Abstract
Background: This work examines the protective effect and mechanisms of early extracorporeal membrane oxygenation with cardiopulmonary resuscitation (CPR) on ventricular-fibrillation-induced post-resuscitation lung injury in a swine cardiac-arrest model. Methods: Sixteen male swine were randomised to conventional CPR (CCPR; n=8; CCPR alone) and extracorporeal CPR (ECPR; n=8; extracorporeal membrane oxygenation with CCPR), with restoration of spontaneous circulation for 6 h as an endpoint. Serological specimens were collected at baseline and restoration of spontaneous circulation for 1, 2, 4, and 6 h; lung tissue specimens were obtained postmortem. Between-group comparisons of recovery success rate, extravascular lung water , pulmonary vascular permeability index, electron microscopic features, and serum and tissue biomarkers (surfactant protein A, surfactant protein D, Clara cell protein 16, superoxide dismutase, malondialdehyde, myeloperoxidase) were undertaken. Results: The CCPR group had non-significantly lower 6-h survival rate ( p> 0.05). Serum levels of surfactant protein A, surfactant protein D, Clara cell protein 16, and malondialdehyde were significantly higher ( p< 0.05), whereas serum superoxide dismutase was significantly lower, in the CCPR than in the ECPR group ( p <0.01). Compared with the ECPR group, tissue surfactant protein A, surfactant protein D, and superoxide dismutase significantly decreased compared to the baseline, whereas malondialdehyde and myeloperoxidase significantly increased ( p< 0.01) in the CCPR group. Extravascular lung water and pulmonary vascular permeability index were significantly higher in the CCPR after 6 h compared to the baseline values and the ECPR group ( p< 0.01). Conclusions: Electron microscopy revealed mostly vacuolated intracellular alveolar type II lamellar bodies and fuzzy lamellar structure and widening and blurring of the blood–gas barrier in the CCPR group in contrast to that in the ECPR group. ECPR was found to have protective pulmonary effects, possibly related to the regulation of alveolar surface-active proteins and mitigated oxidative stress response post-resuscitation.