Effects of positive end-expiratory pressure/recruitment manoeuvres compared with zero end-expiratory pressure on atelectasis during open gynaecological surgery as assessed by ultrasonography: a randomised controlled trial.
- 作者列表："Généreux V","Chassé M","Girard F","Massicotte N","Chartrand-Lefebvre C","Girard M
BACKGROUND:During general anaesthesia, most patients develop atelectasis, which promotes postoperative pulmonary complications. RCTs that investigated perioperative lung protection have failed to reduce postoperative pulmonary complications consistently. Ultrasound imaging could help confirm the effects of different protective ventilatory strategies, but this has not been tested in trials. The objective of this study was to use ultrasonography to evaluate whether lung-protective ventilation measures reduce perioperative atelectasis. METHODS:We conducted a prospective, randomised patient- and assessor-blinded controlled trial in women undergoing open gynaecological surgery. Subjects were randomised to either lung protection or zero end-expiratory pressure (ZEEP; with no recruitment manoeuvres [RMs]). Lung protection entailed PEEP (7 cm H2O) and RMs every 30 min. Lung ultrasonography was undertaken at five predefined time points. The primary outcome was the difference in lung ultrasonography score (LUS) between groups before emergence; a lower LUS indicates better lung aeration. RESULTS:We recruited 45 women (34-85 yr old). Women randomised to lung protection had lower mean (standard deviation) LUS before emergence (6.1 [3.7]), compared with women randomised to ZEEP (11.7 [3.9]; 95% confidence interval for the difference between group means [-7.9 to -3.2]; P<0.0001). This difference did not persist after extubation, with similar mean LUSs in women who had received intraoperative lung protection (7.0 [4.1]), compared with women randomised to receive ZEEP (7.7 [3.1]). Conclusions: As assessed by lung ultrasonography, intraoperative PEEP/RMs decreased aeration loss during general anaesthesia. However, similar degrees of aeration loss were observed after tracheal extubation regardless of intraoperative ventilatory strategy. Clinical trial registration: NCT02055807.
背景: 在全身麻醉期间，大多数患者发生肺不张，这促进了术后肺部并发症。研究围手术期肺保护的 rct 未能一致地减少术后肺部并发症。超声成像可以帮助确认不同保护性通气策略的效果，但这还没有在试验中进行测试。本研究的目的是使用超声检查评估肺保护性通气措施是否减少围手术期肺不张。 方法: 我们在接受开腹妇科手术的女性中进行了一项前瞻性、随机、患者和评估者盲法对照试验。受试者随机接受肺保护或零呼气末压 (ZEEP; 无招募动作 [RMs])。肺保护每 30 min 进行 PEEP (7厘米 H2O) 和 RMs。在 5 个预定时间点进行肺超声检查。主要结局是出现前两组间肺超声评分 (LUS) 的差异; 较低的 LUS 表示肺通气量较好。 结果: 我们招募了 45 名女性 (34-85 岁)。与随机接受 ZEEP 的女性相比，随机接受肺保护的女性出现前的平均 (标准差) LUS 较低 (6.1 [3.7]) (11.7 [3.9]); 组间差异的 95% 置信区间均值 [-7.9 至-3.2]; P
METHODS:BACKGROUND AND PURPOSE:A critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH:C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY RESULTS:Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K2 , and S1P receptors (S1P2 and S1P3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice. CONCLUSIONS AND IMPLICATIONS:S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.
METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.
METHODS::The respiratory tract is lined by a pseudo-stratified epithelium from the nose to terminal bronchioles. This first line of defense of the lung against external stress includes five main cell types: basal, suprabasal, club, goblet and multiciliated cells, as well as rare cells such as ionocytes, neuroendocrine and tuft/brush cells. At homeostasis, this epithelium self-renews at low rate but is able of fast regeneration upon damage. Airway epithelial cell lineages during regeneration have been investigated in the mouse by genetic labeling, mainly after injuring the epithelium with noxious agents. From these approaches, basal cells have been identified as progenitors of club, goblet and multiciliated cells, but also of ionocytes and neuroendocrine cells. Single-cell RNA sequencing, coupled to lineage inference algorithms, has independently allowed the establishment of comprehensive pictures of cell lineage relationships in both mouse and human. In line with genetic tracing experiments in mouse trachea, studies using single-cell RNA sequencing (RNAseq) have shown that basal cells first differentiate into club cells, which in turn mature into goblet cells or differentiate into multiciliated cells. In the human airway epithelium, single-cell RNAseq has identified novel intermediate populations such as deuterosomal cells, 'hybrid' mucous-multiciliated cells and progenitors of rare cells. Novel differentiation dynamics, such as a transition from goblet to multiciliated cells have also been discovered. The future of cell lineage relationships in the respiratory tract now resides in the combination of genetic labeling approaches with single-cell RNAseq to establish, in a definitive manner, the hallmarks of cellular lineages in normal and pathological situations.