严重胸部创伤并发急性呼吸窘迫综合征的临床观察

目的:严重胸部创伤并发急性呼吸窘迫综合征的临床观察。方法:筛选严重胸部创伤合并ARDS的患者32例,对其进行临床治疗(包括:机械通气,合理补液,给予扩血管、抗感染、适量应用激素等)。结果:32例ARDS患者中死亡12例,死亡率为33.33%。结论:文章所述的临床治疗方法,对患者治疗效果显著,治疗后的死亡率也明显降低于统计数据。     

Activation of lung macrophage subpopulations in experimental acute pancreatitis

Pulmonary macrophages exist in two different anatomical compartments in the lower respiratory tract: alveolar macrophages in the alveoli and interstitial macrophages in the interstitium. Depending on the micro-environmental stimulation, macrophages follow different activation pathways. According to their inflammatory response pattern, activated macrophages have been characterized as pro-inflammatory (M1), wound-healing (M2a) and regulatory (M2b). Since acute pancreatitis occurs in parallel with acute lung injury, the profile of the different macrophage subpopulations could be relevant in the progression of the disease. The activation of lung alveolar and interstitial macrophages was assessed in an experimental model of severe acute pancreatitis induced in rats by intraductal infusion of 3.5% sodium taurocholate. Alveolar and interstitial macrophages were obtained and the expression of markers of different activations was evaluated. Activation of nuclear factors PPARγ and NF-κB, which are involved in the acquisition of different phenoytpes, was also measured. Alveolar macrophages acquired an early M1 phenotype characterized by the expression of inflammatory cytokines and NF-κB activation. In contrast, interstitial macrophages followed the inhibitory M2b pathway. In these macrophages, PPARγ became activated and the anti-inflammatory cytokine IL-10 was expressed. These results suggest that alveolar and interstitial macrophages play different roles in acute lung injury associated with acute pancreatitis. Alveolar macrophages promote an early inflammatory response, whereas interstitial macrophages help resolve inflammation.     

82例高原肺挫伤的临床治疗

目的探讨高海拔地区肺挫伤的特点,以提高临床治疗效果。方法回顾性分析82例肺挫伤患者的症状、体征及相关检查和综合治疗。结果 82例患者经综合治疗治愈67例（81.7%）,15例需应用机械通气,死亡9例,死亡率11%。结论高原地区肺挫伤患者承受原发性低氧、低气压和继发性肺创伤的双重打击,高原肺水肿（HAPE）和呼吸窘迫综合症（ARDS）可同时存在。低氧血症出现早,病情变化快,死亡率高。     

不同病因导致急性呼吸窘迫综合征应用体外膜式氧合治疗体会

目的:观察不同病因引起急性呼吸窘迫综合征(ARDS)的患者,应用体外膜式氧合(ECMO)的治疗效果。方法:回顾性分析2007年6月至2008年8月我院3例ARDS应用ECMO病例。发生原因分别是重症肺炎、胸腹联合创伤后合并呼吸机相关性肺炎(VAP)、以及肺栓塞肺动脉内膜血栓剥脱术后灌注肺;观察应用ECMO前基础状态(Base)、用后8 h、24 h、48 h及72 h动脉血气分析、血压、脉搏和呼吸机调整参数。结果:应用ECMO后,例1重症肺炎患者8 h、24 h、48 h及72 h血压、脉搏及氧合等项指标平稳,但ECMO参数下调时,缺氧状态无缓解,最终ECMO辅助14 d后死亡;例2胸腹联合创伤后VAP合并ARDS患者和例3肺栓塞术后灌注肺患者,ECMO辅助8 h、24 h、48 h、72 h血压、脉搏、氧合等项指标明显改善,分别于ECMO辅助4 d后和24 h后停机。结论:不同病因导致的ARDS应用ECMO后可能结果有所不同。ECMO能改善ARDS患者氧合和气体交换,减轻肺部病理损伤,减轻机体因低氧血症带来的多器官损伤,为治疗原发病赢得时间。     

DSM-RX78, a new phosphodiesterase inhibitor, suppresses superoxide anion production in activated human neutrophils and attenuates hemorrhagic shock-induced lung injury in rats

Neutrophils are activated following hemorrhagic shock and the accumulation of neutrophils in the lung is associated with lung injury. This research investigated the effects of a semisynthetic 2-benzoylaminobenzoic acid derivative, methyl 2-(2-fluorobenzamido)benzoate (DSM-RX78), on superoxide anion (O₂⁻) production in formyl-l-methionyl-l-leucyl-l-phenylalanine (FMLP)-activated human neutrophils, and on lung injury in Sprague-Dawley rats subjected to trauma-hemorrhage. DSM-RX78 concentration-dependently inhibited O₂⁻ production, but not elastase release, in FMLP-activated human neutrophils. DSM-RX78 displayed no superoxide-scavenging ability, and it failed to alter the subcellular NADPH oxidase activity. Significantly, DSM-RX78 increased cAMP formation and protein kinase (PK)A activity in FMLP-activated neutrophils, which occurred through the selective inhibition of cAMP-specific phosphodiesterase (PDE) activity but not an increase in adenylate cyclase function or cGMP-specific PDE activity. These results show that DSM-RX78 is a new inhibitor of cAMP-specific PDE. Moreover, DSM-RX78 reduced FMLP-induced phosphorylation of protein kinase B (Akt), but not calcium mobilization. The inhibitory effects of DSM-RX78 on O₂⁻ production and Akt phosphorylation were reversed by PKA inhibitors, suggesting that DSM-RX78 regulates O₂⁻ production of human neutrophils by promoting cAMP/PKA-dependent inhibition of Akt activation. On the other hand, administration of DSM-RX78 significantly attenuated the increase in myeloperoxidase activity and edema in the lung, as well as protein concentrations in bronchoalveolar lavage fluid in rats after trauma-hemorrhagic shock. In summary, these results strongly suggest that DSM-RX78 exerts anti-inflammatory effects, which result from the elevation of cAMP levels and PKA activity through its inhibition of cAMP-specific PDE. Also, our findings show that DSM-RX78 attenuates hemorrhagic shock-induced lung injury in rats.     

An effective antidote for paraquat poisonings: The treatment with lysine acetylsalicylate

Sodium salicylate (NaSAL) has been shown to have a multifactorial protection mechanism against paraquat (PQ)-induced toxicity, due to its ability to modulate inflammatory signalling systems, to prevent oxidative stress and to its capacity to chelate PQ. Considering that currently there is no pharmaceutical formulation available for parenteral administration of NaSAL, the aim of the present study was to evaluate the antidotal feasibility of a salicylate prodrug, lysine acetylsalicylate (LAS), accessible for parenteral administrations. PQ was administered to Wistar rats by gavage (125 mg/kg of PQ ion) and the treatment was performed intraperitoneally with different doses (100, 200 and 400 mg/kg of body weight) of LAS. Survival rate was followed during 30 days and living animals at this endpoint were sacrificed for lung, kidney, liver, jejune and heart histological analysis. It was shown, that the salicylate prodrug, LAS, available in a large number of hospitals, is also effective in the treatment of PQ intoxications. From all tested LAS doses, 200 mg/kg assured animal's full survival. Comparatively to 60% of mortality observed in PQ only exposed animals, the lethality was higher (80%) in the group that received 400 mg/kg of LAS 2 h after PQ administration. The dose of 100 mg/kg of LAS showed only a modest protection (60% of survival). Collagen deposition was observed by histological analysis in survived animals of all experimental groups, being less pronounced in animals receiving 200 mg/kg of LAS, reinforcing the importance of this dose against tissue damage induced by PQ. The results allow us to suggest that LAS should be considered in the hospital treatment of PQ poisonings.     

川芎嗪对油酸-内毒素序贯损伤大鼠心、肺的干预作用

目的：探讨川芎嗪对油酸内毒素序贯致伤大鼠肺脏及心脏的干预作用。方法：采用油酸（Oleic acid OA）内毒素序贯注射复制ARDS大鼠模型,32只健康Wistar大鼠分为对照组（c组）、实验组（OA组）、654—2对照组（OA＋654—2组）、川芎嗪干预组（OA＋川芎嗪组）,在不同时间点观察左室收缩末压（LVSP）、左室舒张末期压力（LVEDP）、左心室最大上升速率及最大下降速率（±dp／dtmax）、动脉血pH、PaO2和PaCO2。结果：OA组PaO2明显低于c组,达到ARDS的标准,OA＋6542组与OA＋川芎嗪组大鼠PaO2、左室收缩未压、＋dp／dtmax（kPa／s）均明显高于OA组（P〈O．05）。OA＋654—2组与0A＋川芎嗪组大鼠左室舒张末压力、-dp／dtmax（kPa／s）均低于OA组（P〈O．05）。结论：川芎嗪对油酸-内毒素序贯ARDS大鼠的心、肺功能有改善作用。     

老年胃肠道术后早期脱呼吸机病人并发ARDS的早期诊治

目的 探讨老年胃肠道术后早期脱呼吸机病人并发ARDS的早期诊断及干预性治疗.方法 利用SIRS量化评分预估ARDS发展,诊断明确后立即给予呼吸支持以及降低全身炎性反应综合征等治疗.结果 317例老年胃肠道术后早期脱呼吸机病人中,用该方案评估,有23例被及时确诊为ARDS,并给予早期干预治疗,其中22例顺利康复痊愈,仅1例死亡,病死率4.3%.结论 该诊疗方案可提高老年胃肠道术后早期脱呼吸机病人并发ARDS的预判准确性及干预治疗效果,明显降低发病率和病死率.     

地震伤患者并发ARDS的危险因素分析

目的探讨分析地震伤患者并发ARDS的危险因素。方法回顾性研究四川省人民医院“5·12”大地震后收治的符合纳入标准的896例地震伤患者的病历资料,采用统计学方法探讨地震伤患者并发ARDS的危险因素。结果统计学分析显示：年龄,严重创伤后的低血压、大量输血、缺氧血症、挤压综合征及气性坏疽和ARDS的发生呈相关性。是地震伤患者并发ARDS的危险因素。结论年龄、严重创伤后的低血压、大量输血、缺氧血症,挤压综合征及气性坏疽是地震伤患者并发ARDS的高危因素。     

The effect of prone positioning in acute respiratory distress syndrome or acute lung injury: a meta-analysis. Areas of uncertainty and recommendations for research

OBJECTIVE: To compare the effects of ventilation in prone and in supine position in patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS). DESIGN: Meta-analysis of randomised controlled trials. DATA SOURCES: BioMedCentral, PubMed, CINAHL, and Embase (to November 2007), with additional information from authors. MEASUREMENTS AND RESULTS: From selected randomised controlled trials comparing positioning in ALI/ARDS we extracted data concerning study design, disease severity, clinical outcomes, and adverse events. Five trials including 1,372 patients met the inclusion criteria for mortality analysis; one trial was added to assess the effects on acquisition of ventilator-associated pneumonia (VAP). The included trials were significantly underpowered and enrolled patients with varying severity. Prone positioning duration and mechanical ventilation strategy were not standardised across studies. Using a fixed-effects model, we did not find a significant effect of prone positioning (proning) on mortality (odds ratio 0.97, 95% confidence interval 0.77-1.22). The PaO(2)/FiO(2) ratio increased significantly more with proning (weighted means difference 25 mmHg, p < 0.00001). Proning was associated with a non-significant 23% reduction in the odds of VAP (p=0.09), and with no increase in major adverse airway complications: OR 1.01, 95% CI 0.71-1.43. Length of intensive care unit stay was marginally and not significantly increased by proning. CONCLUSIONS: Prone position is not associated with a significant reduction in mortality from ALI/ARDS despite a significant increase in PaO(2)/FiO(2), is safe, and tends to decrease VAP. Published studies exhibit substantial clinical heterogeneity, suggesting that an adequately sized study optimising the duration of proning and ventilation strategy is warranted to enable definitive conclusions to be drawn.