. The additive hypotensive effect of acetazolamide was the same for both substances. Once a day by administration of timolol was sufficient in 17 of 20 cases controlled merely by topical administration.

Acetazolamide↗
PubMed1984

Zinc therapy of acetazolamide-induced side-effects.

A double-blind cross-over trial extending over 4 weeks with administration of 0.2 g zinc sulphate 3 times daily and a placebo was carried out on 12 patients having grave acetazolamide-induced side-effects manifesting themselves as gustatory disorder, anorexia, and paraesthesia. All the patients had S-zinc levels within the normal range. These rose during zinc therapy periods, to fall again within placebo periods. Recording of the degrees of subjective side-effects based on interviews showed the side-effects to abate towards the conclusion of the trial period, independently of the randomizing programme. In other words, no significant difference was demonstrable between zinc period and placebo period. Taste tests according to Börnstein showed the gustatory disorders to be related exclusively to beverages containing carbon dioxide. However, in no more than 3 out of 10 patients did the gustatory sense return to normal after administration of zinc and one after placebo. Thus, this controlled trial has not served to disclose any statistically significant effect of zinc administration on acetazolamide-induced side-effects.

Acetazolamide↗
PubMed1991

Neuroretinal rim area in low tension glaucoma: effect of nifedipine and acetazolamide compared to no treatment.

The purpose of this study was to measure the change of neuroretinal rim area in patients with low tension glaucoma on- and off-treatment. Thirty-two patients were followed up for a mean of 2.6 years. Ten patients received treatment with nifedipine, 11 patients with acetazolamide and 11 patients had no treatment. The total change of rim area and the yearly rate of rim area change did not differ statistically significantly between the three groups. Seven patients in each group suffered from cold hands and feet. The response to cold provocation visual field testing was positive in 25% of patients. Neither the history of cold hands and feet nor the cold provocation test result affected the rate of progression of optic disc abnormalities. Nifedipine and acetazolamide treatment seemed to show no advantage over no-treatment in our patients.

Acetazolamide↗
PubMed1996

Time course of the acetazolamide effect in patients with extracranial carotid artery disease.

The acetazolamide test of cerebrovascular reserve is performed as a two-point transcranial Doppler (TCD) measurement of the flow velocity in the middle cerebral artery (MCA) before and 15 to 20 minutes after injection of the carbonic anhydrase inhibitor. The time course was evaluated by bilateral TCD monitoring over 45 minutes in 51 patients with extracranial carotid artery disease. Twenty-nine patients in Group 1 showed a unilateral and 22 patients in Group 2, a bilateral stenosis of the internal carotid artery (ICA). Thirty-one normal hemispheres in 18 normal subjects provided baseline control values. The most useful parameter for the description of the time course was the integral of the mean flow velocity. In both groups integral of the mean flow velocity was significantly reduced compared to that in normal persons (Group 1: 587.2 +/- 538.3 cm, p < 0.01; Group 2: 728.9 +/- 397.1 cm, p < 0.01; normal persons: 967.8 +/- 350.0 cm). The maximal increase of mean flow velocity in a two-point measurement also was significantly lower in the patient groups, but did not reach the same level of significance in Group 2 (Group 1: 19.6 +/- 12.3 cm/sec, p < 0.01; Group 2: 24.2 +/- 10.4 cm/sec, p < 0.05). Thirty-four of 73 hemispheres had reduced integral of the mean flow velocity, but only 29 had a reduced maximal increase. These data indicate that continuous monitoring and evaluation of the time course of the acetazolamide effect provide additional information on cerebrovascular reserve and help to detect an increased number of patients with impaired cerebrovascular reserve.

Acetazolamide↗
PubMed1990

Comparison of the effect of acetazolamide tablets and sustets on diurnal intraocular pressure in patients with chronic simple glaucoma.

Twenty patients with primary open-angle glaucoma uncontrolled on single topical therapy completed a double dummy crossover study to compare acetazolamide tablets with a sustained release formulation (Sustet). The two preparations were equally effective, but no direct relationship was found between the intraocular pressure and the plasma concentration of acetazolamide. No difference between the formulations was found in the frequency or severity of side effects.

Acetazolamide↗
PubMed1993

Prophylactic use of acetazolamide to prevent intraocular pressure elevation following Nd-YAG laser posterior capsulotomy.

Fifty four eyes of 54 patients undergoing Nd-YAG laser posterior capsulotomy were randomly assigned to pretreatment with either 125 mg of oral acetazolamide (group A) or placebo (group B). During the first 3 hours following capsulotomy, an intraocular pressure (IOP) rise of at least 10 mm Hg was recorded in eight of the 26 eyes of group B (30.8%) and in none of the 28 eyes of group A (p < 0.01). A rise of at least 5 mm Hg was recorded in 16/26 (61.5%) and 4/28 (14.3%) eyes respectively (p < 0.001). Three eyes of group B developed an IOP greater than 35 mm Hg. We found that pretreatment with a low dose of acetazolamide is highly effective in preventing IOP elevation following Nd-YAG laser posterior capsulotomy.

Acetazolamide↗
PubMed1975

Treatment with acetazolamide of brain-stem and spinal paroxysmal disturbances in multiple sclerosis.

Nine cases of multiple sclerosis with paroxysmal disorders were treated with acetazolamide. In most cases a brain-stem origin of the seizures was suggested by their particular pattern: crossed syndromes (facial spasm associated with contralateral weakness of the arm and leg, paroxysmal paraesthesiae in one side of the face and weakness of the contralateral leg), paroxysmal dysarthria, and ataxia. One patient with a Brown-Sequard syndrome complained of paroxysmal paraesthesiae in the lower limbs, for which a spinal origin was admitted. In all patients the paroxysmal disorders were promptly suppressed or markedly reduced by acetazolamide.

Acetazolamide↗
PubMed1997

Cerebral blood flow and cerebrovascular response to acetazolamide in patients with chronic alcoholism.

Cerebral blood flow and cerebrovascular response to acetazolamide were studied in 12 patients with chronic alcoholism and 12 age matched healthy controls. Blood flows in the cerebral cortex, thalamus, and putamen were significantly lower in the chronic alcoholic group than in the healthy control group. The increase in blood flow caused by acetazolamide did not show any significant difference between the two groups. These findings suggest that the decreased cerebral blood flow in chronic alcoholism is due to decreased cerebral metabolism.

Acetazolamide↗
PubMed1991

Gastric HCO3- secretion: relationship with Na+ secretion and effect of acetazolamide in humans.

We examined the relationship between gastric HCO3- and Na+ secretion under fasting and sham-fed conditions in nine healthy men and also evaluated the effect of the carbonic anhydrase inhibitor acetazolamide on gastric secretion of HCO3- and Na+. Secretion of H+, K+, and Cl- were also measured. Gastric HCO3- secretion rates under fasting and sham-fed conditions closely paralleled Na+ secretion rates. A maximally tolerated intravenous dose (10 mg/kg) of acetazolamide significantly inhibited H+, Cl- and K+ secretion but did not significantly affect Na+ or HCO3- secretion. Thus the gastric mucosa secretes HCO3- and Na+ in parallel in humans both under fasting and sham-fed conditions. Relative to parietal secretion of HCl, nonparietal secretion of HCO3- and Na+ is resistant to carbonic anhydrase inhibition.

Acetazolamide↗
PubMed1990

Cerebral blood flow and end-tidal PCO2 during prolonged acetazolamide treatment in humans.

One oral dose of 1,000 mg of acetazolamide caused an acute 38% increase in cerebral blood flow (CBF) in eight healthy volunteers. During the following 10 days the subjects took 1,000 mg acetazolamide daily. CBF normalized within the first 2 days. The drug induced mild hyperventilation, gradually decreasing alveolar PCO2 to 70% of the control value at the end of the treatment period. In healthy humans the hyperventilation will not increase brain oxygenation significantly at sea level. But at high altitudes the enhanced ventilatory drive will improve oxygenation of the brain, and this may account for the beneficial effects of the drug on the symptoms of acute mountain sickness. During the treatment there was a significant 10% decrease of the hematocrit but an unaltered hemoglobin concentration. In combination with data in the literature our studies suggest that the initial CBF increase is a consequence of a transient extracellular acidosis dilating brain arterioles, whereas increased ventilatory drive results from a gradually increasing mild intracellular acidosis in the brain.

Acetazolamide↗
PubMed2000

Benzolamide, acetazolamide, and signal transduction in avian intrapulmonary chemoreceptors.

Intrapulmonary chemoreceptors (IPC) are CO(2)-sensitive sensory neurons that innervate the lungs of birds, help control the rate and depth of breathing, and require carbonic anhydrase (CA) for normal function. We tested whether the CA enzyme is located intracellularly or extracellularly in IPC by comparing the effect of a CA inhibitor that is membrane permeable (iv acetazolamide) with one that is relatively membrane impermeable (iv benzolamide). Single cell extracellular recordings were made from vagal filaments in 16 anesthetized, unidirectionally ventilated mallards (Anas platyrhynchos). Without CA inhibition, action potential discharge rate was inversely proportional to inspired PCO(2) (-9.0 +/- 0.8 s(-1). lnTorr(-1); means +/- SE, n = 16) and exhibited phasic responses to rapid PCO(2) changes. Benzolamide (25 mg/kg iv) raised the discharge rate but did not alter tonic IPC PCO(2) response (-9.8 +/- 1.6 s(-1). lnTorr(-1), n = 8), and it modestly attenuated phasic responses. Acetazolamide (10 mg/kg iv) raised IPC discharge, significantly reduced tonic IPC PCO(2) response to -3.5 +/- 3.6 s(-1). lnTorr(-1) (n = 6), and severely attenuated phasic responses. Results were consistent with an intracellular site for CA that is less accessible to benzolamide. A model of IPC CO(2) transduction is proposed.

Acetazolamide↗
PubMed1981

Effects of CO2 and acetazolamide on bicarbonate and fluid transport in rabbit proximal tubules.

Early superficial (SF) and juxtamedullary (JM) proximal convolutions of the rabbit kidney were perfused in vitro to determine the effects of carbonic anhydrase inhibition (10(-4) M acetazolamide) and acute changes in PCO2 (decreases to approximately equal to 15 and increases to approximately equal to 74 mmHg) on potential differences (PD in mV), volume reabsorption (Jv in nl x mm-1 x min-1), and bicarbonate reabsorption (JCO2 in pmol x mm-1 x min-1). At PCO2 37 mmHg early JM exhibited a more lumen-negative PD (-7.5 vs. -5.3), greater Jv (1.13 vs. 0.82), and greater JCO2 (86.7 vs. 44.4) than early Sf. Sf and JM had similar responses to acetazolamide: PD became more negative (-5.2 to -5.9 in SF; -8.8 to -10.1 in JM), Jv decreased (0.92 to 0.68 in SF; 1.11 to 0.76 in JM), and JCO2 decreased (35.7 to 7.7 in SF; 99.2 to 27.4 in JM). Increasing PCO2 to approximately equal to 74 mmHg decreased lumen-negative PD, increased Jv, and increased JCO2 in SF and JM (-5.5 to -4.8, 0.72 to 0.95, and 47.6 to 80.4 in SF; -6.6 to -5.7, 1.19 to 1.47, and 78.0 to 111.3 in JM). Decreasing PCO2 to approximately equal to 15 mmHg increased lumen-negative PD, decreased JCO2, but had no effect on Jv in both segments (-4.9 to -5.8, 51.3 to 6.3, and 0.80 to 0.79 in SF; -7.0 to -7.9, 75.3 to 19.6, and 1.34 to 1.41 in JM). It is concluded that 1) early SF and JM display quantitative heterogeneity, 2) PCO2 changes within the physiologic range produce large changes in HCO3 absorption in early proximal tubules and 3) large changes in HCO3- reabsorption are dissociated from changes in volume reabsorption during hypocapnia.

Acetazolamide↗
PubMed1984

Electrochemical heterogeneity of the cochlear endolymph: effect of acetazolamide.

The electrochemical composition of endolymph (EL) of two adjacent cochlear turns was studied in anesthetized rats. Differences in [K]EL, [Cl]EL, and endocochlear potential (EP) were found between the basal turn (165.6 +/- 3.0 mM, n = 14; 144.6 +/- 2.1 mM, n = 14;96.6 +/- 1.9 mV, n = 5, respectively) and the middle turn (155.7 +/- 2.5 mM, n = 15; 133.2 +/- 1.5 mM, n = 15; 87.0 +/- 1.6 mV, n = 6, respectively). The pH values of inner ear fluids were evaluated with 5,5-dimethyloxazolidine-2,4-dione: EL pH of either turn was not different from blood and perilymph (PL) pH. Acetazolamide (40 mg X kg body wt-1) reduced EP and [Cl]EL at each turn by about 20 and 6%, respectively, but [K]EL was unchanged. The electrochemical differences between the two turns persisted. Acetazolamide produced a 0.2-unit decrease in blood pH while the pH values of EL and PL remained unchanged. These results suggest the existence of an electrochemical gradient within EL from the base to the apex of the cochlea involving K+ and Cl- concentrations. H+ and HCO-3 do not appear to participate in this gradient, and the acid-base status in EL could be maintained both by active H+ transport into EL and by HCO-3 formation in the cochlear epithelium.

Acetazolamide↗
PubMed1983

Effect of acetazolamide on normoxic and hypoxic exercise in humans at sea level.

Acetazolamide (A) is a potent inhibitor of carbonic anhydrase. It has been shown to be efficacious in preventing acute mountain sickness as well as decreasing the O2 desaturation that occurs during sleep in individuals with chronic mountain sickness who live at altitude. Very little data, however, are available about its effect on exercise. We studied six healthy males in a double-blind cross-over design using acetazolamide and placebo (P) during normoxic and hypoxic (fractional inspired O2 = 0.118) progressive work exercise to exhaustion on a bicycle ergometer. A metabolic acidosis was documented in all subjects on A (P less than 0.045). Before exercise, subjects on A had 2.0 and 3.5 l/min increase in minute ventilation (VE) during normoxia (P = not significant) and hypoxia (P less than 0.005), respectively, and a 2.2% increase in arterialized O2 hemoglobin saturation (SaO2) during hypoxia. During normoxic and hypoxic exercise, VE/kpm and SaO2/kpm were significantly higher while the respiratory exchange ratio (R) was significantly lower on A. These effects were greater on hypoxia. During normoxia, maximal O2 consumption (1/min) was lower on A [3.1 +/- 0.4 (A) vs. 3.8 +/- 0.2 (P), P less than 0.025] and higher during hypoxia on A[2.6 +/- 0.7 (A) vs. 2.4 +/- 0.1 (P), P less than 0.05]. The increase in exercise VE on A may result in an increased alveolar and subsequent arterial O2 tension which may be important for exercise at altitude. Carbonic anhydrase inhibition may also affect CO2 transport in the lung, which may explain the lower R.

Acetazolamide↗
PubMed1998

Acetazolamide in the treatment of acute mania. A case report.

Several antiepileptic drugs are also being used in affective disorders. There are some hints that also the carbonic anhydrase inhibitor acetazolamide might be useful in the treatment of bipolar affective disorder. We report a 39-year-old male patient with a history of bipolar affective disorder who presented with his second manic episode. Acetazolamide was added to a low dose of valproic acid and to perazine. A marked decrease of the BRMAS score was achieved. The implications of this case are discussed.

Acetazolamide↗
PubMed1980

Electron microscopic study of the parathyroid gland of the acetazolamide-treated mouse.

Ultrastructural aspects of the parathyroid glands of acetazolamide-treated mice were examined. Many chief cells of the treated mice are deficient in free ribosomes compared with the control mice. Most Golgi complexes are poorly developed and associated with a few prosecretory granules. However, relatively numerous secretory granules are observed in the cytoplasm, and a few secretory granules are present in the peripheral cytoplasm. Large secretory granules (storage granules), homogeneously dense bodies with a low electron density, heterogeneously dense bodies containing osmiophilic substance and/or lipid-like material, multivesicular bodies and lipid droplets have apparently increased in number in many chief cells of the experimental mice. Many transitional forms are recognized between each of the large secretory granules and the bodies mentioned above. These ultrastructural features suggest that parathyroid gland cellular activity is suppressed in response to acetazolamide treatment. In addition, correlations of the occurrence of large secretory granules and various bodies are discussed.

Acetazolamide↗
PubMed1989

Tamm-Horsfall protein accumulation in glomeruli during acetazolamide-induced acute renal failure.

A patient with ocular hypertension was treated with acetazolamide. Acute renal failure developed rapidly and renal biopsy showed mild tubular lesions and crystal formation in a tubular lumen. By immunofluorescence studies with a monoclonal antibody, Tamm-Horsfall protein, normally absent from the proximal segments of the nephron, was detected in most glomeruli. This strongly suggests that tubular obstruction plays a major part in some cases of acetazolamide-induced acute renal failure.

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