间断肺通气对体外循环肺损伤的保护作用

目的研究间断肺通气对体外循环(CPB)肺损伤的保护作用,并探讨其机制。方法将24例风湿性心脏病患者采用随机数字表法分为两组,处理组(n=13)CPB期间每5min间断肺通气一次;对照组(n=11)CPB期间不通气。所有患者均在术前留取血液标本,术后2h行支气管肺泡灌洗,分别测定支气管肺泡灌洗液(BALF)中的中性粒细胞、总蛋白(TP)、肿瘤坏死因子-α(TNF-α)含量、血清总蛋白以及术前、CPB后1h、4h肺氧合指数(OI)。结果处理组BALF中的中性粒细胞、TP、TNF-α含量较对照组显著降低(P<0.01,P=0.02,0.02),CPB后OI较对照组显著降低(P<0.05);两组CPB后1h、4h其OI均较同组CPB前显著增高(P<0.05)。结论间断肺通气可通过减少白细胞与血管内皮的黏附,减轻肺部炎症反应、内皮细胞损伤等,对CPB所致的肺损伤有保护作用。     

非肽内皮素拮抗剂在体外循环中的肺保护作用

目的 研究体外循环（CPB）过程中内皮素（endothelin，ET）在肺损伤中的作用，探讨ET介导肺损伤的可能机制及阿魏酸（FA）对肺的保护作用。方法 将12只犬随机分为两组，建立CPB肺灌注模型。对照组：灌注4C冷晶体心脏停搏液；实验组：于肺动脉近端灌注4CFA保护液；观察两组CPB前后肺组织内ET的浓度、一氧化氮（NO）、丙二醛（MDA）含量及肺组织干湿比（D／W）变化、氧合指数（PaO2／FiO2）、肺血管阻力（PVR）、气道压（AWP）、肺顺应性和组织学变化。结果 CPB后对照组肺内ET合成显著增加（P〈0．05），实验组低于对照组（P〈0．05）；D／W，MDA较对照组降低（P〈0．05）．NO含量较对照组增高（P〈0．05）。CPB后实验组PaO2／FiO2、肺顺应性分别高于对照组（P〈0．05），而AWP、PVR则低于对照组（P〈0．05）；实验组肺损伤较对照组轻。结论 ET参与CPB中的肺损伤过程；用FA进行肺灌注可减轻肺损伤，改善肺功能，具有较好的肺保护作用。     

缺血预处理对肺缺血-再灌注损伤的保护作用及机制

目的　探讨缺血预处理 (IP)对肺缺血 -再灌注 (IR)损伤的保护作用和可能的机制。　方法　建立兔在体IR损伤模型 ,将 36只兔随机分为 IP组、IR组和对照组 ,每组 12只 ,观察各组肺湿 /干重比 ,检测各组肺组织超氧化物歧化酶 (SOD)活性、丙二醛 (MDA)含量及髓过氧化物酶 (MPO)活性 ,对支气管肺泡灌洗液 (BAL F)中白细胞进行分类计数 ,并检测各组肺通透性指数。　结果　 IP组与 IR组比较 ,肺湿 /干重比明显降低 (P<0 .0 1) ;肺组织中 SOD活性显著增高 ,MDA含量和 MPO活性明显降低 (P<0 .0 1) ;BAL F中中性粒细胞分类计数、肺通透性指数明显降低(P<0 .0 1)。IP组与对照组比较 ,上述指标差别无显著性意义 (P>0 .0 5 )。　结论　 IP可通过减轻 IR时肺组织中性粒细胞的浸润与激活 ,提高机体抗氧化自由基的能力 ,而减轻 IR引起的肺损伤。     

抑肽酶在心肺转流术中对肺损伤的保护

目的 探讨心肺转流术（ｃａｒｄｉｏｐｕｌｍｏｎａｒｙ ｂｙｐａｓｓ,ＣＰＢ）导致肺缺血－再灌注损伤,抑肽酶对肺损伤保护的作用。方法 将２４例心内直视手术的患者随机分为对照组和实验组,每组１２例,实验组给予抑肽酶处理。检测ＣＰＢ前后左、右心房血中性粒细胞和血小板计数,围手术期各时段桡动脉血浆中内皮素、血栓素Ｂ２、６－酮－前列腺素Ｆ１α和呼吸指数的变化。结果 对照组ＣＰＢ后左、右心房血中血小板和中性粒细胞计数差异有显著性（Ｐ〈０．０５）;实验组ＣＰＢ前后则差异无显著性;内皮素、血栓素Ｂ２、呼吸指数在ＣＰＢ中、ＣＰＢ后两组比较均差异有显著性（Ｐ〈０．０１）。结论 ＣＰＢ致肺损伤,血小板和中性粒细胞在肺内聚集,内皮素、血栓素Ｂ２、６－酮－前列腺素Ｆ１α在其病理过程中起重要作用。抑肽酶能通过干预这些因素而达到保护肺功能的     

甲泼尼松龙对体外循环肺损伤的预防作用

３０例体外循环心内直视手术病人随机分成对照组与甲泼尼松龙用药组，每组１５。用药组于体外循环前静脉推注甲泼尼松龙１５ｍｇ／ｋｇ。结果表明：用药组能明显抑制肺再灌注早期中性粒细胞、单核细胞及血小板的聚集，减少肺内氧自由基的产生，明显减轻体外循环后肺组织的损伤程度，并从形态学观察得以证实。对临床具有重要的指导意义与实用价值。     

体外循环中白细胞对肺损伤机制及白细胞过渡的肺保护作用

肺损伤为体外循环术后常见的并发症之一，血液与体外循环管道接触，能够活化补体，激活白细胞，白细胞激活后黏附于血管内皮细胞或进入肺组织，释放具有趋化作用的炎性介质及代谢产物，如蛋白酶，氧自由基和花生四烯酸等在肺损伤中起着重要作用，动物实验及临床应用白细胞过滤器在体外循环中对白细胞进行过滤，肺血管阻力明显降低，血氧饱和度，动脉血氧分压升高，尤其对术前缺氧越重和体外循环时间越长的患者作用越明显，因此，在体外循环中进行白细胞过滤能够减轻其对肺的损伤，起到肺保护作用。     

选择素P与心肺转流术后肺损伤

心肺转流中P-selectin的过度表达可以导致或加重肺损伤,特异性阻断P-selectin的表达可以在一定程度上使之得到缓解。现就P-selectin的结构、作用及针对P-selectin的肺损伤治疗和研究现状进行综述。     

体外循环心脏手术肺保护的研究进展

体外循环心脏手术后肺操作的发生率极高，是体外循环心脏手术病人术后并发症和死亡的重要原因之一。本文综述了体外循环心脏手术肺损伤的发生机制及相关的保护性策略研究进展。     

Protective Effects of Isoflurane Pretreatment in Endotoxin-induced Lung Injury

Background: The concept of antiinflammatory effects of volatile anesthetics is well established in vitro and in some organ systems. Their protective role in lung injury, however, remains to be elucidated. The authors hypothesized that in the lung, isoflurane pretreatment may attenuate neutrophil infiltration and reduce endotoxin-induced injury.

Methods: Male C57Bl/6 mice were exposed to aerosolized lipopolysaccharide. Neutrophil recruitment into the pulmonary vasculature and migration into the different lung compartments (interstitium and alveolar air space) were determined by flow cytometry. Capillary protein leakage, formation of lung edema, and concentration of the chemokines keratinocyte-derived chemokine (CXCL1) and macrophage inflammatory protein 2 (CXCL2/3) in bronchoalveolar lavage were compared in mice with or without isoflurane treatment (1.4% inspired for 30 min) at different times before and after endotoxin exposure.

Results: Endotoxin inhalation induced significant neutrophil migration into all lung compartments. Isoflurane pretreatment attenuated both neutrophil recruitment into lung interstitium and alveolar space when given 1 or 12 h before or 1 h after lipopolysaccharide but not at 4, 6, or 24 h before endotoxin exposure. Isoflurane pretreatment 1 or 12 h before lipopolysaccharide also reduced protein leakage and pulmonary edema. Production of CXCL1 and CXCL2/3 in the bronchoalveolar lavage was reduced when isoflurane was given 1 h but not 12 h before lipopolysaccharide, suggesting different mechanisms for early and late protection.     

心肺转流术致未成熟肺损伤及其保护的研究现状

心肺转流术（CPB）所致未成熟肺损伤，是婴幼儿心脏手术后严重的并发症，直接影响心脏手术的成功率，但其损伤机制及如何有效地施保护，一直是个亟待解决的问题。研究结果发现，心肺转流时外源性物质激活补体介导全身炎症是肺损伤的关键，中性粒细胞肺内聚集活化是肺缺血－再灌注损伤的中心五一节。白细胞浸润，释放大量弹性蛋白酶，产生大量的氧自由基，破坏肺泡上皮及血管内皮细胞，导致肺水肿。婴幼儿未成熟肺因其肺组织表面活性物质少，血管内皮细胞通透性高的特点，更易出现肺水肿、肺不张、引起术后肺功能不全。目前，研究的保护措施有药物、表面活性物质和肺动脉灌注等。     

Protective Effects of Nigella sativa Oil in Hyperoxia-Induced Lung Injury

BackgroundOxygen-induced lung injury is believed to lead to the development of bronchopulmonary dysplasia in premature infants. We have evaluated the beneficial effects of Nigella sativa oil (NSO) on rats with hyperoxia-induced lung injury.MethodsThirty newborn Sprague-Dawley rats were randomly divided into 3 groups as hyperoxia (95% O₂), hyperoxia+NSO and control (21% O₂). Pups in the hyperoxia+NSO group were administered intraperitoneal NSO at a dose of 4 ml/kg daily during the study period. Histopathologic, immunochemical, and biochemical evaluations (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], malonaldehyde [MDA] and myeloperoxidase [MPO]) were performed.ResultsIn the histopathologic and immunochemical evaluation, severity of lung damage was significantly lower in the hyperoxia+NOS group (P<.05). Tissue GSH-Px and SOD levels were significantly preserved, and MDA, MPO levels were significantly lower in the hyperoxia+NSO group (P<.05).ConclusionNSO significantly reduced the severity of lung damage due to hyperoxia.     

Protective Effects of Memantine Against Ischemia-Reperfusion Injury in Spontaneously Hypertensive Rats

Summary  Memantine, an uncompetitive NMDA open-channel blocker, has been shown to be effective in preventing neuronal damage after permanent focal cerebral ischemia. Reperfusion after a long period of ischemia may aggravate the progression of neuronal damage. Those drugs that show protective effects after permanent cerebral ischemia, therefore, might fail to do so against ischemia-reperfusion injury. In this study we evaluated the effects of memantine on brain edema formation and ischemic injury volume after transient cerebral ischemia. Male Spontaneously Hypertensive Rats (SHR) weighing 250–300 g were anesthetized with halothane and subjected to 1 hour of temporary middle cerebral artery occlusion by an intraluminal suture. 20 mg/kg of memantine or saline were injected intraperitoneally 5 min. after the induction of ischemia. Physiological parameters and regional cerebral blood flow were monitored during the surgical procedure. Brain water content and ischemic injury volume were measured with the wet dry method and 2,3,5-triphenyl tetrazolium chloride monohydrate (TTC) staining, respectively, at 24 hours after occlusion. There were no statistically significant differences between the groups regarding physiological parameters during the procedure. Memantine treatment (n=9) reduced the brain water content significantly in the cortex compared to saline treatment (n=8; 83.1±0.7% vs. 84.5±1.5%, respectively, p<0.05). The total volume of ischemic brain injury was 300±49 mm³ in the animals treated with saline (n=13). Treatment with 20 mg/kg memantine (n=14) reduced the ischemic injury volume to 233±61 mm³ (P<0.01). These results demonstrate that the harmful effects of recirculation after a period of ischemia can be attenuated by the treatment of memantine, perhaps by its action at the NMDA receptors.     

Set Positive End-expiratory Pressure during Protective Ventilation Affects Lung Injury

Background: The most appropriate method of determining positive end-expiratory pressure (PEEP) level during a lung protective ventilatory strategy has not been established.

Methods: In a lavage-injured sheep acute respiratory distress syndrome model, the authors compared the effects of three approaches to determining PEEP level after a recruitment maneuver: (1) 2 cm H2O above the lower inflection point on the inflation pressure-volume curve, (2) at the point of maximum curvature on the deflation pressure-volume curve, and (3) at the PEEP level that maintained target arterial oxygen partial pressure at a fraction of inspired oxygen of 0.5.

Results: Positive end-expiratory pressure set 2 cm H2O above the lower inflection point resulted in the least injury over the course of the study. PEEP based on adequate arterial oxygen partial pressure/fraction of inspired oxygen ratios had to be increased over time and resulted in higher mRNA levels for interleukin-8 and interleukin-1[beta] and greater tissue inflammation when compared with the other approaches. PEEP at the point of maximum curvature could not maintain eucapneia even at an increased ventilatory rate.