摘要
Background： Study of lung function in survivor from cardiac arrest （CA） caused by pulmonary thromboembolism （PTE） was rare. The aim of this study was to investigate the variations ofpostresuscitation lung function after thrombolysis treatment in a CA porcine model caused by PTE. Methods： After 2 min of untreated CA, pigs of 10-12 weeks with a weight of 30±2 kg （n = 24） were treated with recombinant human tissue plasminogen activator （50 mg）. Cardiopulmonary resuscitation （CPR） and ventilation were initiated after drug administration. Pulmonary function and arterial blood gas parameters were measured at baseline, return of spontaneous circulation （ROSC） immediately, and 1 h, 2 h, 4 h, and 6 h after ROSC. Results： The dynamic lung compliance decreased significantly at ROSC immediately and 1 h after ROSC compared to baseline （21.86 ±2.00 vs. 26.72± 2.20 ml/mmHg and 20.38 ± 1.31 vs. 26.72 ± 2.20 ml/mmHg, respectively; P 〈 0.05; 1 mmHg = 0.133 kPa）. Compared with baseline, airway resistance increased significantly at ROSC immediately and 1 h after ROSC （P 〈 0.05）. Respiratory index also increased after ROSC and showed significant differences among baseline, ROSC immediately, and 2 h after ROSC （P 〈 0.05）. Oxygen delivery decreased at ROSC immediately compared to baseline （P 〈 0.05）. The oxygenation index decreased significantly at any time after ROSC compared to baseline （P 〈 0.05）. Extravascular lung water index and pulmonary vascular permeability index （PVP1） showed significant differences at ROSC immediately compared to baseline and 1 h after ROSC （P 〈 0.05）; PVPI at ROSC inamediately was also different from 6 h after ROSC （P 〈 0.05）. Ventilation/perfusion ratios increased after ROSC （P 〈 0.05）. Histopathology showed fibrin effusion, bleeding in alveoli, and hemagglutinatiun in pulmonary artery. Conclusions： Lung function remains abnormal even after CPR with thrombolysis therapy; it is essential to continue anticoagulation and symptomatic treatment after ROSC.
Background： Study of lung function in survivor from cardiac arrest （CA） caused by pulmonary thromboembolism （PTE） was rare. The aim of this study was to investigate the variations ofpostresuscitation lung function after thrombolysis treatment in a CA porcine model caused by PTE. Methods： After 2 min of untreated CA, pigs of 10-12 weeks with a weight of 30±2 kg （n = 24） were treated with recombinant human tissue plasminogen activator （50 mg）. Cardiopulmonary resuscitation （CPR） and ventilation were initiated after drug administration. Pulmonary function and arterial blood gas parameters were measured at baseline, return of spontaneous circulation （ROSC） immediately, and 1 h, 2 h, 4 h, and 6 h after ROSC. Results： The dynamic lung compliance decreased significantly at ROSC immediately and 1 h after ROSC compared to baseline （21.86 ±2.00 vs. 26.72± 2.20 ml/mmHg and 20.38 ± 1.31 vs. 26.72 ± 2.20 ml/mmHg, respectively; P 〈 0.05; 1 mmHg = 0.133 kPa）. Compared with baseline, airway resistance increased significantly at ROSC immediately and 1 h after ROSC （P 〈 0.05）. Respiratory index also increased after ROSC and showed significant differences among baseline, ROSC immediately, and 2 h after ROSC （P 〈 0.05）. Oxygen delivery decreased at ROSC immediately compared to baseline （P 〈 0.05）. The oxygenation index decreased significantly at any time after ROSC compared to baseline （P 〈 0.05）. Extravascular lung water index and pulmonary vascular permeability index （PVP1） showed significant differences at ROSC immediately compared to baseline and 1 h after ROSC （P 〈 0.05）; PVPI at ROSC inamediately was also different from 6 h after ROSC （P 〈 0.05）. Ventilation/perfusion ratios increased after ROSC （P 〈 0.05）. Histopathology showed fibrin effusion, bleeding in alveoli, and hemagglutinatiun in pulmonary artery. Conclusions： Lung function remains abnormal even after CPR with thrombolysis therapy; it is essential to continue anticoagulation and symptomatic treatment after ROSC.
基金
This work supported by grants from the National Natural Science Foundation of China （No. 81372025） and the 2015 Annual Special Cultivation and Development Project for Technology Innovation Base of Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation （No. Z 151100001615056）.
