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首页> 外文期刊>Life sciences >Muscarinic receptors involved in airway vascular leakage induced by experimental gastro-oesophageal reflux
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Muscarinic receptors involved in airway vascular leakage induced by experimental gastro-oesophageal reflux

机译：毒蕈碱受体参与实验性胃食管反流引起的气道血管渗漏

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Gastro-oesophageal acid reflux may cause airway responses such as cough, bronchoconstriction and inflammation in asthmatic patients. Studies in humans or in animals have suggested that these responses involve cholinergic nerves. The purpose of this study was to investigate the role of the efferent vagal component on airway microvascular leakage induced by instillation of hydrochloric acid (HCI) into the oesophagus of guinea-pigs and the subtype of muscarinic receptors involved. Airway microvascular leakage induced by intra-oesophageal HCI instillation was abolished by bilateral vagotomy or by the nicotinic receptor antagonist, hexamethonium. HCl-induced leakage was inhibited by pretreatment with atropine, a non-specific muscarinic receptor antagonist, and also by pretreatment with either pirenzepine, a muscarinic M, receptor antagonist, or 4-DAMP, a muscarinic M-3 receptor antagonist. Pirenzepine was more potent than atropine and 4-DAMP. These antagonists were also studied on airway microvascular leakage or bronchoconstriction induced by intravenous administration of acetylcholine (ACh). Atropine, pirenzepine and 4-DAMP inhibited ACh-induced airway microvascular leakage with similar potencies. In sharp contrast, 4-DAMP and atropine were more potent inhibitors of ACh-induced bronchoconstriction than pirenzepine. Methoctramine, a muscarinic M-2 receptor antagonist, was ineffective in all experimental conditions. These results suggest that airway microvascular leakage caused by HCI intra-oesophageal instillation involves ACh release from vagus nerve terminals and that M, and M-3 receptors play a major role in cholinergic-mediated microvascular leakage, whereas M-3 receptors are mainly involved in ACh-induced bronchoconstriction. (c) 2008 Elsevier Inc. All rights reserved.
机译：胃食管胃酸反流可能引起气道反应，例如哮喘患者的咳嗽，支气管收缩和炎症。在人类或动物中的研究表明，这些反应涉及胆碱能神经。这项研究的目的是调查迷走神经传出成分对豚鼠食管中盐酸（HCI）的滴注和毒蕈碱受体亚型引起的气道微血管渗漏的作用。通过双侧迷走神经切开术或烟碱样受体拮抗剂六甲铵消除了食道内HCl滴注引起的气道微血管渗漏。盐酸诱导的泄漏可通过非特异的毒蕈碱受体拮抗剂阿托品预处理来抑制，也可以通过毒蕈碱M受体拮抗剂哌仑西平或毒蕈碱M-3受体拮抗剂4-DAMP预处理来抑制。哌仑西平比阿托品和4-DAMP更有效。还研究了这些拮抗剂对静脉内注射乙酰胆碱（ACh）引起的气道微血管渗漏或支气管收缩的作用。阿托品，哌仑西平和4-DAMP以相似的效力抑制ACh诱导的气道微血管渗漏。与之形成鲜明对比的是，与吡仑西平相比，4-DAMP和阿托品是ACh诱导的支气管收缩的更有效抑制剂。甲基辛卡明（一种毒蕈碱M-2受体拮抗剂）在所有实验条件下均无效。这些结果表明，HCI食管内滴注引起的气道微血管渗漏涉及迷走神经末梢释放ACh，M和M-3受体在胆碱能介导的微血管渗漏中起主要作用，而M-3受体主要参与ACh引起的支气管收缩。 （c）2008 Elsevier Inc.保留所有权利。

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