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PubMed1983

Effect of acetazolamide on barbiturate-induced sleeping time in mice. III. Pharmacokinetics of serum elimination and brain distribution.

Effects of acetazolamide (AZA) on the serum elimination and brain distribution of barbital (BA), phenobarbital (PHB), pentobarbital (PEB) and hexobarbital (HB) were studied in mice. When the barbiturates were administered intraperitoneally to mice, the pretreatment of AZA reduced the serum BA and PHB levels, and significantly increased these brain levels. While relatively small and no effects of AZA were observed for the PEB and HB levels, respectively. After the intravenous administration, the serum elimination of these barbiturates were described by the two compartment model. Although the pretreatment of AZA tended to increase the volumes of central compartment and decrease the elimination rate constants for BA, PHB and PEB, the elevated brain levels of the barbiturates could not be explained as the simulated peripheral concentrations. However, it appeared that the prolongation effect of AZA on the BA, PHB and PEB sleeps in mice was associated with the elevated brain barbiturate levels with AZA.

Acetazolamide↗
PubMed1986

Gastroduodenal HCO3-secretion in anesthetized rats: effects of 16,16-dimethyl PGE2, topical acid and acetazolamide.

Alkaline secretion was measured in the whole stomach and in the proximal duodenum (2 cm proximal to the outlet of the common bile duct) of anesthetized rats, under basal conditions and in response to topical acid and 16,16-dimethyl PGE2 (16-dmPGE2) given by various routes. Gastric alkaline secretion was unmasked by intraduodenal administration of omeprazole (30 mg/kg). Both the stomach and duodenum consistently secreted bicarbonate in amounts of 0.2-0.4 microEq/15 min and 1.5-2 microEq/15 min as a basal secretion, respectively. 16-dmPGE2, either given subcutaneously (1-30 micrograms/kg), intravenously (3 micrograms/kg/hr) or by topical application for 30 min (0.3-10 micrograms/ml), (concentration)-dependently increased HCO3- secretion in both tissues, but this effect disappeared quickly after sacrifice with KCI (i.v.). Stimulation of HCO3- secretion was also caused by topical acid to the stomach (100 mM HCI for 10 min) or to the duodenum (10 mM HCI for 10 min), but was completely blocked by pretreatment with indomethacin (5 mg/kg, s.c.). Acetazolamide, given subcutaneously at 100 mg/kg, which gives over 80% inhibition of carbonic anhydrase activity in the gastroduodenal mucosa, had no effect on either basal or stimulated HCO3- secretion caused by 16-dmPGE2 (10 micrograms/kg, s.c.). These results indicate that both endogenous and exogenous (16-dmPGE2) prostaglandins stimulate alkaline secretion in the gastroduodenal mucosa of rats, and this mechanism is independent from the carbonic anhydrase activity of the tissue.

16,16-Dimethylprostaglandin E2↗
PubMed1987

Roles of gastric motility changes in cytoprotection induced by acetazolamide and cysteamine in rats.

The present study was undertaken using acetazolamide (AZ) and cysteamine (Cys) to investigate the relationship between gastric motor activity and the phenomenon of "cytoprotection" in rats. Both AZ (10-100 mg/kg) and Cys (10-100 mg/kg), given either p.o. or s.c., significantly reduced the formation of gastric mucosal injury caused by HCl-ethanol (1 ml of 60% ethanol in 150 mM HCl, p.o.). The protective effect of Cys appeared within 10 min, reached the maximal levels 30 min later, while that of AZ appeared from 30 min after administration and became potent with a latency period after treatment. Neither indomethacin (IM: 5 mg/kg, s.c.) nor N-ethylmaleimide (NEM: 5 mg/kg, s.c.) significantly affected the protective effect of Cys, whereas that of AZ was almost totally antagonized by IM. Both AZ and Cys, given either intragastrically or s.c., significantly inhibited gastric motor activity measured as intraluminal pressure recordings, but had minimal effect on acid and alkaline secretion. IM significantly attenuated the inhibitory effect of AZ on the motor activity, while NEM did not affect the inhibited motor responses caused by AZ and Cys. A significant relationship was found between the inhibitory effects of these two drugs on gastric motor activity and HCl-ethanol-induced mucosal injury, the correlation coefficient being 0.819 (P less than 0.01). When the mucosal folds were visualized with Gentian Violet (1 ml of 0.5% v/v, p.o.), both AZ and Cys significantly prevented the localized staining along the mucosal folds, suggesting dissolution of the folds. These results suggest that both AZ and Cys protect the gastric mucosa against injury caused by HCl-ethanol, probably through a dissolution of mucosal folds due to inhibition of gastric motor activity.

Acetazolamide↗
PubMed2005

Feasibility study of serial lumbar puncture and acetazolamide combination in the management of elevated cerebrospinal fluid pressure in AIDS patients with cryptococcal meningitis in Uganda.

A feasibility study of serial lumbar puncture and acetazolamide combination in managing raised cerebrospinal fluid pressure was undertaken in 18 patients with AIDS and cryptococcal meningitis in Uganda. There were no adverse events related to the intervention and improvement in minimental status score, performance score, symptoms and a reduction in intracranial opening pressure were observed. This method is therefore feasible in AIDS-associated cryptococcal meningitis in a resource-poor setting given the observed safety and possible effectiveness, a larger study is warranted.

AIDS-Related Opportunistic Infections↗
PubMed2002

Effects of acetazolamide and furosemide on ventilation and cerebral blood volume in normocapnic and hypercapnic patients with COPD.

STUDY OBJECTIVES: Effects of chronic metabolic alkalosis and acidosis and their relation to central chemoregulation may differ between normocapnic and chronic hypercapnic patients with COPD. The relationship between responses of inspired ventilation (VI), mouth occlusion pressure (P(0.1)), and cerebral blood volume (CBV), to short-term changes in arterial PCO(2) was measured. PATIENTS AND METHODS: Seventeen patients with chronic hypercapnia and COPD (PaCO(2) > 6.0 kPa) and 16 normocapnic patients with COPD (PaCO(2) < or = 6.0 kPa) [FEV(1) 27% predicted] were studied under baseline metabolic conditions and after 1 week of treatment with oral furosemide, 40 mg/d, or acetazolamide, 500 mg/d. Hypercapnia (change in end-tidal carbon dioxide > 1 kPa) was induced by administering adequate amounts of carbon dioxide in the inspired air. CBV was measured using near-infrared spectroscopy. RESULTS: Compared with baseline metabolic condition, chronic metabolic acidosis and alkalosis did not change ventilatory (Delta VI/Delta PaCO(2)) and cerebrovascular (Delta CBV/Delta PaCO(2)) reactivity. Base excess (BE) decreased by 6.8 +/- 1.1 mEq/L and 6.9 +/- 1.6 mEq/L, respectively, in the normocapnic and chronic hypercapnic COPD groups during metabolic acidosis, resulting in a not-quite-significant leftward shift of both the ventilatory and cerebrovascular carbon dioxide response curve. BE increased by 2.3 +/- 1.2 mEq/L and 1.2 +/- 1.3 mEq/L, respectively, during chronic metabolic alkalosis in both COPD groups, without concomitant shift. Poor correlations between ventilatory and cerebrovascular carbon dioxide responsiveness (Delta CBV/Delta PaCO(2) and Delta VI/Delta PaCO(2), Delta CBV/Delta PaCO(2) and Delta P(0.1)/Delta PaCO(2), respectively) were found irrespective of baseline, respiratory condition, and induced metabolic state. CONCLUSIONS: Normocapnic and chronic hypercapnic COPD patients have the same ventilatory and cerebrovascular carbon dioxide responsiveness irrespective of induced metabolic state.

Acetazolamide↗
PubMed1996

Drug-induced hypoglycemia presenting as acute mountain sickness, after mistaking acetohexamide for acetazolamide.

Acute mountain sickness (AMS) can present with a wide variety of symptoms in unacclimatized persons who rapidly ascend to altitudes > 2500 m. The clinical manifestations of drug-induced hypoglycemia, including adrenergic and neurologic symptoms, have significant overlap with the AMS symptom complex. These similarities can lead to confusion in the diagnosis of hypoglycemia versus AMS, particularly for diabetics ascending to altitude. A case is described in which the oral hypoglycemic agent acetohexamide, instead of acetazolamide, was mistakenly self-administered for the prophylaxis and treatment of altitude illness. Improper self-medication by travelers in remote areas may be more common than is currently recognized.

Acetazolamide↗
PubMed1987

Cyclic AMP-stimulated fluid transport in the thyroid: influence of thyroid stimulators, amiloride and acetazolamide on the dynamics of domes in monolayer cultures of porcine thyroid cells.

Confluent monolayer cultures of porcine thyroid cells form dome-shaped elevations by local separation from the plastic culture dish. Formation of domes by epithelial cells in culture is generally considered to be evidence of fluid transport. A computer-controlled data acquisition system was developed to quantitate fluid transport in thyroid cultures by serial measurements of dome elevation. Thyrotrophin (10 mU/ml), prostaglandin E2 (PGE2; 0.01-1 mumol/l), forskolin (1 mumol/l), 8-(4-chlorophenylthio)adenosine 3':5'-cyclic monophosphate (0.5 mmol/l) and 3-isobutyl-1-methyl-xanthine (0.5 mmol/l) promoted increases in dome height over 5-120 min. Dome growth in the presence of PGE2 (1 mumol/l) was inhibited by amiloride (0.1-100 mumol/l), ouabain (200 mumol/l), or by removal of bicarbonate and glucose from the medium. In media of reduced bicarbonate concentration (1 mmol/l compared with the control concentration of 10 mmol/l), dome growth was inhibited by acetazolamide (0.01-1 mmol/l). These data are consistent with cyclic AMP-stimulated transport of fluid from apical to basal pole of the cells, dependent on sodium entry through the apical pole by an Na+/H+ exchanger.

Acetazolamide↗
PubMed2002

Acetazolamide-induced muscle weakness in hypokalemic periodic paralysis.

A 46-year-old man with hypokalemic periodic paralysis (HypoPP) and diabetes mellitus (DM) had worsened muscle weakness after acetazolamide (ACZ) treatment. During the paralytic episode, serum potassium levels were reduced, and serum chloride and insulin levels were increased. The data suggested proximal renal tubular acidosis due to ACZ. We determined arterial-venous concentrations of potassium, insulin and glucose across the forearm. Venous potassium levels were markedly reduced. ACZ is thought to potentiate potassium uptake into muscles. Hyperinsulinemia and DM could contribute to ACZ-induced exacerbation in our patient. We should pay more attention to ACZ-treated HypoPP patients with hyperinsulinemia and DM.

Acetazolamide↗
PubMed1991

Drug-induced hypotension SEP test and acetazolamide test using 133Xe SPECT in patients with occlusive carotid disease--selection of candidates for extracranial-intracranial bypass.

The correlation between the drug-induced hypotension somatosensory evoked potential (SEP) test and regional cerebral blood flow changes after acetazolamide administration was studied. Fourteen patients presenting with transient ischemic attack, reversible ischemic neurological deficits, or minor completed stroke were evaluated. All patients had no or only localized low-density areas on computed tomographic scans, and unilateral occlusion or severe stenosis of the internal carotid or middle cerebral artery on cerebral angiograms. The Diamox asymmetry enhancement (DAE) was studied to detect reduced cerebral perfusion reserve in the affected hemispheres. The DAE was 7.9 +/- 5.8% in seven patients positive in the SEP test, significantly higher than -1.5 +/- 2.9% in patients negative in the SEP test. Postoperative SEP tests were negative in all five patients who underwent extracranial-intracranial (EC-IC) bypass surgery, suggesting that the EC-IC bypass improved the cerebral perfusion reserve in the affected hemispheres. The DAE decreased significantly in four of these patients. This study disclosed a significant correlation between the drug-induced hypotension SEP test and DAE. These parameters are considered important for evaluating patients with hemodynamic compromise and/or suitable candidates for EC-IC bypass.

Acetazolamide↗
PubMed1989

The acetazolamide challenge: imaging techniques designed to evaluate cerebral blood flow reserve.

Cerebral blood flow was analyzed by the stable xenon (Xe)/CT scanning technique in 29 patients with significant vascular lesions before and after administration of an acetazolamide (Diamox) vasodilatory challenge. Three response types were identified: I, normal flow before Diamox with flow augmentation after Diamox; II, low flow before Diamox with flow augmentation after Diamox; and III, low or normal flow before Diamox with no augmentation or decreased flow after Diamox. Twenty-four percent of the patients studied qualified for category III. We believe that patients in this category represent a group of individuals without blood flow reserve whose clinical management should include careful consideration of their hemodynamic status. The Xe/CT scanning technique with the addition of Diamox flow challenge is a clinically accessible and effective method for assessing cerebral blood flow and blood flow reserve.

Acetazolamide↗
PubMed1992

Interaction of catecholamine and acetazolamide in the action on the endolymphatic sac direct current potential.

Our recent studies have revealed that catecholamines depress the endolymphatic sac DC potential (ESP) by beta-adrenergic action, and that acetazolamide (ACTZ), a potent carbonic anhydrase inhibitor, decreases the ESP. The interaction of ACTZ and isoproterenol (Iso), a nonselective beta agonist, in their action on the ESP was examined in the guinea pig. Intravenous administration of Iso (6.25 micrograms/kg/min) and ACTZ (10 mg/kg) reduced the ESP amplitude by 38.5 +/- 5.9% (n = 8) and 39.8 +/- 3.7% (n = 8), respectively. Co-administration of both agents reduced the ESP amplitude by 62.3 +/- 3.3% (n = 8). The ESP change induced by co-administration was significantly larger than that by the administration of each agent alone. Co-treatment with Iso and ACTZ at doses producing near-maximum reduction of the ESP depressed almost all parts of oxygen-dependent components of the ESP. The results suggest that Iso and ACTZ decrease the ESP via mechanisms different from each other, and that oxygen-dependent components of the ESP are composed of Iso- and ACTZ-sensitive parts.

Acetazolamide↗
PubMed1981

Acetazolamide interferes with the protective effect of prostaglandin E2 in the rat gastric mucosa.

Oral prostaglandin E2 protected the gastric mucosa against the damage induced by intraperitoneal indomethacin in the rat. Blocking of the gastric alkaline secretion by subcutaneous acetazolamide potentiated the ulcerogenic action of indomethacin and reduced or abolished the protective effect of a submaximal dose prostaglandin E2. The results are compatible with the hypothesis that stimulation of the alkaline secretion is one of the mechanisms by which prostaglandin E2 protects the gastric mucosa.

Acetazolamide↗
PubMed1986

Effect of dextran-bound acetazolamide on rabbit corneal endothelial ion fluxes.

The effects of a carbonic anhydrase inhibitor, acetazolamide, bound to a 72,000 dalton dextran (DBI) on bicarbonate and sodium fluxes across the isolated rabbit corneal endothelium have been examined. When DBI was present on the aqueous-facing endothelial surface, there was a marked inhibition of both the stromal to endothelial unidirectional and net flux of bicarbonate. This suggests that the exit of bicarbonate from the cell into the aqueous-facing solution is influenced by the enzyme carbonic anhydrase. No change was found in sodium fluxes under these same incubation conditions. When DBI was present on the stromal-facing surface of the endothelium, no changes were found in unidirectional or net bicarbonate fluxes; the sodium flux from stroma to endothelium was increased, however, with no change in net flux. This data implies that the link between sodium and bicarbonate movement across the endothelium is not a direct coupling between the transport of the two ions in the form of a symport (Na+:HCO3-) at the apical cell border.

Acetazolamide↗
PubMed1996

Effect of acetazolamide and melittin on polarization of the frog gastric mucosa proton pump.

We have shown that polarization of an electrogenic H+/K+ ATPase pump located in the secretory (luminal) membrane of the frog gastric mucosa is the major factor contributing to the change in open circuit potential difference (OCPD) induced by voltage clamping. This transmucosal polarization was markedly reduced by H2 blockers famotidine and cimetidine, and by the H+/K+-ATPase inhibitors omeprazole and SCH 28080. SCN-, a nonspecific H+ secretion inhibitor, did not affect the polarization. In the present experiments, the effects of two other inhibitors of H+ secretion were examined, namely, acetazolamide (AA), a carbonic anhydrase inhibitor, and melittin (MEL), an inhibitor of the H+/K+-ATPase enzyme. When AA 10(-3) M or MEL 10(-5) M was added to the nutrient solution, H+ secretion was completely inhibited. While MEL markedly reduced the polarization induced by voltage clamp, AA did not affect the polarization. These data support the concept that MEL directly affects the electrogenic H+/K+-ATPase pump while the inhibition of H+ secretion by AA is by an indirect mechanism. The data further support the electrogenicity of the H+/K+-ATPase.

Acetazolamide↗
PubMed2003

[Development of quantification analysis software for measuring regional cerebral blood flow by the modified split-dose method with (123)I-IMP before and after acetazolamide loading].

We developed a quantification analysis software program for measuring regional cerebral blood flow (rCBF) at rest and under acetazolamide (ACZ) stress by the modified split-dose (MSD) method with iodine-123 N-isopropyl-p-iodoamphetamine (IMP) and compared the rCBF values measured by the MSD method and by the split dose (123)I-IMP SPECT (SD) method requiring one continuous withdrawal of arterial blood. Since the MSD method allows the input of two arterial blood sampling parameter values, the background subtraction procedure for obtaining ACZ-induced images in the MSD method is not identical to the procedure in the SD method. With our software program for rCBF quantification, the resting rCBF values determined by the MSD method were closely correlated with the values measured by the SD method (r=0.94), and there was also a good correlation between the ACZ-induced rCBF values obtained by the MSD method and by the SD method (r=0.81). The increase in rCBF under ACZ stress was estimated to be approximately 26% by the SD method and 38% by the MSD method, suggesting that the MSD method tends to overestimate the increase in rCBF under ACZ stress in comparison with the SD method, but the variability of the rCBF values at rest and during ACZ stress analyzed by the MSD method was smaller than the variability with the SD method. Further clinical studies are required to validate our rCBF quantification analysis program for the MSD method.

Acetazolamide↗
PubMed1999

Cascade of acetazolamide-induced vasodilatation.

UNLABELLED: Acetazolamide (AZ) has been found to be effective in inducing vasodilatation. To evaluate the mechanism by which AZ acts, we compared the effects of this agent on vascular PGI2, endothelin (ET-1), and NOx, with those induced by CO2 gas inhalation. METHOD: Blood flow (BF) was measured in the liver, kidneys, stomach wall, and abdominal muscle of anesthetized white rabbits with a laser flow meter at baseline and again after sequential doses of AZ (4 mg/kg) or CO2 inhalation. Cardiac output and serum concentrations of PGI2, ET-1, and NOx were also measured in these animals. RESULTS: AZ increased BF in the liver and kidneys, but had no effect on BF in the stomach wall or abdominal muscle. The level of NOx was decreased following the administration of AZ, while PGI2 and ET-1 levels remained unchanged. In contrast, CO2 inhalation increased PCO2, and decreased pH, significantly. CO2 elevated BF in the liver, kidneys, stomach wall, and abdominal muscle, as well as serum levels of PGI2 and ET-1, while having no effect on NOx levels. The alterations in BF, PGI2, ET-1, and NOx in response to AZ, suggest that the mechanism of AZ-induced vasodilatation may involve a cascade that is triggered by CO2 retention similar to that caused by the inhalation of CO2.

6-Ketoprostaglandin F1 alpha↗
PubMed2000

Cerebellar vasoreactivity in stroke patients with crossed cerebellar diaschisis assessed by acetazolamide and 99mTc-HMPAO SPECT.

UNLABELLED: Crossed cerebellar diaschisis (CCD) tends to persist or even worsen after supratentorial infarction. Several studies have shown impairment of cerebral vasomotor responsiveness in the hemispheric area of diaschisis in patients with hemispheric infarction. This finding has led to the concern that the lack of CCD reversibility might be associated with chronic circulatory abnormalities. We therefore assessed the vasoreactivity in the cerebellar hemisphere in which diaschisis is manifested using acetazolamide (ACZ) and SPECT. METHODS: Eight stroke patients with CCD (5 with unilateral hemispheric infarcts and 3 with unilateral intracerebral hemorrhage) had 99mTc-HMPAO SPECT scanning at rest and 20 min after intravenous injection of 1.0 g ACZ. The time interval after stroke ranged from 25 to 904 d. From the total counts obtained from each cerebellar hemisphere, the asymmetry index (AI) was calculated as (unaffected - affected cerebellar hemisphere)/unaffected cerebellar hemisphere x100. RESULTS: After ACZ, the mean AI (8.7+/-6.6) was significantly decreased (P<0.05) compared with that at rest (17.7+/-5.8). Seven of the 8 patients showed decrease in the AI after ACZ. In 1 patient, the direction of the asymmetry was reversed after ACZ so that the AI was negative. The ACZ-induced change in the AI did not show a significant correlation with the time interval after stroke, whether calculated in absolute terms or as a percentage change. CONCLUSION: This study shows that normal vascular supply is maintained in the CCD-affected cerebellar hemisphere over long periods of time after a stroke. Thus, the lack of CCD reversibility may not be attributed to a chronic circulatory insufficiency. The results lend support to the concept of functional deactivation and subsequent transneuronal degeneration as a likely explanation for CCD. It is unclear whether decreased AI after ACZ indicates a higher vascular response of the affected cerebellar hemisphere than that of the normal side.

Acetazolamide↗