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Inhibition of hypoxia-induced calcium responses in pulmonary arterial smooth muscle by acetazolamide is independent of carbonic anhydrase inhibition.乙酰唑胺对肺动脉平滑肌缺氧诱导的钙反应的抑制作用与碳酸酐酶抑制无关。
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Carbonic anhydrase. Its preparation and properties.碳酸酐酶。其制备方法及性质。
J Physiol. 1933 Dec 5;80(2):113-42. doi: 10.1113/jphysiol.1933.sp003077.
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Pulmonary vasodilation by acetazolamide during hypoxia is unrelated to carbonic anhydrase inhibition.乙酰唑胺在低氧期间引起的肺血管舒张与碳酸酐酶抑制无关。
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The structure and function of carbonic anhydrase isozymes in the respiratory system of vertebrates.脊椎动物呼吸系统中碳酸酐酶同工酶的结构与功能。
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Beta-adrenergic receptor stimulation and adenoviral overexpression of superoxide dismutase prevent the hypoxia-mediated decrease in Na,K-ATPase and alveolar fluid reabsorption.β-肾上腺素能受体刺激和超氧化物歧化酶的腺病毒过表达可预防缺氧介导的钠钾ATP酶活性降低及肺泡液体重吸收减少。
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Isolation of highly pure alveolar epithelial type I and type II cells from rat lungs.从大鼠肺中分离高纯度的I型和II型肺泡上皮细胞。
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Upregulation of alveolar epithelial active Na+ transport is dependent on beta2-adrenergic receptor signaling.肺泡上皮细胞主动钠转运的上调依赖于β2-肾上腺素能受体信号传导。
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高碳酸血症期间的碳酸酐酶II与肺泡液体重吸收

Carbonic anhydrase II and alveolar fluid reabsorption during hypercapnia.

作者信息

Chen Jiwang, Lecuona Emilia, Briva Arturo, Welch Lynn C, Sznajder Jacob I

机构信息

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.

出版信息

Am J Respir Cell Mol Biol. 2008 Jan;38(1):32-7. doi: 10.1165/rcmb.2007-0121OC. Epub 2007 Aug 9.

DOI:10.1165/rcmb.2007-0121OC
PMID:17690328
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2176133/
Abstract

Carbonic anhydrase II (CAII) plays an important role in carbon dioxide metabolism and intracellular pH regulation. In this study, we provide evidence that CAII is expressed in both type I (AECI) and type II (AECII) alveolar epithelial cells by RT-PCR and Western blotting in freshly isolated rat cells. These results were further confirmed by double immunostaining with CAII antibodies and AECI- or AECII-specific markers in freshly isolated alveolar epithelial cells and rat lung tissues. Inhibition of CAII by acetazolamide or methazolamide delayed the decrease in the intracellular pH observed during hypercapnia in cultured AECI, AECII, and AECI-like cells. In an isolated-perfused rat lung model, alveolar fluid reabsorption significantly decreased during high CO(2) exposure, which was not prevented by carbonic anhydrase inhibition. Thus, we provide evidence that CAII is expressed in rat alveolar epithelial cells and does not regulate lung alveolar fluid reabsorption during hypercapnia.

摘要

碳酸酐酶II(CAII)在二氧化碳代谢和细胞内pH调节中发挥着重要作用。在本研究中,我们通过逆转录聚合酶链反应(RT-PCR)和蛋白质免疫印迹法,在新鲜分离的大鼠细胞中证实了CAII在I型(AECI)和II型(AECII)肺泡上皮细胞中均有表达。在新鲜分离的肺泡上皮细胞和大鼠肺组织中,用CAII抗体与AECI或AECII特异性标志物进行双重免疫染色,进一步证实了这些结果。在培养的AECI、AECII和AECI样细胞中,乙酰唑胺或甲醋唑胺对CAII的抑制作用延缓了高碳酸血症期间观察到的细胞内pH的下降。在离体灌注大鼠肺模型中,高二氧化碳暴露期间肺泡液体重吸收显著降低,碳酸酐酶抑制并不能阻止这种情况。因此,我们提供的证据表明,CAII在大鼠肺泡上皮细胞中表达,并且在高碳酸血症期间不调节肺泡液体重吸收。