BACKGROUND: Atelectasis results in impaired compliance and gas exchange and, in extreme cases, increased microvascular permeability, pulmonary hypertension, and right ventricular dysfunction. It is not known whether such atelectasis-induced lung injury is due to the direct mechanical effects of lung volume reduction and alveolar collapse or due to the associated regional lung hypoxia. The authors hypothesized that addition of supplemental oxygen to an atelectasis-prone ventilation strategy would attenuate the pulmonary vascular effects and reduce the local levels of vasoconstrictor eicosanoids. METHODS: In series 1, anesthetized, atelectasis-prone mechanically ventilated rats were randomly assigned to one of six groups based on the inspired oxygen concentration and ventilated without recruitment. Series 2 was performed to determine the cardiac and pulmonary vascular effects of 21% versus 100% inspired oxygen. In series 3, computed tomography scans were performed after ventilation with a recruitment strategy (21% O2) or no recruitment strategy (21% O2 or 100% O2). In series 4, functional residual capacity was measured in animals where the gas was 21% or 100% O2. RESULTS: The partial pressure of arterial oxygen increased with increasing inspired oxygen, but the alveolar-arterial oxygenation gradient was also greater with higher inspired oxygen. Ventilation with 21% O2 (but not with 100% O2) was associated with progressive pulmonary vascular impedance and increased pulmonary vascular permeability. Prostaglandin F2alpha was increased by mechanical ventilation, especially without supplemental oxygen. Computed tomography scans demonstrated no atelectasis in recruited lungs, and atelectasis in nonrecruited lungs that was greater with supplemental oxygen. Increased atelectasis with 100% O2 (vs. 21% O2) was demonstrated by measurement of functional residual capacity. CONCLUSIONS: Although supplemental oxygen worsened atelectasis in this model, it prevented the pathologic effects of atelectasis, including microvascular leak and pulmonary hypertension. Atelectasis-induced lung injury seems to be mediated by hypoxia rather than by the direct mechanical effects of atelectasis.
BACKGROUND: Atelectasis results in impaired compliance and gas exchange and, in extreme cases, increased microvascular permeability, pulmonary hypertension, and right ventricular dysfunction. It is not known whether such atelectasis-induced lung injury is due to the direct mechanical effects of lung volume reduction and alveolar collapse or due to the associated regional lung hypoxia. The authors hypothesized that addition of supplemental oxygen to an atelectasis-prone ventilation strategy would attenuate the pulmonary vascular effects and reduce the local levels of vasoconstrictor eicosanoids. METHODS: In series 1, anesthetized, atelectasis-prone mechanically ventilated rats were randomly assigned to one of six groups based on the inspired oxygen concentration and ventilated without recruitment. Series 2 was performed to determine the cardiac and pulmonary vascular effects of 21% versus 100% inspired oxygen. In series 3, computed tomography scans were performed after ventilation with a recruitment strategy (21% O2) or no recruitment strategy (21% O2 or 100% O2). In series 4, functional residual capacity was measured in animals where the gas was 21% or 100% O2. RESULTS: The partial pressure of arterial oxygen increased with increasing inspired oxygen, but the alveolar-arterial oxygenation gradient was also greater with higher inspired oxygen. Ventilation with 21% O2 (but not with 100% O2) was associated with progressive pulmonary vascular impedance and increased pulmonary vascular permeability. Prostaglandin F2alpha was increased by mechanical ventilation, especially without supplemental oxygen. Computed tomography scans demonstrated no atelectasis in recruited lungs, and atelectasis in nonrecruited lungs that was greater with supplemental oxygen. Increased atelectasis with 100% O2 (vs. 21% O2) was demonstrated by measurement of functional residual capacity. CONCLUSIONS: Although supplemental oxygen worsened atelectasis in this model, it prevented the pathologic effects of atelectasis, including microvascular leak and pulmonary hypertension. Atelectasis-induced lung injury seems to be mediated by hypoxia rather than by the direct mechanical effects of atelectasis.
Authors: Maurizio Cereda; Yi Xin; Hooman Hamedani; Justin Clapp; Stephen Kadlecek; Natalie Meeder; Johnathan Zeng; Harrilla Profka; Brian P Kavanagh; Rahim R Rizi Journal: J Appl Physiol (1985) Date: 2015-12-10
Authors: Laura A Wilding; Joe A Hampel; Basma M Khoury; Stacey Kang; David Machado-Aranda; Krishnan Raghavendran; Jean A Nemzek Journal: J Am Assoc Lab Anim Sci Date: 2017-03-01 Impact factor: 1.232
Authors: Maurizio Cereda; Kiarash Emami; Stephen Kadlecek; Yi Xin; Puttisarn Mongkolwisetwara; Harrilla Profka; Amy Barulic; Stephen Pickup; Sven Månsson; Per Wollmer; Masaru Ishii; Clifford S Deutschman; Rahim R Rizi Journal: J Appl Physiol (1985) Date: 2010-12-02
Authors: Maurizio Cereda; Kiarash Emami; Yi Xin; Stephen Kadlecek; Nicholas N Kuzma; Puttisarn Mongkolwisetwara; Harrilla Profka; Stephen Pickup; Masaru Ishii; Brian P Kavanagh; Clifford S Deutschman; Rahim R Rizi Journal: Crit Care Med Date: 2013-02 Impact factor: 7.598
Authors: Ting Wang; Christine Gross; Ankit A Desai; Evgeny Zemskov; Xiaomin Wu; Alexander N Garcia; Jeffrey R Jacobson; Jason X-J Yuan; Joe G N Garcia; Stephen M Black Journal: Am J Physiol Lung Cell Mol Physiol Date: 2016-12-15 Impact factor: 5.464
Authors: Lesley M Foley; Robert S B Clark; Alberto L Vazquez; T Kevin Hitchens; Henry Alexander; Chien Ho; Patrick M Kochanek; Mioara D Manole Journal: Pediatr Res Date: 2016-09-16 Impact factor: 3.756
Authors: Pablo Cruces; Benjamin Erranz; Felipe Lillo; Mauricio A Sarabia-Vallejos; Pablo Iturrieta; Felipe Morales; Katherine Blaha; Tania Medina; Franco Diaz; Daniel E Hurtado Journal: BMJ Open Respir Res Date: 2019-10-28