Ackerman N B, Coalson J J, Kuehl T J, Stoddard R, Minnick L, Escobedo M B, Null D M, Robotham J L, deLemos R
Crit Care Med. 1984 Jun;12(6):512-6. doi: 10.1097/00003246-198406000-00009.
During experiments designed to develop an appropriate ventilatory strategy for high-frequency ventilation (HFV) in the premature baboon with hyaline membrane disease (HMD), we observed the development of pulmonary interstitial emphysema (PIE). Four study groups of 5 animals each received positive-pressure ventilation and positive end-expiratory pressure (PPV/PEEP) or HFV and 1 of 3 sighing techniques. Pathologically, all animals ventilated with PPV/PEEP or HFV with a carefully controlled intermittent sigh developed dilatation of the distal conducting airway and alveolar duct, with poorly expanded pulmonary saccules. The imposition of a sigh with inappropriate timing or excessive volume ruptured the dilated airway walls and caused interstitial air to accumulate. This was evident from the location of striking dilation of the distal airways and pseudocysts in areas of atelectasis. Thus, early in the course of HMD when saccular aeration is minimal, the pathogenesis of PIE is related to airway rather than alveolar rupture.
在旨在为患有透明膜病(HMD)的早产狒狒制定合适的高频通气(HFV)通气策略的实验过程中,我们观察到了肺间质肺气肿(PIE)的发展。四个研究组,每组5只动物,分别接受正压通气和呼气末正压(PPV/PEEP)或高频通气以及三种叹息技术中的一种。从病理上看,所有接受PPV/PEEP通气或接受精心控制的间歇性叹息的高频通气的动物,其远端传导气道和肺泡管均出现扩张,肺小囊扩张不良。时机不当或气量过大的叹息会使扩张的气道壁破裂,导致间质空气积聚。这从肺不张区域远端气道和假囊肿的明显扩张位置可以明显看出。因此,在HMD病程早期,当肺小囊充气极少时,PIE的发病机制与气道破裂而非肺泡破裂有关。