Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACETAZOLAMIDE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed2005

Acetazolamide improves central sleep apnea in heart failure: a double-blind, prospective study.

RATIONALE: Acetazolamide is a mild diuretic and a respiratory stimulant. It is used to treat periodic breathing at high altitude. OBJECTIVES: To determine the therapeutic efficacy of acetazolamide on central sleep apnea associated with heart failure. METHODS: Twelve male patients with stable systolic heart failure whose initial polysomnograms showed more than 15 episodes per hour of apnea and hypopnea participated in the study. The patients were randomized to a double-blind cross-over protocol with acetazolamide or placebo, taken 1 h before bedtime for six nights with 2 wk of washout. MEASUREMENTS: Polysomnography, pulmonary function tests, arterial blood gases, and left ventricular ejection fraction were obtained initially along with a sleep questionnaire, history, and physical examination. Baseline measurements were repeated at the end of each arm. MAIN RESULTS: There were no significant differences between parameters at baseline and placebo. In comparing placebo with acetazolamide, the hourly number of episodes of central apnea (49 +/- 28 vs. 23 +/- 21 [mean +/- SD]; p = 0.004) and the percentage of total sleep time spent below an arterial oxyhemoglobin saturation of 90% (19 +/- 32 vs. 6 +/- 13%; p = 0.01) decreased significantly. Acetazolamide improved subjective perception of overall sleep quality (p = 0.003), feeling rested on awakening (p = 0.007), daytime fatigue (p = 0.02), and falling asleep unintentionally during daytime (p = 0.002). CONCLUSIONS: In patients with heart failure, administration of a single dose of acetazolamide before sleep improves central sleep apnea and related daytime symptoms.

Acetazolamide↗
PubMed2006

Effects of acetazolamide on ventilatory, cerebrovascular, and pulmonary vascular responses to hypoxia.

RATIONALE: Acute mountain sickness (AMS) may affect individuals who (rapidly) ascend to altitudes higher than 2,000-3,000 m. A more serious consequence of rapid ascent may be high-altitude pulmonary edema, a hydrostatic edema associated with increased pulmonary capillary pressures. Acetazolamide is effective against AMS, possibly by increasing ventilation and cerebral blood flow (CBF). In animals, it inhibits hypoxic pulmonary vasoconstriction. OBJECTIVES: We examined the influence of acetazolamide on the response to hypoxia of ventilation, CBF, and pulmonary vascular resistance (PVR). METHODS: In this double-blind, placebo-controlled, randomized study, nine subjects ingested 250 mg acetazolamide every 8 h for 3 d. On the fourth test day, we measured the responses of ventilation, PVR, and CBF to acute isocapnic hypoxia (20 min) and sustained poikilocapnic hypoxia (4 h). Ventilation was measured with pneumotachography. Hypoxia was achieved with dynamic end-tidal forcing. The maximum pressure difference across the tricuspid valve (DeltaPmax, a good index of PVR) was measured with Doppler echocardiography. CBF was measured by transcranial Doppler ultrasound. RESULTS: In normoxia, acetazolamide increased ventilation and reduced DeltaPmax, but did not influence CBF. The ventilatory and CBF responses to acute isocapnic hypoxia were unaltered, but the rise in DeltaPmax was reduced by 57%. The increase in DeltaPmax by sustained poikilocapnic hypoxia observed after placebo was reduced by 34% after acetazolamide, the ventilatory response was increased, but the CBF response remained unaltered. CONCLUSIONS: Acetazolamide has complex effects on ventilation, PVR, and CBF that converge to optimize brain oxygenation and may be a valuable means to prevent/treat high-altitude pulmonary edema.

Acetazolamide↗
PubMed1981

Carbonic anhydrase distribution in rodent embryos and its relationship to acetazolamide teratogenesis.

The carbonic anhydrase inhibitor, acetazolamide, leads to a unique distal postaxial right forelimb deformity in rats and CBA/J mice, but SWV mice are completely resistant. Using Hansson's histochemical method, the distribution of carbonic anhydrase and its inhibition by acetazolamide in rat, CBA/J mouse, and SWV mouse embryos were compared. Carbonic anhydrase activity was demonstrable in many tissues of sensitive rat and CBA/J mouse embryos and in resistant SWV mouse embryos. The forelimb buds of resistant and sensitive embryos possess carbonic anhydrase activity in the area between the ectoderm and adjacent mesenchyma with no localization of enzyme activity corresponding to the malformation seen in acetazolamide teratogenesis. This suggests that carbonic anhydrase in the forelimbs is not the primary site of action for acetazolamide. A distinctive staining pattern of nucleated erythrocytes in resistant embryos indicated the presence of a low activity form of carbonic anhydrase in nearly half of the erythrocytes. A five-to tenfold greater amount of acetazolamide was needed to completely inhibit carbonic anhydrase activity in nucleated erythrocytes from resistant embryos than in those from sensitive embryos. The existence of a low activity form of carbonic anhydrase in SWV embryo erythrocytes may be the basis of resistance to acetazolamide teratogenesis.

Abnormalities, Drug-Induced↗
PubMed2004

Theophylline and acetazolamide reduce sleep-disordered breathing at high altitude.

A randomised, double-blind, placebo-controlled study was conducted to evaluate the effects of theophylline and acetazolamide in the treatment of sleep-disordered breathing (SDB) after fast ascent to high altitude (3,454 m). The study was conducted at a high-altitude research laboratory and included 30 healthy male volunteers. Study medication was either oral slow release theophylline (2x250 mg x day(-1)), oral acetazolamide (2x250 mg x day(-1)) or a matched placebo tablet. Polysomnographic measurements were performed during two consecutive nights, and acute mountain sickness, pulse rate, oxyhaemoglobin saturation and arterial blood gases were assessed three times a day. Without active medication, the apnoea/hypopnoea index (AHI) was highly pathological (median 16.2 x h(-1), range 2-92). Both theophylline and acetazolamide normalised SDB (median AHI 2.5 x h(-1), range 0-11; 4.2 x h(-1), range 0-19, respectively) and reduced oxyhaemoglobin desaturations during sleep (median desaturation index placebo 41.5 x h(-1), range 6-114; acetazolamide 6.5 x h(-1), range 3-28; theophylline 8.5 x h(-1), range 3-32). Compared with the high amount of central apnoeas or hypopnoeas, the number of obstructive events during sleep was very low in all groups (<4 x h(-1)). In contrast to theophylline, acetazolamide significantly improved basal oxyhaemoglobin saturation during sleep (86.2 +/- 1.7% versus 81.0 +/- 3.0%). The authors conclude that both oral slow release theophylline and acetazolamide are effective to normalise high-altitude sleep-disordered breathing.

Acetazolamide↗
PubMed1999

Effects of maternal acetazolamide treatment on body weights and incisor development of the fetal rat.

The incisor development of fetal rats on gestation day 19 was well correlated with their fetal weights. The number of odontoblasts in the mandibular incisors, an index of incisor development, increased more than that of the maxillary incisors with increase in fetal body weights. Maternal acetazolamide treatments were observed to suppress the mean fetal weight and to retard incisor development. A smaller incisor size, a thinner predentin layer, and fewer odontoblasts were characteristic of the acetazolamide group. There was also a good correlation between the fetal weights and the number of odontoblasts in the acetazolamide group. From these results, we postulated that the retarded incisor development of the fetal rats caused by the maternal acetazolamide treatment was related to their suppressed fetal weights. However, the regression coefficient of the fetal weights and the number of odontoblasts in the acetazolamide group was smaller than that of the vehicle control group. It may indicate that retarded incisor development in response to maternal acetazolamide treatment is to some extent independent of suppressed fetal weight.

Acetazolamide↗
PubMed1986

Difference in the effects of acetazolamide and ammonium chloride acidosis on ventilatory responses to CO2 and hypoxia in humans.

The effects of acetazolamide, a potent carbonic anhydrase inhibitor, and ammonium chloride (NH4Cl) on arterial blood gas tension, resting ventilation, and ventilatory responses to CO2 (HCVR) and hypoxia (HVR) were studied in healthy male subjects. Both drugs induced chronic metabolic acidosis with the reduction in plasma bicarbonate by a mean of 7.0 +/- 2.0 (S.D.) mM after acetazolamide and by 5.6 +/- 1.8 mM after NH4Cl. The ratio in the decrement of PaCO2 to that of plasma bicarbonate (delta PaCO2/delta [HCO3-]) was 1.51 in the former and 0.98 in the latter. Both drugs increased inspiratory minute ventilation (VI) predominantly due to increased tidal volume (VT) with acetazolamide and to increased respiratory frequency (f) with NH4Cl. In HCVR, the increments in CO2- ventilation slope and in ventilation at PETCO2 60 mmHg after drug administration were 0.77 +/- 0.51 l X min-1 X mmHg-1 and 20.0 +/- 11.2 l/min with acetazolamide and 0.59 +/- 0.40 l X min-1 X mmHg-1 and 8.0 +/- 2.8 l/min with NH4Cl, respectively. On the other hand, HVR both in terms of delta VI/delta SaO2 slope and of ventilation at SaO2 75% significantly increased after NH4Cl but not after acetazolamide administration. Thus, augmented VT and HCVR in the acetazolamide group and increased f and HVR in the NH4Cl group suggested that the central chemosensitive mechanism in the former and the peripheral chemosensitive mechanism in the latter may predominantly be responsible for the elevated ventilatory activities.

Acetazolamide↗
PubMed1981

Determination of acetazolamide in biological fluids by high-performance liquid chromatography.

A high-performance liquid chromatographic (HPLC) assay for acetazolamide is presented. A 100-microliter sample is mixed with an aliquot of the internal standard solution and the mixture, buffered at pH 4.5, is extracted with ethyl acetate. The extract is evaporated to dryness and the residue is analyzed by HPLC, using a reverse-phase octadecylsilane column. The wavelength of the detection is 254 nm. The coefficient of variation (CV) in the within-day analysis of replicate 10-microgram/ml acetazolamide samples in human blood plasma was 6.5%, while the between-day CV was 7.1%. The procedures was developed for the 1-25 microgram/ml acetazolamide concentration range. The internal standard used is similar in chemical structure to acetazolamide and can be readily prepared in one step from a commercially available precursor. In addition to blood serum or plasma, the assay can also use aqueous and vitreous humor samples. Theophylline and acetaminophen interfere in the assay. The technique was used to determine the concentration of acetazolamide in the blood serum of human volunteers after an oral dose of the drug, and in the aqueous and vitreous humors of rabbits after an intravenous dose of acetazolamide.

Acetazolamide↗
PubMed2000

Diaschisis and acetazolamide reactivity in brainstem infarction.

Regional cerebral blood flows (rCBF) were studied in 6 patients with lateral medullary infarction and 4 patients with pontine infarction, using stable xenon computed tomography method. In lateral medullary infarction, the rCBF and acetazolamide reactivity were decreased in the ipsilateral cerebellum and the rCBF was decreased with normal acetazolamide reactivity in the contralateral frontal lobe in one patient accompanying ipsilateral cerebellar infarction. rCBF was decreased with normal acetazolamide reactivity in the cerebellum in 3 patients, and both rCBF and acetazolamide reactivity were decreased in the whole brain in 2 patients. In pontine infarction, rCBF was decreased in ipsilateral frontal lobe and contralateral cerebellum in one patient, rCBF was decreased in the cerebellum with normal acetazolamide reactivity in the other patients. The hypoperfusion with normal acetazolamide reactivity was considered to be due to diaschisis. The rCBF decrease in the remote areas in patients with brainstem infarction was considered to be due to diaschisis or underlying arteriosclerosis.

Acetazolamide↗
PubMedDate not supplied

[Assessment of cerebrovascular reserve capacity in patients with carotid artery disease using transcranial Doppler sonography and acetazolamide].

AIM: In our study we utilised transcranial Doppler sonography (TCD) and the test with intravenously administered acetazolamide (reversible inhibitor of carbonic anhydrase) which causes vasodilatation of the brain resistance vessels to assess cerebrovascular reserve capacity (CVRC) in patients with symptomatic and asymptomatic carotid stenosis. MATERIAL: 25 patients (22 male, 3 female; aged 46-82; mean 62 years) with carotid artery disease were examined. They were qualified for the operation because of that. METHOD: Blood flow wave spectrum in the right and left middle cerebral artery (MCA) was analysed. 2 MHz pulsed-wave transducer was placed over the appropriate temporal acoustic window. We measured mean blood flow velocity (Vmean) in both MCAs. The records were taken: a) at rest, b) 15 minutes after 1.0 g of acetazolamide was administered intravenously. Cerebrovascular reserve (CVRC) was calculated as the maximal percentage increase in the appropriate MCA after the administration of acetazolamide in comparison with its value at rest. The values of CVRC were analysed statistically. RESULTS: 15 minutes after acetazolamide was injected CVRC was 44 +/- 15% (mean +/- SD) (range 0-74) in asymptomatic hemispheres. In 30 patients (97%) CVRC was 46 +/- 12% (23-74) and in 1 patient (3%) 0% (case nr 7). In the group of symptomatic hemispheres CVRC was 12 +/- 15% (-16-36) after acetazolamide administration. In 12 patients (63%) from this group CVRC was positive: 20 +/- 11% (3-33), in 4 patients (21%) CVRC was 0% (cases nr 8, 9, 22, 23) and in other 3 patients (16%) CVRC was negative: -7 +/- 8 (-16(-)-3) (cases nr 4, 12, 19). CONCLUSION: 1. The group of patients with symptomatic hemispheres have statistically lower CVRC in comparison with the group of asymptomatic hemispheres. 2. There was no statistical difference between the mean values of CVRC in patients with bilateral, severe carotid stenosis and the ones with unilateral changes. 3. We believe that such a test performed by means of TCD and intravenously injected acetazolamide can indicate a subgroup of patients with carotid stenosis for whom carotid endarterectomy is necessary at the earliest time because of possible early neurological complications appearance which are related to the lack or serious impairment of CVRC.

Acetazolamide↗
PubMed2000

[Perfusion SPECT with (99m)Tc-HMPAO in type I diabetics with no background of central neurologic symptoms. A study of activation with acetazolamide].

OBJECTIVE: This study aimed to assess if activation with acetazolamide increases the diagnostic capacity of baseline SPECT with (99m)Tc-HMPAO in the study of brain perfusion in type I diabetic patients with no history of neurological symptoms. MATERIAL AND METHODS: A baseline SPECT was carried out in 11 diabetes mellitus type I patients with no neurological symptoms with 555 MBq of (99m)Tc-HMPAO; 1 g of acetazolamide was administered during the examination and a second SPECT was obtained 20' later with the same methodology used in the baseline SPECT. The images were visually analyzed. The post-acetazolamide studies were analyzed with (CBS) and without (WBS) baseline image subtraction and both methods were compared. RESULTS: The baseline SPECT showed 48 hypoperfused cortical areas. The post-acetazolamide SPECT analyzed without baseline image subtraction detected 14 new hypoperfused areas and those analyzed with it detected 26 areas. 69% of the baseline hypoperfused areas were hyporeactive in the WBS analysis and 54% in the CBS analysis. CONCLUSION: The perfusion SPECT with acetazolamide improves the diagnostic capacity of the baseline perfusion (99m)Tc-HMPAO SPECT, and makes it possible to classify the abnormalities as metabolic or vascular, with a preference for the post-acetazolamide CBS imaging analysis.

Acetazolamide↗
PubMed2001

Abolition of pentagastrin-stimulated alkaline tide using the carbonic anhydrase inhibitor acetazolamide.

BACKGROUND: Alkaline tide is the transient increase in blood and urine pH following stimulation of gastric acid secretion. It is attributed to HCO3- release from parietal cells in parallel with H+ secretion. The enzyme carbonic anhydrase is thought to be responsible for HCO3- production from CO2 and OH- in the parietal cell. OBJECTIVE: To examine the effect of pretreatment with the carbonic anhydrase inhibitor, acetazolamide, on the alkaline tide phenomenon. METHODS: Ten patients with dyspepsia and demonstrable alkaline tide were tested on three separate days. The pH and base excess were determined in arterialized venous blood before and 45 minutes after an intramuscular injection of pentagastrin. The pH of the urine was measured before and 120 min after pentagastrin injection. Measurements were performed after pentagastrin alone on day 1, following pretreatment with acetazolamide 60 min before pentagastrin on day 2, and after the administration of acetazolamide alone on day 3. RESULTS: Following the administration of pentagastrin alone, the blood base excess increased by 1.61 +/- 0.2 mEq/L (mean +/- standard deviation) and the calculated alkaline tide at 45 min was 33.99 +/- 4.49 mEq. On day 2 with prior administration of acetazolamide, base excess decreased by 0.21 +/- 0.39 mEq/L, and the calculated alkaline tide was -3.28 +/- 7.57 mEq, which was significantly lower than on day 1 (P = 0.0001). On day 3, following acetazolamide alone, the base excess values decreased by 0.53 +/- 0.2 mEq/L and the alkaline tide was -10.05 +/- 3.33 mEq; there was no significant difference compared with day 2 (P = 0.44). CONCLUSION: Pretreatment with acetazolamide abolished the alkaline tide induced by pentagastrin. This finding supports the view that carbonic anhydrase has a major role in the alkaline tide phenomenon.

Acetazolamide↗
PubMed2004

Effects of acetazolamide and anordiol on osmotic water permeability in AQP1-cRNA injected Xenopus oocyte.

AIM: To study the effects of acetazolamide and anordiol on osmotic water permeability in aquaporin 1 (AQP1)-cRNA injected Xenopus oocyte and their mechanisms. METHODS: AQP1 gene constructed in pBluescript was transcripted into cRNA in vitro and then the cRNA was injected in Xenopus oocytes. The effects of acetazolamide and anordiol on the water transport function of AQP1 were observed by assaying the osmotic swelling of oocytes. In addition, their effects on protein expression of AQP1 were quantitatively investigated by Western blotting method. RESULTS: After incubation for 15 min or 72 h, acetazolamide, a carbonic anhydrase inhibitor, equally reduced the water permeability of AQP1-cRNA injected oocyte in a dose-dependent manner. After incubation for 72 h, anordiol, an antiestrogen with partial estrogenic activity, reduced the osmotic water permeability dose dependently as well; however, no discernable action was observed after incubation with anordiol for 15 min. The Western blotting analysis showed that acetazolamide did not influence the protein expression of AQP1. However, after incubation for 72 h with anordiol (10 micromol/L), the quantity of AQP1 in the oocyte membrane was decreased dramatically (P<0.05). CONCLUSION: Both acetazolamide and anordiol inhibited the osmotic water permeability of AQP1-cRNA injected oocyte, but their mechanisms were different. Acetazolamide functionally inhibited the osmotic water permeability of AQP1, whereas anordiol primarily decreased the amount of AQP1 protein in the oocyte membrane.

Acetazolamide↗
PubMed1991

[The responses of somatosensory evoked potentials and cerebral blood flow to acetazolamide in patients with occlusive carotid disease].

The correlation between somatosensory evoked potential (SEP) and regional cerebral blood flow (rCBF) changes after acetazolamide administration was studied in six patients presented with transient ischemic attack (TIA) or minor completed stroke. All patients had no or only localized low density area on computed tomography, and severe occlusive disease in the ipsilateral common or internal carotid artery on cerebral angiography. In two patients with internal carotid artery occlusion, both marked decrease in ipsilateral N20 amplitude and prolongation of ipsilateral N20 latency were observed from 5-10 minutes after acetazolamide injection. These changes gradually improved and resolved 30-45 minutes after acetazolamide injection. In these cases, stable xenon CT revealed paradoxical rCBF decrease in the territory of the ipsilateral middle cerebral artery after acetazolamide injection. Especially, rCBF in the ipsilateral centrum semiovale fell to less than 20 ml/100 g/min. The other patients showed no change in SEPs and no paradoxical decrease in rCBF after acetazolamide injection. These results suggest that SEP test with acetazolamide loading could be valuable to evaluate a certain group of the patients with severely disturbed cerebral perfusion reserve in the carotid territory and suitable candidate for extracranial-intracranial arterial bypass (EC/IC bypass), although further investigations is needed.

Acetazolamide↗
PubMed1990

[Gastric lesions induced by ethanol and indomethacin: cytoprotective effect of acetazolamide].

A study was made of the effect of acetazolamide (a potent carbonic anhydrase inhibitor) on the production of lesions by absolute alcohol and of the effect of indomethacin (inhibitor of cyclooxygenase) on the gastric cytoprotection produced by S-adenosylmethionine (sulfhydryl compound). Acetazolamide significantly reduced gastric mucosa lesions induced by oral administration of absolute alcohol. It did not modify those produced by indomethacin. Pretreatment with acetazolamide potentiated the production of S-adenosylmethionine in response to alcohol injury, but it did not modify the protective effect of S-adenosylmethionine against injury by indomethacin. Since acetazolamide did not alter gastric secretion of HCO3-, it is concluded that carbonic anhydrase-dependent gastric alkali secretion did not intervene in the gastric acetazolamide-induced cytoprotective mechanism. The same effect was produced by stimulation of the biosynthesis of endogenous prostaglandins. This provides a physiologic rationale for the use of acetazolamide in acute gastric disease and gastroduodenal peptic ulcer.

Acetazolamide↗
PubMed1989

[CO2 elimination in ophthalmic surgery after administration of acetazolamide].

The authors studied the influence on CO2 elimination in lungs of acetazolamide given before ophthalmic surgery. The changes in PaCO2, PETCO2, (a-ET) PCO2, ventilation volume (VE), and respiratory rate (RR) were measured before and 6 hours after administration of acetazolamide (500mg, p. o.). Comparison of PETCO2, PaCO2, (a-ET) PCO2, VE and RR after the operation with or without treatment with acetazolamide showed that (a-ET) PCO2 increased significantly and the increase of PaCO2 in post-anesthesia period was less with the treatment of acetazolamide. In other words, ventilation was stimulated by acetazolamide as the decrease in VE was less in post-anesthesia period. It may be concluded that oral administration of acetazolamide 500mg does not interfere with CO2 elimination.

Acetazolamide↗
PubMed1985

Acetazolamide and exercise in sojourners to 6,300 meters--a preliminary study.

To examine the effect of acetazolamide on resting acid-base balance and on exercise performance at extreme altitude, we studied four members of the American Medical Research Expedition to Mount Everest at an altitude of 6,300 meters. After an initial progressive exercise test to exhaustion on a bicycle ergometer, subjects were re-studied after taking acetazolamide 250 mg every 8 h for three doses. We measured venous blood during rest for determination of hemoglobin, hematocrit, 2,3-diphosphoglycerate (DPG), bicarbonate, pH, P50, and arterial oxygen saturation by ear oximeter. The results showed that pH, bicarbonate, and DPG:hemoglobin ratio were lower on acetazolamide, whereas P50 at in vivo conditions was unchanged. Exercise ventilation and oxygen consumption for the same workload were slightly higher after acetazolamide, whereas VCO2/VO2 respiratory exchange ratio (R) was lower, and oxygen saturation was unchanged. Two of four subjects had decreased time at maximum workload on acetazolamide; none had an increased performance. The results of this study show that partial carbonic anhydrase inhibition in individuals sojourning to very high altitude produces a further base deficit and a metabolic acidosis, stimulates ventilation, and may impair maximum exercise performance. Although acetazolamide effectively prevents acute mountain sickness, it does not improve performance, and may even impair exercise performance at extreme altitude.

Acetazolamide↗
PubMed1979

Acidosis inhibits the hypocalcemic effect of acetazolamide.

The effect of acetazolamide on calcium metabolism was examined using sham-operated, ureter-ligated and nephrectomized rats. Acetazolamide doses from 10 to 500 mg/kg produced significant hypocalcemic effects in ureter-ligated and nephrectomized rats. However, doses of acetazolamide up to 1000 mg/kg were devoid of hypocalcemic activity when administered to sham-operated rats. Sham-operated rats exhibited an acidotic response to acetazolamide while ureter-ligated rats did not. Attenuation of this drug-induced acidotic response with i.p. injections of tris(hydroxymethyl)amino-methane uncovered a hypocalcemic effect of acetazolamide in sham-operated rats. Also, the hypocalcemia associated with acetazolamide treatment of ureter-ligated rats was negated when an acidosis was induced by prior injection of NH4Cl. These data indicate that the administration of inhibitors of carbonic anhydrase produces a hypocalcemia when a metabolic acidosis is not present.

Acetazolamide↗
PubMed1982

Acute mountain sickness and acetazolamide. Clinical efficacy and effect on ventilation.

Sixty-four climbers participated in a randomized clinical trial of acetazolamide prophylaxis for acute mountain sickness (AMS) during rapid, active ascent of MT Rainier. Twenty-nine (93.6%) of 31 climbers receiving acetazolamide and 25 (75.8%) of 33 receiving placebo attained the summit. Time spent ascending from sea level to the summit (4,394 m) averaged 33.5 hours (range, 23 to 48 hours). On the summit AMS was less common in climbers receiving acetazolamide, and they experienced less headache, nausea, drowsiness, shortness of breath, and dizziness and a greater sense of satisfaction and psychological well-being. Minute ventilation on the summit was significantly greater in subjects taking acetazolamide (24.9 +/- 2.0 L/min compared with 16.9 +/- 3.8 L/min). Expired vital capacity was also greater on the summit in the acetazolamide group (6.9 +/- 0.4 L compared with 5.8 +/- 0.4 L). We conclude that acetazolamide is effective in the prophylaxis of AMS for climbers attempting rapid, active ascent. Increased ventilation at altitude, producing an increased alveolar oxygen tension, may be related to the observed amelioration of symptoms.

Acetazolamide↗