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PubMed1980

Autoradiographic localization of carbonic anhydrase in the rabbit ciliary body.

The high binding affinity of acetazolamide for carbonic anhydrase (K1 congruent to 10(-8) M) was employed to demonstrate the distribution of the enzyme in the rabbit ciliary body by incubating the tissue with 3H-acetazolamide (1.5 Ci/mmol). Specificity of binding was ascertained by displacing 3H-acetazolamide with a high concentration of unlabeled ethoxzolamide (K1 congruent to 10(-9) M). Wedges of the globe anterior to the ora serrata were incubated in bicarbonate buffered physiological saline, 95% O2/5% CO2, at 0 degrees C for 2 hr with either 3H-acetazolamide (0.2 microM), 3H-acetazolamide and unlabeled ethoxzolamide (100 microM), or physiological saline alone. They were then washed for 2 hr in fresh physiological saline and processed for autoradiography. The autoradiographs showed the label localized in both pigmented and nonpigmented layers of ciliary body epithelium in the pars plicata and in the iridial processes. The epithelia of both crests and troughs showed localization of label. In contrast, no concentration of label was found in the stroma of the ciliary body, including vascular endothelium, and in the epithelia of the pars plana. In sections that were incubated with 3H-acetazolamide in the presence of an excess of unlabeled ethoxzolamide, no localization of label occurred. These findings suggest that the epithelia of the pars plicata, but not those of the pars plana, contain carbonic anhydrase. This is consistent with hypotheses restricting aqueous humor formation to the pars plicata.

Acetazolamide↗
PubMed1986

Disturbance of CO2 elimination in the lungs by carbonic anhydrase inhibition.

Carbonic anhydrase in the red blood cell and in the pulmonary endothelium facilitates the elimination of CO2 in the lungs. Although a carbonic anhydrase inhibitor, such as acetazolamide which is frequently used in patients with glaucoma or with metabolic alkalosis, is known to impair the CO2 elimination in the lungs, the dose-response curve of CO2 elimination with acetazolamide has not been well documented in CO2 homeostasis. In the present study, the effects of inhibited carbonic anhydrase were tested in 8 anesthetized dogs; various dosages of acetazolamide were used. When the administered clinical dosage of acetazolamide increased from 5 to 20 mg/kg, PaCO2, PVCO2, arterial-alveolar PCO2 difference (a-ADCO2), and physiological VD/VT ratio increased progressively to 52.0 +/- 2.1 Torr, 58.0 +/- 3.0 Torr, 23.4 +/- 1.2 Torr, and by 19.2 +/- 1.8% (S.E.) respectively, whereas inhibition rate of red blood cell carbonic anhydrase (RCA) activity increased progressively to 73.1 +/- 2.1% (S.E.). On the other hand, PACO2 decreased to 27.1 +/- 1.8 Torr (S.E.) upon the first injection of 5 mg/kg of acetazolamide, but PACO2 did not change further upon 3 additional 5 mg/kg injections. Mixed venous-arterial PCO2 difference [V-a)PCO2), VCO2, and anatomical VD/VT ratio were unchanged by the administration of any doses of acetazolamide.

Acetazolamide↗
PubMed2000

Pharmacokinetics of acetazolimide after intravenous and oral administration in horses.

OBJECTIVE: To determine the pharmacokinetics of acetazolamide administered IV and orally to horses. ANIMALS: 6 clinically normal adult horses. PROCEDURE: Horses received 2 doses of acetazolamide (4 mg/kg of body weight, IV; 8 mg/kg, PO), and blood samples were collected at regular intervals before and after administration. Samples were assayed for acetazolamide concentration by high-performance liquid chromatography, and concentration-time data were analyzed. RESULTS: After IV administration of acetazolamide, data analysis revealed a median mean residence time of 1.71 +/- 0.90 hours and median total body clearance of 263 +/- 38 ml/kg/h. Median steady-state volume of distribution was 433 +/- 218 ml/kg. After oral administration, mean peak plasma concentration was 1.90 +/- 1.09 microg/ml. Mean time to peak plasma concentration was 1.61 +/- 1.24 hours. Median oral bioavailability was 25 +/- 6%. CONCLUSIONS AND CLINICAL RELEVANCE: Oral pharmacokinetic disposition of acetazolamide in horses was characterized by rapid absorption, low bioavailability, and slower elimination than observed initially after IV administration. Pharmacokinetic data generated by this study should facilitate estimation of appropriate dosages for acetazolamide use in horses with hyperkalemic periodic paralysis.

Acetazolamide↗
PubMed2001

[Effects of Rholida on the free radical metabolism and serum creatine kinase after exercise at plateau].

Objective. To study the effect of Rholida on free radical metabolism and serum creatine kinase CK) after exercise at plateau. Method. After staying at high altitude (4100 m) for 20 d, 40 healthy young men were divided into 4 groups randomly (Rholida, Acetazolamide, Xi' s capsule and control, 10 men each group). And their SOD, MDA, GSH-Px CK, and CK-MB were determined respectively. Before, after taking drugs and after finishing the 5 min-stair-exercise. Result. Before taking drugs and after exercise, MAD GSH-Px, CK, CK-MB, increased as compared with quiet state (P<0.05, P<0.01), but SOD showed no significant chang (P>0.05). After taking drugs for 6 d, those who took Rholida, Acetazolamide and Xi's capsule, their MAD, GSH-Px CK, CK-MB increased after exercise as compared with quiet state (P<0.05). In Rholida group SOD increased and had significant change (P<0.05); but there was no significant change in Acetazolamide, Xi' s capsule group, SOD increased, MDA decreased (P<0.05), CK, CK-MB had no significant change (P>0.05), GSH-Px increased in Xi's group (P<0.05), but not in Acetazolamide group (P>0.05). SOD, GSH-Px increased, MDA, CK-MB decreased in Rholida group after taking drugs and the changes were significant (P<0.01). In Acetazolamide and Xi's capsule group, GSH-Px increased significantly, MDA, CK, CK-MB decreased significantly (P<0.05), but SOD didn't (P>0.05). Conclusion. Rholida, Acetazolamide, Xi's capsule could regulate the disorder of free radical metabolism at plateau and Rholida had advantage over the others.

Acetazolamide↗
PubMed1998

[Assessment of cerebrovascular reactivity in patients with symptomatic and asymptomatic atherosclerotic carotid artery lesions].

AIMS: Strokes caused by hemodynamically significant internal carotid artery stenoses and occlusions are believed to be embolic or hemodynamic of origin. The aim of the study was to assess cerebral hemodynamic compromises of significant carotid artery stenosis of occlusion using vasodilatory testing (acetazolamide test) in asymptomatic and symptomatic patients. PATIENTS AND METHODS: 36 patients with unilateral, hemodynamically significant carotid stenosis were investigated using transcranial Doppler acetazolamide-test. There were 12 asymptomatic and 24 symptomatic patients. The middle cerebral artery mean blood flow velocity was measured at rest and after intravenous injection of 1 g acetazolamide. The absolute mean blood flow velocities and the cerebrovascular reactivity was compared at the stenotic and non-stenotic side. In a further analysis the mean velocities and the cerebrovascular reactivity values of the stenotic side were compared. Results of acetazolamide test performed on 28 healthy volunteers were used as control values. RESULTS: There were no side-differences between the middle cerebral artery mean blood flow velocity and cerebrovascular reactivity values in the asymptomatic group. In the symptomatic group, however middle cerebral artery mean velocity and cerebrovascular reactivity after acetazolamide was significantly lower on the stenotic side, than on the non-stenotic one. Comparing the different groups non-stenotic sides did not differ to each other in their cerebral blood flow velocity and cerebrovascular reactivity. In the symptomatic patients, however, cerebral blood flow velocity and cerebrovascular reserve capacity after acetazolamide was lower, than that of the stenotic side of asymptomatic patients and controls. CONCLUSIONS: The transcranial Doppler is a suitable method for detecting altered cerebral hemodynamics in significant carotid stenosis. Impaired cerebrovascular reactivity may refer to the impairment of cerebral autoregulatory mechanisms.

Acetazolamide↗
PubMed1995

Doppler study of the ophthalmic artery in patients with carotid occlusive disease.

Assessing the adequacy of collateral circulatory pathways has become increasingly important in the investigation of cerebral circulation. Using transorbital Doppler ultrasonography (TOD), we examined the ophthalmic artery (OA) in patients with hemodynamic significant internal carotid artery (ICA) occlusive disease. The velocity and the direction of flow in the OA were studied in 45 patients (occlusion n = 27, stenosis > 75% n = 18), and in 30 age matched controls, under baseline conditions and within 30 minutes after the i.v. administration of 1 g acetazolamide as a vasodilatory stimulus. Based on the direction of flow before and after acetazolamide, the 45 patients could be separated into four groups with increasing degree of ICA lesions. In group I the OA flow was anterograde, but the velocity decreased after acetazolamide. In group II the OA direction became retrograde after acetazolamide, indicating collateral flow to the brain. In patients with retrograde OA flow following acetazolamide injection (group II-IV), the vessel reacted similarly to an intracranial artery, with marked increase in velocity when vasoreactivity was tested. TOD and the acetazolamide test provide useful information about potential collateral OA flow to the brain in patients with ICA occlusive disease.

Adult↗
PubMed1986

Urea synthesis and CO2/HCO3- compartmentation in isolated perfused rat liver.

With physiological portal HCO3- and CO2 concentrations of 25mM and 1.2mM in the perfusate, respectively, acetazolamide inhibited urea synthesis from NH4Cl in isolated perfused rat liver by 50-60%, whereas urea synthesis from glutamine was inhibited by only 10-15%. A decreased sensitivity of urea synthesis from glutamine to acetazolamide inhibition was also observed when the extracellular HCO3- and CO2 concentrations were varied from 0-50mM and 0-2.4mM, respectively. Stimulation of intramitochondrial CO2 formation at pyruvate dehydrogenase with high pyruvate concentrations (7mM) was without effect on the acetazolamide sensitivity of urea synthesis from NH4Cl. Urea synthesis was studied under conditions of a limiting HCO3- supply for carbamoyl-phosphate synthesis. In the absence of externally added HCO3- or CO2, when 14CO2 was provided intracellularly by [U-14C]glutamine or [1-14C]-glutamine oxidation, acetazolamide had almost no effect on label incorporation into urea, whereas label incorporation from an added tracer H14CO3- dose was inhibited by about 70%. 14CO2 production from [U-14C]glutamine was about twice as high as from [1-14C]glutamine, indicating that about 50% of the CO2 produced from glutamine is formed at 2-oxoglutarate dehydrogenase. The fractional incorporation of 14CO2 into urea was about 13% with [1-14C]-as well as with [U-14C]glutamine. Addition of small concentrations of HCO3- (1.2mM) to the perfusate increased urea synthesis from glutamine by about 70%. This stimulation of urea synthesis was fully abolished by acetazolamide. The carbonate-dehydratase inhibitor prevented the incorporation of added HCO3- into urea, whereas incorporation of CO2 derived from glutamine degradation was unaffected. Without HCO3- and CO2 in the perfusion medium, when 14CO2 was provided by [1-14C]-pyruvate oxidation, acetazolamide inhibited urea synthesis from NH4Cl as well as 14C incorporation into urea by about 50%. Therefore carbonate-dehydratase activity is required for the utilization of extracellular CO2 or pyruvate-dehydrogenase-derived CO2 for urea synthesis, but not for CO2 derived from glutamine oxidation. This is further evidence for a special role of glutamine as substrate for urea synthesis.

Ammonium Chloride↗
PubMed1990

Treatment of humoral hypercalcemia of malignancy in rats with inhibitors of carbonic anhydrase.

The enzyme carbonic anhydrase has been suggested as a critical participant in osteoclast-mediated bone resorption. In humoral hypercalcemia of malignancy (HHM) intense osteoclastic bone resorption is principally responsible for the observed hypercalcemia. We therefore undertook to examine the effect of the carbonic anhydrase inhibitor acetazolamide on the hypercalcemia induced by the H500 Leydig cell tumor in Fisher rats, a well-described model of HHM. Acetazolamide treatment for 10 h at 10 mg/h resulted in a significant fall in serum calcium in the five drug-treated animals (14.2 +/- 0.9 to 11.5 +/- 0.1 mg/dl, p less than 0.05). Conversely, the six animals infused with vehicle alone showed a significant rise in serum calcium (12.5 +/- 0.5 to 13.8 +/- 0.1 mg/dl, p less than 0.05). At the end of the infusion, the acetazolamide-treated animals had a significantly lower mean serum calcium than those receiving vehicle alone (11.5 +/- 0.1 versus 13.8 +/- 0.1, p less than 0.05). There was no significant change in serum phosphorus, urine calcium, urine phosphorus, or nephrogenous cyclic AMP excretion between the two groups. Acetazaolamide and HTS 5-(3-hydroxybenzoyl)-2-thiophenesulfonamide, another carbonic anhydrase inhibitor, both significantly inhibited in vitro bone resorption induced by 5 X 10(-9) M 36Tyr(1-36)-PTHrP-amide (PTHrP, parathyroid hormone-related protein). Acetazolamide also inhibited the resorption induced by 10(-8) M (1-141)-PTHrP and 2.5 X 10(-9) M (1-74)-PTHrP. We conclude that acetazolamide is effective in lowering the serum calcium in animals with humoral hypercalcemia of malignancy. The data are consistent with the hypothesis that the mechanism of action for this effect is direct inhibition of osteoclast-mediated bone resorption.

Acetazolamide↗
PubMed1988

Effect of alteration of cerebrospinal fluid bulk flow on nicotine cerebrospinal fluid exit transfer kinetics.

This study was undertaken to determine if a compound which alters the bulk flow of cerebrospinal fluid (CSF) alters the elimination kinetics of a compound in the CSF. Acetazolamide was chosen as the CSF bulk flow-altering agent. It produces a relatively large effect on the flow process, affecting both choroidal and extrachoroidal CSF production, and has been shown to affect CSF flow following iv administration. The compound monitored was nicotine. Acetazolamide was administered orally for one week before and intravenously during the experiment. Nicotine was administered by a bolus injection directly into the CSF via the cisterna magna. The results indicate that the introduction of acetazolamide into the general circulation increases the rate of removal of nicotine from the CSF. Subjects receiving acetazolamide had elevated CSF pressures. The increase in CSF pressure associated with the administration of acetazolamide suggests pressure as a possible factor in the observed increase in the rate of removal of nicotine.

Acetazolamide↗
PubMed1990

Carbonic anhydrase inhibition and cerebral cortical oxygenation in the rat.

We report here the results of our study of the carbonic anhydrase inhibitor acetazolamide on cerebral vascular and metabolic function, correlated with the effects of this agent on systemic arterial blood gases and pH. We found that the effects of acetazolamide were to increase PaO2, decrease bicarbonate ion concentration and decrease pH. While these effects were maintained for many hours after both high and low dose acetazolamide, the cerebral metabolic and vascular effects of the drug were transient. The central effects of carbonic anhydrase inhibition were consistent with increased oxygen delivery and increased tissue oxygenation. Hypoxia such as encountered at altitude, represents a challenge to the mechanisms which control blood flow in the brain. The decreased arterial oxygen content at altitude is a ventilatory drive which has the effect of 1) increasing somewhat the PaO2; 2) decreasing the PaCO2; 3) alkalinizing the blood. The decreased PaCO2 then leads to decreased CBF compounding the problem of hypoxemia. In this situation, increasing CBF helps to relieve the tissue hypoxia. This has been done by either increased inhalation of CO2 (Harvey et al., 1988) or by acetazolamide (Cain and Dunn, 1966; Forwand et al., 1968). A common feature in both treatments might be increased tissue CO2 retention (Kjällquist et al., 1969; Meyer et al., 1961) and tissue acidification (Heuser et al., 1975). The two treatments are not identical since acetazolamide seems to have additional effects on cerebral metabolism that elevated CO2 does not. Thus, we can deduce that the primary pathologic effects of acute hypoxia are due to the decreased cerebral blood flow produced by hyperventilation-induced hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1987

The nature of the neutral Na+-Cl(-)-coupled entry at the apical membrane of rabbit gallbladder epithelium: I. Na+/H+, Cl-/HCO3- double exchange and Na+-Cl- symport.

Cl- influx at the luminal border of the epithelium of rabbit gallbladder was measured by 45-sec exposures to 36Cl- and 3H-sucrose (as extracellular marker). Its paracellular component was evaluated by the use of 25 mM SCN- which immediately and completely inhibits Cl- entry into the cell. Cellular influx was equal to 16.7 mu eq cm-2 hr-1 and decreased to 8.5 mu eq cm-2 hr-1 upon removal of HCO3- from the bathing media and by bubbling 100% O2 for 45 min. When HCO3- was present, cellular influx was again about halved by the action of 10(-4) M acetazolamide, 10(-5) to 10(-4) M furosemide, 10(-5) to 10(-4) M 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (SITS), 10(-3) M amiloride. The effects of furosemide and SITS were tested at different concentrations of the inhibitor and with different exposure times: they were maximal at the concentrations reported above and nonadditive. In turn, the effects of amiloride and SITS were not additive. Acetazolamide reached its maximal action after an exposure of about 2 min. When exogenous HCO3- was absent, the residual cellular influx was insensitive to acetazolamide, furosemide and SITS. When exogenous HCO3- was present in the salines, Na+ removal from the mucosal side caused a slow decline of cellular Cl- influx; conversely, it immediately abolished cellular Cl- influx in the absence of HCO3-. In conclusion, about 50% of cellular influx is sensitive to HCO3-, inhibitable by SCN-, acetazolamide, furosemide, SITS and amiloride and furthermore slowly dependent on Na+. The residual cellular influx is insensitive to bicarbonate, inhibitable by SCN-, resistant to acetazolamide, furosemide, SITS and amiloride, and immediately dependent on Na+. Thus, about 50% of apical membrane NaCl influx appears to result from a Na+/H+ and Cl-/HCO3- exchange, whereas the residual influx seems to be due to Na+-Cl- cotransport on a single carrier. Whether both components are simultaneously present or the latter represents a cellular homeostatic counter-reaction to the inhibition of the former is not clear.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed2004

Effect of bicarbonate on retinal vasculature and acidosis-induced retinopathy in the neonatal rat.

BACKGROUND: Systemic acidosis induces preretinal neovascularization (NV) analogous to retinopathy of prematurity (ROP) in the neonatal rat. Sodium bicarbonate is used in human neonates to treat acidosis. The effects of alkali administration on the developing retinal vasculature and on acidosis-induced retinopathy (AIR) are unknown. We investigated the effect of sodium bicarbonate gavage on the retinal vasculature of normal and acidotic neonatal rats to determine (1) whether bicarbonate treatment is associated with preretinal NV and (2) whether AIR can be prevented with systemic bicarbonate treatment. METHODS: The extent of acidosis and alkalosis were initially determined from carotid arterial blood samples. In the bicarbonate-alone study, newborn rats were randomized into litters of 25 and received bicarbonate doses of 15 mmol/kg twice daily and 20 mmol/kg once daily from days 2 to 7. Control animals received saline gavage. In the AIR treatment study, acidosis was induced in neonatal rats by intraperitoneal injection of acetazolamide 200 mg/kg from days 2 to 7. Acetazolamide-treated rats received either additional bicarbonate gavage or no additional treatment. Eyes were enucleated on day 13, and the retinal vasculature was assessed for NV using ADPase staining techniques and light microscopy. RESULTS: Systemic alkalosis (peak pH 7.55+/-0.02; mean +/- SD) was confirmed with bicarbonate gavage, and partial reversal of acidosis was confirmed when acetazolamide-treated rats received bicarbonate. Surviving rats receiving bicarbonate 15 mmol/kg twice daily (28% survival) and 20 mmol/kg bicarbonate once daily (45% survival) had an incidence of preretinal NV of 9% and 8%, respectively. No NV was seen in saline-control rats. In the acetazolamide-treated rats, the incidence of preretinal NV in surviving rats was numerically lower in bicarbonate-treated rats than acetazolamide-only controls (8% versus 24%, p=0.065) but with only 19% survival in the bicarbonate-treated rats. CONCLUSIONS: In the neonatal rat, alkalosis induced by bicarbonate gavage is associated with a low incidence of mild, preretinal NV similar to ROP. Although treating acidotic rats with bicarbonate may reduce the incidence of preretinal NV, treatment was associated with an unacceptable mortality rate.

Acetazolamide↗
PubMed2000

Inhibition of membrane-bound carbonic anhydrase enhances subretinal fluid absorption and retinal adhesiveness.

BACKGROUND: The clinical use of currently available carbonic anhydrase (CA) inhibitors is limited by systemic side-effects, thought to result from the inhibition of intracellular CA isoenzymes. This study investigates how benzolamide, a carbonic anhydrase inhibitor which does not readily penetrate cell membranes, modulates retinal pigment epithelium functions relative to acetazolamide, which diffuses into the cytosol. METHODS: Small retinal detachments were made in Dutch rabbits by injecting saline into the subretinal space. Detachment height was measured using a dual He-Ne beam YAG laser focusing system, and the fluid absorption rate was calculated before and after intravenous injections of saline, acetazolamide or benzolamide. Retinal adhesiveness was determined by peeling the retina from the RPE and measuring the amount of adherent pigment. RESULTS: The baseline fluid absorption rate of 0.04 microl/mm(2)/h was unchanged after injection of 0.9% NaCl or low-dose benzolamide (5 mg/kg). The absorption increased to about 0.14 microl/mm(2)/h after higher benzolamide doses (20-40 mg/kg) and to 0.13 microl/mm(2)/h after acetazolamide (20 mg/kg). Both acetazolamide and benzolamide significantly slowed the post-enucleation failure of retinal adhesiveness. CONCLUSION: Since benzolamide had effects similar to acetazolamide, inhibition of membrane-bound CA appears to be sufficient to enhance subretinal fluid absorption and retinal adhesiveness. Membrane-specific CA inhibitors may therefore be of clinical value if they minimize side-effects from intracellular CA inhibition.

Absorption↗
PubMed1984

Effect of carbonic anhydrase inhibition on the DC potential difference between cerebrospinal fluid and blood.

The effect of cerebral carbonic anhydrase inhibition on the DC potential difference between cerebrospinal fluid (CSF) and blood (PD) was studied in anesthetized dogs by perfusing the ventriculocisternal system with artificial CSF containing the carbonic anhydrase inhibitor, acetazolamide. The slope of the PD vs. arterial blood pH (delta PD/delta pHa) was calculated from PD and pHa values obtained during room-air breathing, respiratory acidosis, and respiratory alkalosis. delta PD/delta pHa decreased from -26.3 +/- 1.9 millivolts per pH unit (mV/U) before acetazolamide administration to 17.6 +/- 2.1 after acetazolamide (P less than 0.02). The PD at pH 7.4 (PD7.4) increased slightly from 2.9 +/- 0.5 mV before acetazolamide treatment to 3.9 +/- 0.6 after acetazolamide (P less than 0.02). The results suggest that carbonic anhydrase could be involved in generating the PD between CSF and blood.

Acetazolamide↗
PubMed2004

Neodymium:yttrium-aluminum-garnet capsulotomy and intraocular pressure in pseudophakic patients with glaucoma.

OBJECTIVE: To determine the 1- and 3-hour changes in intraocular pressure after neodymium:yttrium-aluminum-garnet (Nd:YAG) capsulotomy in pseudophakic patients with glaucoma and to determine the effect of acetazolamide and apraclonidine on these changes. DESIGN: Randomized controlled trial. PARTICIPANTS: Pseudophakic patients with glaucoma requiring Nd:YAG posterior capsulotomy (n = 76). INTERVENTION: Patients undergoing Nd:YAG posterior capsulotomy were randomly allocated to receive no therapy, oral acetazolamide (250 mg), or topical apraclonidine 1% within 1 hour before capsulotomy. MAIN OUTCOME MEASURES: Intraocular pressures 1 and 3 hours after laser therapy were recorded. RESULTS: Data were available for 76 eyes in 76 patients. Twenty-nine patients received no therapy; 24, oral acetazolamide; and 23, apraclonidine. One fifth (6/29) of patients with glaucoma developed a pressure rise of > or =5 mmHg if untreated, and 3% (1/29) developed a pressure rise of >10 mmHg. In comparison, no patients in the acetazolamide group developed a pressure rise of > or =5 mmHg (P = 0.02), and 1 of 24 in the apraclonidine group (P = 0.08) developed such a pressure rise, with none developing a pressure rise of >10 mmHg. When comparing all treated with nontreated, a reduction in the proportion with pressure rise was found (P = 0.01). All of the patients who developed a pressure rise of > or =5 mmHg did so within the first hour. CONCLUSIONS: In the absence of therapy, clinically significant post-Nd:YAG pressure rises occur in one fifth of patients with glaucoma undergoing capsulotomy. Oral acetazolamide and topical apraclonidine reduce the frequency and magnitude of pressure rises and are of comparable effectiveness. In this study, all clinically important pressure rises developed within the first hour.

Acetazolamide↗
PubMed1999

Differences in regional cerebral blood flow in two types of leuko-araiosis.

Cerebral blood flow and cerebrovascular acetazolamide reactivity were investigated in patients with periventricular hyperintensity and in patients with leuko-araiosis in centrum semiovale. Fifteen patients with periventricular hyperintensity, 15 patients with leuko-araiosis in centrum semiovale and 15 age-matched controls without leuko-araiosis were studied. The regional cerebral blood flow was measured using the stable xenon CT method before and 20 min after intravenous injection of 17 mg/kg acetazolamide. The blood flow and the cerebrovascular acetazolamide reactivity in the area of leuko-araiosis were significantly lower in the periventricular hyperintensity group and the leuko-araiosis in centrum semiovale group than the control group. The blood flow in the cerebral cortex was significantly lower in the leuko-araiosis in centrum semiovale group than in the periventricular hyperintensity group and the control group. The cerebrovascular acetazolamide reactivity in the cerebral cortex did not show any significant difference among the three groups. The blood flow in the cerebral cortex was decreased in patients with leuko-araiosis in centrum semiovale but the cerebrovascular acetazolamide reactivity in the cerebral cortex was normal in patients with leuko-araiosis.

Acetazolamide↗
PubMed1998

Medical control of intraocular pressure after cataract surgery.

PURPOSE: To compare the effectiveness of 2 medications commonly used to prevent intraocular pressure (IOP) elevation in the early period after cataract surgery. SETTING: Palo Alto Veterans Affairs Health Care System, Palo Alto, California, USA. METHODS: This prospective study comprised 202 eyes of patients scheduled for cataract extraction who agreed to participate. Patients were randomized to receive oral acetazolamide, 500 mg 1 hour preoperatively; oral acetazolamide, 500 mg immediately postoperatively; apraclonidine hydrochloride 1%, 2 drops 1 hour preoperatively; or artificial tears (control group). Intraocular pressure was measured preoperatively and 4 to 6 and 24 hours postoperatively. RESULTS: Preoperative IOP was not significantly different among the 4 groups. At 4 to 6 hours postoperatively, only preoperative acetazolamide was significantly more effective than the control medication (P = .038); at 24 hours there were no significant differences among the 4 groups. Postoperative IOP elevation in excess of 35 mm Hg at 6 or 24 hours decreased significantly in the preoperative acetazolamide group (3/46 eyes) compared with the control group (14/54 eyes). There was no statistically significant difference in IOP elevation between eyes having extracapsular cataract extraction and those having phacoemulsification, independent of treatment group. CONCLUSION: The results favor preoperative acetazolamide to control postcataract IOP elevation. The method of cataract removal did not affect postoperative IOP elevation.

Acetazolamide↗
PubMed1999

Survival of glaucoma patients.

PURPOSE: To investigate the survival of patients with capsular or simple glaucoma compared with that of the common population, with particular attention to the impact of sex and use of acetazolamide (Diamox). METHODS: The 30 year survival of 1147 patients with capsular or simple glaucoma who were finally hospitalized at the Eye Department, Rikshospitalet, Oslo, from 1961 to 1970, are analysed, using log rank tests. The time varying impacts of sex and acetazolamide on survival are also studied using a regression model. RESULTS: There was a significant increased mortality for patients with acetazolamide, and for men also those not using it. The observed mortality for men was initially lower than the average Norwegian population, but later the mortality increased more rapidly in the glaucoma group. This may be explained by a selection of the healthiest patients to Rikshospitalet, and actually indicates that the excess mortality is even higher than calculated here. CONCLUSION: The analysis of data indicated increased mortality for glaucoma patients when the disease had lasted for some time. This was especially pronounced for men using acetazolamide. A similar study from a period when acetazolamide was not in common use and an analysis of causes of death is also asked for.

Acetazolamide↗