Objective To investigate the expression of aquaporin-1( AQP-1) in pulmonary tissues of asthma mice and the effects of acetazolamide( AZ) on AQP-1 expression. Methods Forty C57BL/6 mice were randomly divided into five groups. Group A was treated with phosphate buffer as a non-asthmatic group.The mice in group B, C, D, and E were sensitized with ovalbumin( OVA) and challenged with aerosol OVA to establish asthma model. The mice in group B, C, and D were interperitoneally injected with AZ at doses of 300, 200, 100 mg/kg, respectively during the challenge period. Results ①Wet/dry weight ratio of lung tissues in group E was significantly higher than that in group A( P lt;0. 05) , while it was lower in B, C and D groups than group E. ②The total number of cells, the number of eosinophils, and interleukin-5( IL-5) inBALF of group E were higher than those in group A( P lt;0. 05) , and interferon-γ( IFN-γ) level was lower in group E than in group A ( P lt; 0. 05) . After AZ treatment, the total number of cells, the number of eosinophils, neutrophils and lymphocytes were significantly decreased( P lt; 0. 05) , which were positively correlated with the dose of AZ. ③AQP-1 were expressed in tracheal epithelium, microvascular endothelial cell and bronchial peripheral vascular bed, and the expression in group E was significantly higher than that in group A( P lt;0. 01) . AQP-1 expression was significantly decreased after the intervention of AZ ( P lt;0. 05) .The decrease was positively correlated with the dose of AZ. The expression of AQP-1 mRNA showed no significant difference among these groups( P gt;0. 05) . Conclusions AQP-1 was over-expressed in the lung tissue of mice with asthma. AZ can inhibit the expression of AQP-1 and relieve lung inflammatory cells infiltrationin a dose-dependent manner. It is the protein expression of AQP-1 not the AQP-1 mRNA which were significantly different in different groups, suggesting that AZ affected AQP-1 in the post-transcriptional stage.
OBJECTIVE:To evaluate the therapeutic effect of acetazolamide treatment on chronic cystoid macular edema (CME). METHODS:Thirty-seven patients (40 eyes)with documented chronic CME of various causes were prospectively treated for 4-week periods with acetazolamide or a placebo in a randomised,crossover study that compared their effects on the reduction of macular edema and improvement of visual functions. Central retinal artery(CRA) blood flow was determined using Doppler velocimetry and vessel diameter measurement using computerised digital image analysis of monochromatic fundus photographs on 10 patients (12 eyes)with CME pre-and post-administration of acetazolamide. RESULTS:More than half the patients showed a response to acetazolamide with partial or complete resolution of. edema. Thirty eyes had improved in visual acuity in the treated patients. Statistically significant improvement were seen in 10deg; thresholds of visual field and ERG b wave amplitude. No improvement was seen when the patients received placebo. There were significant increase of blood flow velocity in CRA and retinal vessels diameter after acetazolamide were administered 3 hours later in CME patients (Plt;0.05). CONCLUSION: Acetazolamide could be of value in reducing the degree of edema and improving visual function to chronic CME. The improvement on retinal circulation might be a major cause to limit the CME. （Chin J Ocul Fundus Dis,1997,13: 89-92）
In 2019, the American Wilderness Medical Society updated and released a new version of the practice guidelines based on the practice guidelines for the prevention and treatment of acute altitude illness first published in 2010 and updated in 2014. This article interprets the guidelines, focusing on effective measures to prevent and treat different forms of acute altitude illness, as well as suggestions for specific methods to manage the disease, with a view to providing help for clinicians in better practice.
In recent years, the potential benefits of acetazolamide in managing fluid overload in acute decompensated heart failure (ADHF) have attracted the attention of researchers. This article reviews the pharmacological mechanism of acetazolamide, how it improves patient symptoms and clinical prognosis in the treatment of heart failure, and the research progress in clinical application. The aim is to provide theoretical and research basis for clinicians to adjust and choose the comprehensive application plan of diuretics for ADHF, and to provide new ideas and directions for further research and development of new drugs targeting diuretic resistance in ADHF patients.