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PubMed1990

[Diagnosis of hemodynamic compromise in patients with chronic cerebral ischemia; the detection of impaired vasodilatory capacity with 133Xe SPECT and acetazolamide (Diamox) test].

To evaluate the efficacy of 133Xe SPECT and Diamox test, for selecting patients with hemodynamic compromise, tests using 133Xe inhalation method and single photon emission computed tomography (SPECT) with acetazolamide (Diamox) were performed in twenty-three patients with chronic cerebral ischemia, before and after extracranial-intracranial bypass surgery or carotid-endarterectomy. All patients complained of TIA, RIND, or minor completed stroke, and cerebral angiography of all patients demonstrated severe stenosis or occlusion in the ipsilateral internal carotid artery or middle cerebral artery. Cerebral blood flow (CBF) was also measured 15 minutes after intravenous administration of 10-12 mg/kg Diamox, which is known as a cerebral vasodilatory agent (Diamox test). Our results revealed that all patients could be divided into four types according to the findings of their resting rCBF and Diamox reactivity. The patients who had normal resting rCBF and normal Diamox reactivity (type 1) were considered to have well-developed collateral circulation and normal cerebral perfusion pressure (CPP) in spite of severe occlusive lesions in the carotid system. Moderate vasodilatation due to reduced CPP was considered to occur in patients who had normal resting rCBF and decreased Diamox reactivity (type 2). The resting rCBF remained unchanged, but Diamox reactivity improved to the normal range after surgery in the patients of type 2 (p less than 0.01), which indicated the improvement of CPP and the resolution of the autoregulatory vasodilatation. Maximum vasodilatation or dysautoregulation was considered to occur due to the inadequate collateral flow and the severely reduced CPP in patients whose findings revealed decrease in the resting rCBF and impaired Diamox reactivity (type 3).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1990

Normoxic and acute hypoxic exercise tolerance in man following acetazolamide.

The influence of acetazolamide (ACZ) upon the ability to perform and sustain maximal and submaximal exercise bouts under normoxic and hypoxic conditions was examined in four groups of healthy male subjects (N = 27). ACZ (500 mg) or inert placebo (Pla) was administered prior to exercise in a quasi-randomized, double-blind, crossover fashion. ACZ was shown to lower venous pH (ACZ, 7.31 +/- 0.01, vs Pla, 7.35 +/- 0.08) and bicarbonate (ACZ, 22.4 +/- 0.27 mM, vs Pla, 25.4 +/- 0.6 mM) and to elevate urine pH (ACZ, 7.36 +/- 0.06, vs Pla, 5.84 +/- 0.19) and tended to elevate VE (P = 0.07) at rest. Peak VO2 measured using a continuous incremental protocol was unaltered in normoxia, while peak VCO2 and RER were lowered by ACZ. No significant effect of ACZ upon VO2, VCO2, RER, or heart rate (HR) was observed during submaximal exercise (75% of peak VO2) although VE was increased by 14% and time to exhaustion (EXHt) was reduced by 29%. During acute hypoxia at a simulated altitude of 4,270 m (Pbar = 446 mm Hg), no significant differences were noted in VE, VO2, VCO2, RER, HR, or arterial saturation (SaO2) at rest. Prior to exercise, venous pH (ACZ, 7.39 +/- 0.04, vs Pla, 7.44 +/- 0.007) and bicarbonate were lower with ACZ (ACZ, 21.6 +/- 0.46 mM, vs Pla, 24.2 +/- 0.25 mM), while urine pH was higher (ACZ, 7.6 +/- 0.07, vs Pla, 5.9 +/- 0.25). Other than a higher PCO2 and lower venous lactate with ACZ, no significant differences were identified at peak VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1975

CO2 retention as a basis for increased toxicity of salicylate with acetazolamide: avoidance of increased toxicity with benzolamide.

Two carbonic anhydrase inhibitors, acetazolamide and benzolamide, are capable of increasing the toxicity of sodium salicylate in mice. Beginning at about 2 mg/kg, each of the inhibitors, in combination with a fixed (400 mg/kg) dose of salicylate, generates a dose-mortality curve that reaches a plateau at about 60% deaths at 6 to 8 mg/kg. This effect can be duplicated by 8 to 10% inspired CO2. It appears that the respiratory acidosis secondary to the inhibition of red cell carbonic anhydrase is responsible for the increased toxicity; earlier work by others shows that acidosis increases the concentration of salicylate in the brain. In the treatment of salicylate poisoning by carbonic anhydrase inhibitors, the goal is to alkalinize the urine and increase the excretion of salicylate. With the newer inhibitor, benzolamide, it is possible to dissociate the respiratory acidosis from the renal effect. Maximal alkalinization of the urine is possible with a dose (about 1 mg/kg) below that which generates a respiratory acidosis. With this dose, there is no increase in the early toxicity of salicylate.

Acetazolamide↗
PubMed1978

pH-induced difference spectrophotometric assay of acetazolamide, hydrochlorothiazide, and furosemide.

On the basis of pH-induced spectral changes for acetazolamide, hydrochlorothiazide, and furosemide, 3 different spectrophotometric methods are described. The methods were successfully applied to the assay of these drugs in different pharmaceutical formulations (tablets and ampoules). The accuracy of the analysis is increased by using the suggested methods as compared with conventional spectrophotometry.

Acetazolamide↗
PubMed1989

Udder edema in cattle: effects of diuretics (furosemide, hydrochlorothiazide, acetazolamide, and 50% dextrose) on serum and urine electrolytes.

Blood and urine chemical values at parturition in clinically normal Holstein cows (n = 12) were compared with the same values in Holstein cows developing udder edema (n = 12). There was no statistically significant mean difference between the 2 groups for the serum and urine chemical data. Furosemide (500 mg) given IV caused a significant increase in serum calcium and sodium, urine chloride, potassium, and sodium, and fractional excretional ratio of chloride, potassium, and sodium. There was a significant mean decrease in the serum potassium, urine creatinine, osmolality, pH, and specific gravity. Hydrochlorothiazide (250 mg) given IV caused a significant mean increase in serum chloride, urine chloride, potassium, and sodium, and fractional excretion ratio of chloride, potassium, and sodium. There was a significant mean decrease in serum potassium and sodium, urine osmolality, pH, and specific gravity. Acetazolamide (500 mg) given IV caused a significant mean increase in blood urea nitrogen, serum chloride and glucose, urine sodium, and fractional excretion ratio of sodium, while causing a significant mean decrease in serum potassium, sodium, and phosphorus, and urine creatinine. Dextrose (500 g) given IV as a 50% solution caused a statistical mean increase in serum glucose, urine chloride, potassium, and sodium, and fractional excretion ratio of chloride and potassium. A statistical mean decrease occurred in the packed cell volume, blood urea nitrogen, serum calcium, potassium, sodium, and phosphorus, urine creatinine, osmolality, and pH.

Acetazolamide↗
PubMedDate not supplied

[Hypercapnia induced by acetazolamide and its effect on pulmonary circulation. Experimental study].

In order to evaluate the isolated hemodynamic effects of acute hypercapnea on pulmonary circulation, we designed a canine model in which vascular pressures. PaO2, and arterial pH were maintained within normal limits. Six mongrel dogs were studied. Hypercapnea was achieved by a single intravenous doses of acetazolamide (120 mg/Kg) while maintaining mechanical ventilation constant. Both arterial and mixed venous PCO2 increased from 27 to 41 mm Hg and from 31 to 46 mm Hg respectively, and remained constant through the rest of the experiment (up to 3 Hs). With hypercapnea, total pulmonary vascular resistance increased from 312 +/- 156 to 435 +/- 173 d.s.cm-5 (p less than 0.05) and the stroke index decreased from 20.7 +/- 8.3 to 13.2 +/- 4.8 ml/beat (p less than 0.05). There were no changes either in pulmonary capillary wedge pressure or in the right ventricular end diastolic pressure. The above changes suggest a pulmonary vasoconstrictor effect of hypercapnea in the absence of other known vasoactive factors.

Acetazolamide↗
PubMed1988

Tomographic cerebral blood flow measurements in patients with ischemic cerebrovascular disease and evaluation of the vasodilatory capacity by the acetazolamide test.

Cerebral blood flow (CBF) was measured in a series of patients with ischemic cerebrovascular disease using xenon-133 inhalation and single photon emission computer tomography. The spontaneous course of CBF changes in a consecutive series of stroke patients was evaluated. A quite heterogeneous pattern of flow changes was observed: In patients with large cortical/subcortical infarcts, extensive hypoperfused areas were observed, often significantly larger than the corresponding hypodense lesion on the CT scan. Smaller CT lesions caused relatively smaller flow changes. Patients with lacunar infarcts showed only a discrete reduction of CBF, but comprising most of the ipsilateral hemisphere. Repeated CBF studies in the chronic phase showed, that the clinical improvement commonly noted in stroke patients is not related to a CBF increase. On the contrary, the CBF lesions tended to become somewhat larger and more demarcated even in cases where the finding of a normal angiogram and a transient state of hyperemia suggested a dissolution of the intracerebral embolus. The pathogenetic mechanisms for these persisting low flow areas in CT intact structures was discussed. One possibility was a selective neuronal cell damage in the peri-infarct areas caused by the ischemic insult. Such lesions would leave the structures macroscopically intact, but decrease both the metabolic demands and CBF. However, this interpretation finds little support in recent microscopic neuropathological studies in man. A more likely possibility was then considered to be disconnection (diaschisis) where the reduced flow is due to a decreased neuronal function caused by undercutting of afferent or efferent nervefibers. A crossed cerebellar diaschisis was observed in all patients with major infarcts in the forebrain. These findings were observed already in the acute phase, but persisted quite unchanged throughout the subacute and chronic phases. The patients with lacunar infarcts showed cerebellar diaschisis in the acute phase only, suggesting that a transient suppression of remote areas is possible too. In order to differentiate between permanent flow changes caused by a functional impairment and a possible hemodynamic component, CBF was measured before and after administration of a potent cerebral vasodilator, acetazolamide (Diamox). In normal cases tested with Diamox, an even CBF increase is noted throughout the hemispheres, while the cerebral metabolic rate for oxygen remains stable. In patients having a severe stenosis or occlusion of the internal carotid artery, this vasodilatory stress test will identify the patients having poor collateral capacity via the circle of Willis.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetazolamide↗
PubMed1986

Acetazolamide enhancement of HIPDM brain flow distribution imaging.

Six patients with symptomatic cerebral vascular disease were studied with 133Xe regional cerebral blood flow measurements and HIPDM cerebral imaging after the administration of acetazolamide. The results obtained from this small group suggest this technique may have high sensitivity for detection of cerebral vascular disease.

Acetazolamide↗
PubMed1987

Udder edema in cattle: effect of furosemide, hydrochlorothiazide, acetazolamide, or 50% dextrose on venous blood pressure.

Before injection of diuretic drugs, blood pressures were determined in the cranial superficial epigastric veins (milk vein) and jugular veins of 15 Holstein cows with udder edema at parturition and of 15 healthy (control) cows at parturition. Cows with udder edema had a significant (P less than or equal to 0.05) mean increase in cranial superficial epigastric venous pressure at parturition, compared with that of control cows. After IV administration of 500 mg of furosemide in cows with udder edema, the mean cranial superficial epigastric venous blood pressure significantly (P less than or equal to 0.05) decreased within 5 minutes, remained at the decreased pressure for 90 minutes, and then returned to near pretreatment pressures by 210 minutes after furosemide injection; however, furosemide did not significantly affect the jugular venous blood pressure of these cows. Furosemide injection did not significantly affect the cranial superficial epigastric or jugular venous blood pressure in the control cows. After IV administration of hydrochlorothiazide (250 mg), acetazolamide (500 mg), or 50% dextrose (500 g), the cranial superficial epigastric and jugular venous blood pressures in cows with udder edema at parturition were not significantly different from those in cows without udder edema at parturition during the 210-minute evaluation period after injection of the drugs.

Acetazolamide↗
PubMed1987

Acetazolamide effect on the inward permeability of the blood-retinal barrier to carboxyfluorescein.

The inward permeability of the blood-retinal barrier to carboxyfluorescein was determined in 12 cynomolgus monkeys. Probenecid (175 mg/kg), an inhibitor of active outward transport of carboxyfluorescein, did not affect the inward permeability, indicating that the inward permeability is independent of the active outward transport system. However, acetazolamide (20 mg/kg), which causes increased outward fluid movement across the retinal pigment epithelium (RPE), significantly reduced the inward permeability. Thus, inward diffusion of carboxyfluorescein interacts with outward fluid flow across the RPE. Since carboxyfluorescein has low lipid solubility and remains extracellular, it is concluded that the pathway of fluid movement and carboxyfluorescein diffusion across the RPE is paracellular.

Acetazolamide↗
PubMed1985

[Familial paroxysmal ataxia sensitive to acetazolamide. 3 cases in a new European family].

UNLABELLED: This family is the tenth reported world-wide and the second reported in Europe. Two of 3 brothers, their mother and probably their maternal grandmother were affected. CLINICAL FEATURES: paroxysmal bouts of ataxia and dysarthria, nystagmus of permanent gaze, the dominant autosomal transmission, the benign nature of the affection and the remarkable efficacy of acetazolamide were typical of familial paroxysmal ataxia. Specific points emphasized are the presence of a mild pyramidal syndrome as a permanent finding in 2 of these patients, and the anomalies of visual (longer lag period) and somesthetic (slowed conduction rate in the lemniscus medialis) evoked potentials probably the result of extension into other pathways than the cerebellar system. The finding of some degree of glucose intolerance, noted previously (Aimard, Vighetto et al., 1983) raises the question of the place of this disease in the group of paroxysmal ataxias due to pyruvic metabolism disorders.

Acetazolamide↗
PubMed1979

Changes in the surface fine structure of rat third ventricular ependyma following chronic acetazolamide treatment.

Participation of non-choroidal elements, particularly of ventricular ependyma, in CSF production is well recognized. The present investigation is an attempt to elucidate possible surface changes in the ventricular lining following chronic acetazolamide administration in the rat. A progressive time-dependent change was observed in the ependyma of the third ventricle. In the dorsal ciliated zone the appearance of dilatations and surface evaginations on cilial shafts were the predominent features. The ventral non-cilated area was characterized by eruption of blebs and microvilli with apical swellings. The significance of these surface fine structural changes are discussed in the light of available studies. It appears that the ependyma is stimulated into increased activity. However, the precise nature of such a response--whether secretory or absorptive--must remain conjectural until correlative scanning and transmission electron microscopic data become available.

Acetazolamide↗
PubMed1983

Effects of thyrotropin, acetazolamide, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, perchlorate, ouabain and furosemide on pH and HCO3- concentrations in cells and luminal fluid of turtle thyroid as calculated from the distribution of [14C]dimethyloxazolidine-2,4-dione.

[14C]Dimethyloxazolidine-2,4-dione was used to determine the pH and bicarbonate concentration ([HCO3-]) in follicular cells and luminal fluid (LF) of turtle thyroids. Values of cellular and luminal pH and [HCO3-] were derived from the steady-state [14C]dimethyloxazolidine-2,4-dione values in whole gland and in the follicular LF sampled by micropipettes inserted into the follicular lumen and by resolution of the [14C]dimethyloxazolidine-2,4-dione uptake curve into its components by a computer program. In extracellular fluid of control turtles at 24 degrees C, the pH was 7.66, [HCO3-] was 33.1 mmol/l and pCO2 was 33.6 mm Hg. In thyroidal follicular cells, pH was 7.26 and [HCO3-] was 14.3 mmol/l; and in LF, pH was 7.32 and [HCO3-] was 16.5 mmol/l. These data provide evidence that H+ and HCO3- do not distribute according to their electrochemical gradients across both the basal and apical membranes of thyroid. Thyrotropin increased cell pH to 7.70 and [HCO3-] to 39.8 mmol/l; luminal pH and [HCO3-] were also markedly increased. Acetazolamide reduced [HCO3-] in both cells and LF. 4-Acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid increased cellular pH and [HCO3-] but did not alter these parameters in LF. Both ouabain and furosemide increased cellular pH and [HCO3-] and decreased luminal pH and [HCO3-]. Methimazole increased cellular pH and [HCO3-], decreased LF [HCO3-] and did not affect the LF pH.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1984

The role of urinary physiological changes in the genesis of urothelial lesions in mice given 4-ethylsulfonylnaphthalene-1-sulfonamide, acetazolamide, and oxamide.

BALB/c female mice were administered several compounds, including 4-ethylsulfonylnaphthalene-1-sulfonamide, acetazolamide, and oxamide, in the diet for six weeks. Fresh urine samples were analyzed three times per week for pH, osmolality, micro-crystals, and protein; and a histopathological evaluation was made of the urothelium at the end of the six weeks test. Incidences of hyperplasia, nodular hyperplasia, vacuolization, ulceration and acute inflammation of the bladder urothelium appeared to be related to the osmolality of the urine and the micro-crystalluria experienced by the mice. Correlation coefficients between lesions and urinary osmolality or crystals were -0.69 (p less than 0.0001) and 0.31 (p less than 0.03), respectively, at the 5% significance level.

Acetazolamide↗
PubMedDate not supplied

Amelioration of cisplatin-induced nephrotoxicity by the diuretic acetazolamide in F344 rats.

Renal toxicity following a single iv nonlethal dose (6 mg/kg) of cisplatin (CDDP) was investigated in male F344 rats pretreated with 20 mg/kg of acetazolamide (ACZ) sc 30 minutes before CDDP administration. There was a decrease in nephrotoxicity as indicated by a smaller elevation of BUN, a milder histopathologic lesion, and a more rapid recovery of BUN in ACZ-pretreated animals. Renal platinum content of rats receiving ACZ was significantly lower than that in animals treated with CDDP alone. There was no change in platinum level in the plasma or the liver but there was a decreased platinum excretion in urine during 24 hours after treatment. Reduction of platinum concentration in the kidney might account for protection against the renal toxicity. The diuretic ACZ might be useful in the hydration regimens used clinically to prevent renal toxicity from CDDP.

Acetazolamide↗