Hyperinflation deteriorates arterial oxygenation and lung injury in a rabbit model of ARDS with repeated open endotracheal suctioning.
BACKGROUND
Hyperinflation (HI) is performed following open endotracheal suctioning (OES), whose goals include: to stimulate a cough, recover oxygenation and improve compliance. However, it may also induce unintended consequences, including: lung stress and strain, failure to maintain high distending pressure, and subsequently cycling recruitment and derecruitment. Here, our aim was to investigate the effects of hyperinflation after repeated OES on sequential alteration of arterial oxygenation and lung injury profile using a saline lavage-induced surfactant depleted ARDS rabbit model.


METHODS
Briefly, 30 Japanese White Rabbits were anesthetized and ventilated in pressure-controlled setting with a tidal volume of 6-8 ml/kg. Animals were divided into four groups, i.e.; Control, ARDS, OES, and HI. Saline-lavage-induced lung injury was induced except for Control group. Thereafter, rabbits were ventilated with positive-end expiratory pressure (PEEP) at 10 cm H2O. The ARDS group received ventilation with the same PEEP without derecruitment. As intervention, OES and HI were performed in ARDS animals. OES was performed for 15 seconds at 150 mm Hg, whereas HI was performed with PEEP at 0 cm H2O and peak inspiratory pressure at +5 cm H2O for a minute. Total duration of the experiment was for 3 hours. OES and HI were performed every 15 minutes from beginning of the protocol.


RESULTS
PaO2 was maintained at about 400 mm Hg in both control and ARDS groups for the duration of this study, while in both OES and HI groups, PaO2 decreased continuously up to 3 hours, dropped to a mean (±SD) of 226 ± 28.9 and 97.0 ± 30.7 mmHg at 3 h, respectively. HI group had the lowest PaO2 in the present investigation. Histological lung injury score was the highest in HI group than other three groups. Pulmonary TNF-α and IL-8 levels were the highest in HI group compared to other groups, but without significant alterations at circulatory level in all the experimental groups.


CONCLUSIONS
We show in the present study that hyperinflation following repeated OES deteriorate arterial oxygenation and the severity of lung injury in a rabbit model of ARDS undergoing mechanical ventilation.
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. megmagmeggen@yahoo.co.jp.
Junko
J
Kamiyama
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. jsubrina@gmail.com.
Subrina
S
Jesmin
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. gongehead@yahoo.co.jp.
Hideaki
H
Sakuramoto
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. nobu-shimojyo06@ob.md.tsukuba.ac.jp.
Nobutake
N
Shimojyo
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. majedul1987@yahoo.com.
Majedul
M
Islam
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. hagiya916@yahoo.co.jp.
Keiichi
K
Hagiya
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. suganomd@gmail.com.
Masato
M
Sugano
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. iwhyh1029@gmail.com.
Takeshi
T
Unoki
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. s1321258@u.tsukuba.ac.jp.
Masami
M
Oki
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. kawano_s@md.tsukuba.ac.jp.
Satoru
S
Kawano
Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan. mizutani@md.tsukuba.ac.jp.
Taro
T
Mizutani
D000704:Analysis of Variance; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D016209:Interleukin-8 / Q000378:metabolism; D055370:Lung Injury / Q000209:etiology*; D008297:Male; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011175:Positive-Pressure Respiration / Q000009:adverse effects*; D011817:Rabbits; D011897:Random Allocation; D012128:Respiratory Distress Syndrome / Q000628:therapy*; D013396:Suction / Q000009:adverse effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D002245:Carbon Dioxide; D010100:Oxygen