Acute ischaemic lung injury due to pulmonary vascular obstruction

Kawabata, Yoshinori; Shimizu, Yoshihiko; Hoshi, Eishin; Ikeya, Tomohiko; Kurashima, Kazuyoshi; Takayanagi, Noboru

doi:10.1111/his.12979

Cited by 1 publication

(2 citation statements)

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“…Indeed, bronchial perfusion increases in the presence of higher alveolar O 2 and CO 2 ( 23 ); both might have been obtained by inhaled CO 2 through direct effect (for CO 2 ) and higher regional ventilation of the left lung (for O 2 ). Our observation suggests that the reduction of tissue hypoperfusion might be a novel mechanism underlying the protective effect of inhaled CO 2 ( 8 , 9 , 24 ).…”

Section: Discussionmentioning

confidence: 75%

“…Pathologic changes in lung perfusion in acute respiratory failure include a spectrum of functional and anatomical alterations ranging from impaired regional vaso-regulation to perfusion micro-thrombotic defects to pulmonary embolism ( 1 , 2 ). These changes might contribute to ventilation-induced lung injury (VILI) through several mechanisms, including alveolar hypocapnia ( 3 , 4 ), inhomogeneous distribution of ventilation ( 5 – 7 ), and regional hypoperfusion ( 8 , 9 ). Notably, these mechanisms may be at play even when ventilation is delivered within protective limits.…”

Section: Introductionmentioning

confidence: 99%

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Inhaled CO2 vs. Hypercapnia Obtained by Low Tidal Volume or Instrumental Dead Space in Unilateral Pulmonary Artery Ligation: Any Difference for Lung Protection?

et al. 2022

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BackgroundUnilateral ligation of the pulmonary artery (UPAL) induces bilateral lung injury in pigs undergoing controlled mechanical ventilation. Possible mechanisms include redistribution of ventilation toward the non-ligated lung and hypoperfusion of the ligated lung. The addition of 5% CO2 to the inspiratory gas (FiCO2) prevents the injury, but it is not clear whether lung protection is a direct effect of CO2 inhalation or it is mediated by plasmatic hypercapnia. This study aims to compare the effects and mechanisms of FiCO2vs. hypercapnia induced by low tidal volume ventilation or instrumental dead space.MethodsHealthy pigs underwent left UPAL and were allocated for 48 h to the following: Volume-controlled ventilation (VCV) with VT 10 ml/kg (injury, n = 6); VCV plus 5% FiCO2 (FiCO2, n = 7); VCV with VT 6 ml/kg (low VT, n = 6); VCV plus additional circuit dead space (instrumental VD, n = 6). Histological score, regional compliance, wet-to-dry ratio, and inflammatory infiltrate were assessed to evaluate lung injury at the end of the study. To investigate the mechanisms of protection, we quantified the redistribution of ventilation to the non-ligated lung, as the ratio between the percentage of tidal volume to the right and to the left lung (VTRIGHT/LEFT), and the hypoperfusion of the ligated lung as the percentage of blood flow reaching the left lung (PerfusionLEFT).ResultsIn the left ligated lung, injury was prevented only in the FiCO2 group, as indicated by lower histological score, higher regional compliance, lower wet-to-dry ratio and lower density of inflammatory cells compared to other groups. For the right lung, the histological score was lower both in the FiCO2 and in the low VT groups, but the other measures of injury showed lower intensity only in the FiCO2 group. VTRIGHT/LEFT was lower and PerfusionLEFT was higher in the FiCO2 group compared to other groups.ConclusionIn a model of UPAL, inhaled CO2 but not hypercapnia grants bilateral lung protection. Mechanisms of protection include reduced overdistension of the non-ligated and increased perfusion of the ligated lung.

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Section: Discussionmentioning

confidence: 75%