Biomedical subjects
Publications and source records attributed to Marc de Perrot.
We present a simplified model of lung xenotransplantation from hamster to rat with a total non-suture technique using 14G cuffs for the main pulmonary artery, the trachea and the left atrium. This technique provides a technically easier and more reliable model to study xenotransplantation of the lung.
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OBJECTIVE: Although mechanical ventilation can potentially worsen preexisting lung injury, its importance in the setting of lung transplantation has not been explored. This study was undertaken to examine the effect of 2 ventilatory strategies on the development of ischemia-reperfusion injury after lung transplantation. METHODS: In a rat lung transplant model animals were randomized into 2 groups defined by the ventilatory strategy during the early reperfusion period. In conventional mechanical ventilation the transplanted lung was ventilated with a tidal volume equal to 50% of the inspiratory capacity of the left lung and a low positive end-expiratory pressure. In minimal mechanical stress ventilation the transplanted lung was ventilated with a tidal volume equal to 20% of the inspiratory capacity of the left lung, and positive end-expiratory pressure was adjusted according to the shape of the pressure-time curve to minimize pulmonary stress. RESULTS: After 3 hours of reperfusion, oxygenation from the transplanted lung was significantly higher with minimal mechanical stress ventilation than with conventional ventilation. In addition, elastance, cytokine levels, and morphologic signs of injury were significantly lower in the group with minimal mechanical stress ventilation. CONCLUSIONS: This study demonstrates that the mode of mechanical ventilation used in the early phase of reperfusion of the transplanted lung can influence ischemia-reperfusion injury, and a protective ventilatory strategy on the basis of minimizing pulmonary mechanical stress can lead to improved lung function after lung transplantation.
STUDY OBJECTIVES: To assess the mortality rate and the incidence of cardiopulmonary complications after pneumonectomy for non-small cell lung carcinoma (NSCLC) and to identify possible associated risk factors. DESIGN: Observational study of patients who underwent pneumonectomy. Potential risk factors were analyzed from a local database including all thoracic surgical cases. SETTING: A university hospital and a chest medical center. PATIENTS AND METHODS: From January 1, 1990, to April 30, 2000, 193 consecutive pneumonectomies were performed for NSCLC in two affiliated institutions. The following information was recorded: demographic, clinical, functional, and surgical variables; as well as intraoperative and postoperative events. The risk of mortality and cardiopulmonary complications was evaluated using multiple logistic regression analysis to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: After undergoing pneumonectomy, all patients were successfully extubated in the operating room and then transferred to a postanesthesia care unit (126 patients) or ICU (67 patients). The 30-day mortality rate was 9.3%, and cardiovascular and/or pulmonary complications occurred in 47% of cases. Coronary artery disease (CAD) was a predictor of 30-day mortality (OR, 2.9; 95% CI, 1.1 to 8.9). Cardiac morbidity (mainly arrhythmias) was significantly related to advanced age (OR, 3.7; 95% CI, 1.6 to 8.6) and pathologic stages III/IV (OR, 1.4; 95% CI, 1.1 to 4.7), whereas continuous epidural analgesia was associated with a reduced incidence of respiratory complications (OR, 0.2; 95% CI, 0.1 to 0.6). CONCLUSIONS: Pneumonectomy for lung cancer is a high-risk procedure, the risk for which is significantly related to the presence of CAD and advanced pathologic stages. Importantly, the provision of epidural analgesia contributes to lower the risk of respiratory complications.
CONTEXT: Recent clinical trials have demonstrated a decrease in multiple organ dysfunction syndrome (MODS) and mortality in patients with acute respiratory distress syndrome (ARDS) treated with a protective ventilatory strategy. OBJECTIVE: To examine the hypothesis that an injurious ventilatory strategy may lead to end-organ epithelial cell apoptosis and organ dysfunction. DESIGN AND SETTING: In vivo animals: 24 rabbits with acid-aspiration lung injury were ventilated with injurious or noninjurious ventilatory strategies. In vitro: rabbit epithelial cells were exposed to plasma from in vivo rabbit studies. In vivo human: plasma samples from patients included in a previous randomized controlled trial examining a lung protective strategy were analyzed (lung protection group, n = 9 and controls, n = 11). MAIN OUTCOME MEASURES: In vivo animals: biochemical markers of liver and renal dysfunction; apoptosis in end organs. In vitro: induction of apoptosis in LLC-RK1 renal tubular epithelial cells. In vivo human: correlation of plasma creatinine and soluble Fas ligand. RESULTS: The injurious ventilatory strategy led to increased rates of epithelial cell apoptosis in the kidney (mean [SE]: injurious, 10.9% [0.88%]; noninjurious, 1.86% [0.17%]; P<.001) and small intestine villi (injurious, 6.7% [0.66%]; noninjurious, 0.97% [0.14%]; P<.001), and led to the elevation of biochemical markers indicating renal dysfunction in vivo. Induction of apoptosis was increased in LLC-RK1 cells incubated with plasma from rabbits ventilated with injurious ventilatory strategy at 4 hours (P =.03) and 8 hours (P =.002). The Fas:Ig, a fusion protein that blocks soluble Fas ligand, attenuated induction of apoptosis in vitro. There was a significant correlation between changes in soluble Fas ligand and changes in creatinine in patients with ARDS (R = 0.64, P =.002). CONCLUSIONS: Mechanical ventilation can lead to epithelial cell apoptosis in the kidney and small intestine, accompanied by biochemical evidence of organ dysfunction. This may partially explain the high rate of MODS observed in patients with ARDS and the decrease in morbidity and mortality in patients treated with a lung protective strategy.