Continuous tracheal gas insufflation during protective mechanical ventilation in juvenile piglets with acute lung injury induced by endotoxin

Low tidal volume mechanical ventilation is difficult to correct hypoxemia, and prolonged inhalation of pure oxygen can lead to oxygen poisoning. We suggest that continuous tracheal gas insufflation （TGI） during protective mechanical ventilation could improve cardiopulmonary function in acute lung injury. Totally 12 healthy juvenile piglets were anesthetized and mechanically ventilated at PEEP of 2 cmH2O with a peak inspiratory pressure of 10 cmH2O. The piglets were challenged with lipopolysaccharide and randomly assigned into two groups （n=6 each group）： mechanical ventilation （MV） alone and TGI with continuous airway flow 2 I/min. FIO2 was set at 0.4 to avoid oxygen toxicity and continuously monitored with an oxygen analyzer. Tidal volume, ventilation efficacy index and mean airway resistant pressure were significantly improved in the TGI group （P〈0.01 or P〈0.05）. At 4 hours post ALl, pH decreased to below 7.20 in the MV group, and improved in the TGI group （P〈0.01）. Similarly, PaCO2 was stable and was significantly lower in the TGI group than in the MV group （P〈0.01）. PaO2 and PaO2/FIO2 increased also in the TGI group （P〈0.05）. There was no significant difference in heart rate, respiratory rate, mean artery pressure, central venous pressure, dynamic lung compliance and mean resistance of airway between the two groups. Lung histological examination showed reduced inflammation, reduced intra- alveolar and interstitial patchy hemorrhage, and homogenously expanded lungs in the TGI group. Continuous TGI during MV can significantly improve gas exchange and ventilation efficacy and may provide a better treatment for acute lung injury.

Lung recruitment maneuver effects on respiratory mechanics and extravascular lung water index in patients with acute respiratory distress syndrome

BACKGROUND：Animal experiments showed that recruitment maneuver （RM） and protective ventilation strategy of the lung could improve oxygenation and reduce extravascular lung water. This study was to investigate the effects of RM on respiratory mechanics and extravascular lung water index （EVLWI） in patients with acute respiratory distress syndrome （ARDS）. METHODS：Thirty patients with ARDS were randomized into a RM group and a non-RM group. In the RM group, after basic mechanical ventilation stabilized for 30 minutes, RM was performed and repeated once every 12 hours for 3 days. In the non-RM group, lung protective strategy was conducted without RM. Oxygenation index （PaO2/FiO2）, peak inspiratory pressure （PIP）, Plateau pressure （Pplat）, static pulmonary compliance （Cst） and EVLWI of patients before treatment and at 12, 24, 48, 72 hours after the treatment were measured and compared between the groups. Hemodynamic changes were observed before and after RM. One-way ANOVA, Student＇s t test and Fisher＇s exact test were used to process the data. RESULTS：The levels of PaO2/FiO2 and Cst increased after treatment in the two groups, but they were higher in the RM group than in the non-RM group （P〈0.05）. The PIP and Pplat decreased after treatment in the two groups, but they were lower in the RM group than in the non-RM group （P〈0.05）. The EVLWI in the two groups showed downward trend after treatment （P〈0.05）, and the differences were signifcant at all time points （P〈0.01）; the EVLWI in the RM group was lower than that in the non-RM group at 12, 24, 48 and 72 hours （P〈0.05 or P〈0.01）. Compared with pre-RM, hemodynamics changes during RM were significantly different （P〈0.01）; compared with pre-RM, the changes were not significantly different at 120 seconds after the end of RM （P〉0.05）. CONCLUSIONS： RM could reduce EVLWI, increase oxygenation and lung compliance. The effect of RM on hemodynamics was transient.

Sarin Induced Lung Pathology and Protection by Standard Therapy Regime

The effects of atropine, diazepam and pralidoxime were studied for their ability to block the pathological lesions induced by sarin. Rats were exposed to an aerosol of sarin at a concentration of 51.2mg-m for 15 min following the pretreatment with one of the following combinations: atropine (10 mg/kg, i.m.) and diazepam (0.5 mg/kg, i.m.); atropine and pralidoxime (25 mg/kg, i.m.); diazepam and pralidoxime; atropine, diazepam and pralidoxime. Lung exposed to sarin aerosols revealed an increased cellular proliferation with progressive diffused interstitial thickening on the 4th day following exposure. On the 16th day, loss of alveolar space and consolidation of large areas of all lobes were observed. Sarin also caused damage to the respiratory bronchioles. All the therapy regime blocked the development of lung lesions in the descending orders: atropine, diazepam and pralidoxime, atropine and diazepam > diazepam and pralidoxime > atropine and pralidoxime. The result suggests that diazepam in combination with atropine and pralidoxime could be an effective drug combination regime for the lung lesions.

Intratracheally Administered Liposomal α-Tocopherol Protects the Lung against Long-Term Toxic Effects of Paraquat

Paraquat is a broad-spectrum herbicide known to produce lung injury via oxidative stress-mediated mechanisms. Different pharmacological strategies have been explored to reduce the formation of these reactive oxygen species and/or prevent their toxic effects in the treatment of paraquat poisoning. The present study was carried out to investigate whether the antioxidant (L-tocopherol, incorporated into liposomes and delivered directly to the lungs of rats, could protect the organ against the long-term toxic effects of paraquat.Plain liposomes (composed of dipalmitoylphosphatidylcholine, DPPC) or α-tocopherol liposomes (8 mg α-tocopherol/kg body weight) were administered intratracheally to animals 24 h prior to an intraperitoneal injection of paraquat dichloride (20 mg/kg) and rats wefe killed 0, 1, 4, 6, 8, 10, 12, 16, 19 or 24 days after paraquat treatment. Results of this study showed that lungs of animals treated with paraquat were extensively damaged,as evidenced by significant increases in lung weight and decreases in lung angiotensin converting enzyme (ACE) and alkaline phosphatase enzyme (AKP) activities. Moreover,paraquat treatme; resulted in a significant reduction in the number of neutrophils in the blood of rats with a concurrent increase in the pulmonary myeloperoxidase activity,suggestive of neutrophil infiltration in the lungs of treated animals. Pretreatment of rats with liposomes alone did not significantly alter the paraquat-induced changes of all parameters examined. On the other hand, pretreatment of rats with (t-tocopherol liposomes,24 h prior to paraquat challenge, attenuated paraquat-induced changes in ACE, AKP and myeloperoxidase activities but failed to prevent increases in lung weight. Thus, pretreatment of rats with liposome-associated α-tocopherol appears to protect the lung against some of the toxic effects of paraquat

特殊患者的肺保护性通气策略

机械通气可导致呼吸机相关性肺损伤(ventilator-associated lung injury, VALI),主要包括容积伤、气压伤、不张伤、生物伤和剪切伤。肺保护性通气策略(lung protective ventilation strategy, LPVS)是近几年来针对VALI而发展起来的机械通气新策略,其目的为尽可能的保护肺组织减少机械通气性损害。LPVS主要包括小潮气量、最佳的呼气末正压、肺复张等;LPVS的实施可以改善肺顺应性和肺泡处的气体交换,减少肺水肿和感染的发生,降低术后肺部并发症(postoperative pulmonary complications, PPCs)的发生率。本文拟讨论对于某些特殊患者应用肺保护性通气策略方面的进展。