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本文引用的文献

1
Prescribing of β-adrenoceptor antagonists in asthma: an observational study.β-肾上腺素能受体拮抗剂在哮喘中的应用:一项观察性研究。
Thorax. 2011 Jun;66(6):502-7. doi: 10.1136/thoraxjnl-2011-200067. Epub 2011 Apr 1.
2
Response to salbutamol in patients with mild asthma treated with nadolol.纳多洛尔治疗的轻度哮喘患者对沙丁胺醇的反应。
Eur Respir J. 2010 Oct;36(4):963-5. doi: 10.1183/09031936.00003210.
3
Beta2-adrenoceptor signaling is required for the development of an asthma phenotype in a murine model.在小鼠模型中,β2-肾上腺素能受体信号传导是哮喘表型发展所必需的。
Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2435-40. doi: 10.1073/pnas.0810902106. Epub 2009 Jan 26.
4
Beta blockers for asthma: a double-edged sword.用于治疗哮喘的β受体阻滞剂:一把双刃剑。
Lancet. 2009 Jan 10;373(9658):104-5. doi: 10.1016/S0140-6736(09)60018-0.
5
The safety and effects of the beta-blocker, nadolol, in mild asthma: an open-label pilot study.β受体阻滞剂纳多洛尔治疗轻度哮喘的安全性及疗效:一项开放标签的试点研究。
Pulm Pharmacol Ther. 2008;21(1):134-41. doi: 10.1016/j.pupt.2007.07.002. Epub 2007 Jul 17.
6
Changes in beta 2-adrenoceptor and other signaling proteins produced by chronic administration of 'beta-blockers' in a murine asthma model.在小鼠哮喘模型中,长期施用“β受体阻滞剂”所产生的β2-肾上腺素能受体及其他信号蛋白的变化。
Pulm Pharmacol Ther. 2008;21(1):115-24. doi: 10.1016/j.pupt.2007.06.003. Epub 2007 Jul 4.
7
Standardisation of spirometry.肺活量测定法的标准化
Eur Respir J. 2005 Aug;26(2):319-38. doi: 10.1183/09031936.05.00034805.
8
The selectivity of beta-adrenoceptor antagonists at the human beta1, beta2 and beta3 adrenoceptors.β-肾上腺素能受体拮抗剂对人β1、β2和β3肾上腺素能受体的选择性。
Br J Pharmacol. 2005 Feb;144(3):317-22. doi: 10.1038/sj.bjp.0706048.
9
A comparison of lung function methods for assessing dose-response effects of salbutamol.评估沙丁胺醇剂量反应效应的肺功能方法比较
Br J Clin Pharmacol. 2004 Aug;58(2):134-41. doi: 10.1111/j.1365-2125.2004.02105.x.
10
Effects of acute and chronic administration of beta-adrenoceptor ligands on airway function in a murine model of asthma.急性和慢性给予β-肾上腺素能受体配体对哮喘小鼠模型气道功能的影响。
Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4948-53. doi: 10.1073/pnas.0400452101.

氢可酮对急性β-肾上腺素能受体阻滞剂和组胺诱导的支气管收缩的影响。

Effects of hydrocortisone on acute β-adrenoceptor blocker and histamine induced bronchoconstriction.

机构信息

Asthma and Allergy Research Group, Centre for Cardiovascular and Lung Biology, Division of Medical Sciences, University of Dundee, Dundee, UK.

出版信息

Br J Clin Pharmacol. 2012 May;73(5):717-26. doi: 10.1111/j.1365-2125.2011.04143.x.

DOI:10.1111/j.1365-2125.2011.04143.x
PMID:22077869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3403199/
Abstract

AIMS

β-adrenoceptor blockers are avoided in asthma due to concerns of bronchoconstriction. We investigated the safety of acute exposure to propranolol in asthmatics, sequentially challenged with histamine to mimic an asthma exacerbation and evaluated the role of intravenous hydrocortisone in potentiating salbutamol reversibility.

METHODS

Persistent atopic asthmatics, requiring ≤ 1000 µg day(-1) budesonide, performed a randomized double-blind placebo-controlled crossover study. Following 10 mg or 20 mg of oral propranolol, patients received 400 mg intravenous hydrocortisone or placebo, followed by histamine challenge with nebulized salbutamol 5 mg and ipratropium 500 µg recovery.

RESULTS

Thirteen patients completed per protocol. Hydrocortisone did not potentiate salbutamol recovery post propranolol and histamine challenge vs. placebo (mean difference in FEV(1) 0.04 ml, 95% CI -0.07, 0.15, P= 0.417). β-adrenoceptor blocker induced bronchoconstriction was demonstrated by spirometry and impulse oscillometry. For the placebo visit, FEV(1) fell 4.7% 2 hours post propranolol (95% CI 1.8, 7.5, P= 0.008) whilst total airway resistance (R5%) increased 31.3% (95% CI 15.6, 47.0, P= 0.04). On both visits FEV(1) % and R5% returned to baseline after salbutamol post histamine.

CONCLUSION

Nebulized salbutamol and ipratropium produced a full recovery after propranolol and histamine induced bronchoconstriction, independent of hydrocortisone use. Since the greatest risk of β-adrenoceptor blockade is after first dose, our findings offer reassurance to those undertaking further evaluation of chronic β-adrenoceptor blockade as a potential treatment for mild-to-moderate asthma.

摘要

目的

由于担心支气管收缩,β-肾上腺素受体阻滞剂在哮喘中被避免使用。我们研究了急性暴露于普萘洛尔在哮喘患者中的安全性,这些患者先后接受组胺挑战以模拟哮喘加重,并评估静脉注射氢化可的松在增强沙丁胺醇逆转中的作用。

方法

需要≤1000μg 布地奈德/天的持续性特应性哮喘患者进行了一项随机、双盲、安慰剂对照交叉研究。口服普萘洛尔 10mg 或 20mg 后,患者接受 400mg 静脉注射氢化可的松或安慰剂,随后用雾化沙丁胺醇 5mg 和异丙托溴铵 500μg 进行组胺挑战以恢复。

结果

13 名患者按方案完成。与安慰剂相比,氢化可的松并没有增强普萘洛尔和组胺挑战后的沙丁胺醇恢复(FEV1 的平均差异为 0.04ml,95%CI-0.07,0.15,P=0.417)。通过肺量计和脉冲振荡测量法证实了β-肾上腺素受体阻滞剂引起的支气管收缩。在安慰剂就诊时,FEV1 在普萘洛尔后 2 小时下降了 4.7%(95%CI 1.8,7.5,P=0.008),而总气道阻力(R5%)增加了 31.3%(95%CI 15.6,47.0,P=0.04)。在两次就诊中,在组胺后用沙丁胺醇后,FEV1%和 R5%均恢复至基线。

结论

在普萘洛尔和组胺引起的支气管收缩后,雾化沙丁胺醇和异丙托溴铵产生了完全恢复,与氢化可的松的使用无关。由于β-肾上腺素受体阻滞剂的最大风险是在第一次给药后,我们的发现为那些正在进一步评估慢性β-肾上腺素受体阻滞剂作为轻度至中度哮喘潜在治疗方法的人提供了保证。