Oyarzun M J, Clements J A
Am Rev Respir Dis. 1978 May;117(5):879-91. doi: 10.1164/arrd.1978.117.5.879.
In a previous study, we showed that increasing minute ventilation (VE) in rabbit lung by adding a dead space augmented pulmonary surfactant in the airspaces by a cholinergically mediated mechanism. Using the same model in the present study of 148 rabbits, we found that increasing VE augmented airspace phospholipid, the main component of surfactant, from 2.50 +/- 0.61 (mean +/- SD) mg per g of lung during normal VE to 3.15 +/- 1.22 (mean +/- SD) mg per g of lung during increased VE (P = 0.02). Both blocking beta-adrenergic receptors with propranolol or sotalol and inhibiting prostaglandin synthetase with indomethacin or sodium meclofenamate prevented the expected increase in phospholipid during increased VE (P is less than 0.05). The beta-2 agonist, terbutaline, increased phospholipid by 43 per cent during normal VE (P is less than 0.01), and propranolol blocked this increase (P is less than 0.05). Isoproterenol, arachidonic acid, prostaglandins E1, E2, F2alpha, and a cyclic endoperoxide analog of prostaglandin H2 (U-46619) injected during normal VE failed to increase phospholipid. We concluded that acetylcholine (previous study), beta-adrenergic mediators, and prostaglandins are involved in controlling alveolar surfactant during increased VE.
在之前的一项研究中，我们发现通过增加无效腔来提高家兔肺的分钟通气量（VE），可通过胆碱能介导机制增加肺泡内的肺表面活性物质。在本研究中，我们使用相同模型对148只家兔进行实验，发现增加VE可使表面活性物质的主要成分——肺泡磷脂增加，在正常VE时为每克肺组织2.50±0.61（均值±标准差）毫克，增加VE后升至每克肺组织3.15±1.22（均值±标准差）毫克（P = 0.02）。使用普萘洛尔或索他洛尔阻断β - 肾上腺素能受体，以及使用吲哚美辛或甲氯芬那酸钠抑制前列腺素合成酶，均可阻止增加VE时磷脂的预期增加（P＜0.05）。β₂激动剂特布他林在正常VE时可使磷脂增加43%（P＜0.01），而普萘洛尔可阻断这一增加（P＜0.05）。在正常VE时注射异丙肾上腺素、花生四烯酸、前列腺素E₁、E₂、F₂α以及前列腺素H₂的环内过氧化物类似物（U - 46619）均未能增加磷脂。我们得出结论，乙酰胆碱（之前的研究）、β - 肾上腺素能介质和前列腺素参与了增加VE时肺泡表面活性物质的调控。
