动态通气参数对急性呼吸窘迫综合征犬肺损伤的作用机制

目的 探讨机械通气动态通气参数对ARDS犬肺内肺炎症介质的影响及其作用途径.方法 取36条健康杂种犬,采用气管内盐酸吸入法建立ARDS模型,随机(随机数字法)分为对照组,ARDS模型组及实验犬组,实验犬组随机分成A,B,c,D四组,每组6条.A组:小潮气量(6 mL/kg),低吸气流速[6mL/kg·s)],高通气频率(30次/min);B组:大潮气量(20mL/kg),高吸气流速[20mL/(kg·s)],高通气频率(30次/min);C组:大潮气量(20 mL/kg),高吸气流速[17 mL/(kg·s)],低通气频率(15次/min);D组:大潮气量(20 mL/kg),低吸气流速[10 mL/(kg·s)],低通气频率(15次/min).机械通气4 h后处死动物,留取肺组织标本行免疫组化、Western blotting检测TNF-α,IL-8,p38 MAPK蛋白的变化,RT-PCR测定TNF-α,IL-8 mRNA的表达,流式细胞仪检测NF-κB活性.结果 B组IL-8蛋白表达明显较A,D组高,c组IL-8蛋白表达较B组有下降趋势,但B,C组之间差异无统计学意义;B组TNF-α的灰度比值明显较其他组高(P<0.01),但与C组比较差异无统计学意义(P>0.05);B组p38 MAPK表达明显较A,D组高(P<0.01);A,D组之间的p38 NAPK表达差异无统计学意义(P>0.05).B组NF-κB p65(33.56±2.85)%表达较A(10.35±0.6)%,D(7.11±0.47)%两组差异有统计学意义,B组与C组(30.87±1.16)%之间差异无统计学意义.结论 在相同的大潮气量基础上,高吸气流速和高通气频率可以激活肺组织p38 MAPK及NF-κB通道,炎症介质的释放增加,导致呼吸机相关性肺损伤,小潮气量机械通气可减轻炎症反应.     

动态通气参数对急性呼吸窘迫综合征犬肺外炎症反应和肺外脏器功能的影响

目的 观察机械通气动态通气参数对急性呼吸窘迫综合征(ARDS)犬肺外炎症介质水平及肺外脏器功能的影响.方法 36条健康杂种犬,按照随机数字表法分为正常对照组(N组)、ARDS模型组(M组)及机械通气A-D组6组.采用气管内盐酸吸入法建立ARDS模型,按下述方案行机械通气.A组(LVLYHR):小潮气量、低吸气流速、高通气频率;B组(HVHFHR):大潮气量、高吸气流速、高通气频率;C组(HVHFLR):大潮气量、高吸气流速、低通气频率;D组(HVIYLR):大潮气量、低吸气流速、低通气频率.分组机械通气后4 h后处死动物,留取血清用放射性免疫吸附法行IL-8和TNF-α检测;留取肝肾组织行病理学检查.数据处理运用方差分析,以P<0.05为差异具有统计学意义.结果 B组、C组血中IL-8和TNF-α含量显著高于M组、A组、D组(P<0.05),A组、D组和M组差异无统计学意义(P>0.05).N组与其他相比差异具有统计学意义(P<0.05).B组肝肾组织病理学改变最为严重,C组较B组稍有减轻.A组和D组的病理学改变较B、C组明显减轻,A组和M组改变接近.结论 大潮气量、高吸气流速、高通气频率机械通气可以使血清炎症介质水平升高,加重肺外器官的炎症反应;降低通气频率及吸气流速,对防治多器官功能衰竭有重要意义.     

肺透明膜病患儿机械通气时呼吸力学动态变化及临床意义

目的探讨肺透明膜病患儿机械通气时呼吸力学的变化特征及其临床意义。方法126例机械通气的肺透明膜病患儿,按照有无并发症分为有并发症组(43例)和无并发症组(83例)。于第1次机械通气后2、24、48和72h及第1次脱机前进行血气分析及呼吸力学指标监测。结果与机械通气2～72h比较,无并发症组和有并发症组患儿脱机前呼吸系统动态顺应性〔分别为(0.55±0.10)ml·cmH2O-1·kg-1和(0.43±0.10)ml·cmH2O-1·kg-1〕和每分通气量〔MV,分别为(0.65±0.10)L/min和(0.62±0.30)L/min〕均明显增加,氧合指数〔OI,OI=吸入氧浓度×平均气道压×100/动脉血氧分压,分别为(10.2±1.9)mmHg(1mmHg=0.133kPa)和(13.6±4.3)mmHg〕均明显降低。无并发症组呼吸系统动态顺应性和MV在机械通气后48h明显高于有并发症组;两组气道阻力和肺过度膨胀系数均无明显变化。呼吸系统动态顺应性与OI呈显著负相关(r=0.208,P<0.01),与MV呈显著正相关(r=0.218,P<0.01)。无并发症组均一次性脱机成功,脱机成功时呼吸系统动态顺应性平均为(0.55±0.10)ml·cmH2O-1·kg-1,MV平均为(0.65±0.20)L/min;有并发症组28例脱机失败,脱机失败时呼吸系统动态顺应性平均为(1.03±0.30)ml·cmH2O-1·kg-1,MV平均为(0.33±0.30)L/min。结论动态监测肺透明膜病患儿机械通气时呼吸力学的变化,可以判断肺部病变的严重程度,预测呼吸循环系统并发症发生的可能性,评估通气策略,掌握脱机指征。     

不同潮气量机械通气治疗儿童重症肺炎系统性评价

目的比较不同潮气量机械通气治疗儿童重症肺炎的疗效。方法将治疗的重症肺炎患儿120例按随机数字表分为3组,每组40例,均行机械通气治疗,A组潮气量为6~8ml/kg,B组为8~10ml/kg,C组为10~12ml/kg,比较3组呼吸力学参数变化,对患儿进行急性肺损伤(ALI)及小儿死亡危险(PRISMⅢ)评分,并比较3组静息能量消耗变化。结果撤机前A、B组肺动态顺应性(Cdyn)高于C组,C组气道阻力(AR)低于A、B组;A、B组ALI评分低于C组;撤机后C组静息能量消耗值高于A、B组,差异均有统计学意义(P0.05)。结论不同潮气量机械通气对重症肺炎患儿呼吸功能的缓解作用相当,小潮气量、中潮气量机械通气对肺顺应性改善优于大潮气量,但大潮气量机械通气对机体的整体恢复较好。     

脂氧素对机械通气所致肺损伤的实验研究

目的 研究脂氧素对机械通气致肺损伤的保护作用及相关保护机制.方法 36只健康雄性SD大鼠按随机数字表分组.采用大潮气量通气制作大鼠VILI模型.麻醉和气管切开及气管内插管后,对照组(Control组)保留自主呼吸;大潮气量组(HV组)采用大潮气量通气[潮气量(VT)30 mL/kg,呼吸频率(RR)40次/min];大潮气量组+脂氧素处理组(HV+LX组)于机械通气前5 min静脉注射脂氧素10 μg/kg,其余两组注射等量生理盐水.通气时间均为2 h.每组大鼠实验过程中监测血流动力学和动脉血气;通气2 h后处死大鼠取肺组织,测定肺湿/干质量(W/D)比值和髓过氧化物酶(MPO)活性,酶联免疫吸附法(ELISA)测定肺泡灌洗液(BALF)中核转录因子(NF-κB)和白细胞介素-8(IL-8)含量;苏木素-伊红(HE)染色观察肺组织病理学改变并进行肺泡损伤评分(DAD损伤评分).结果 与Control组相比,HV组和HV+LX组的动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)、平均动脉压(MAP)均呈下降趋势;动脉血pH值呈上升趋势.HV+LX组MAP显著高于HV组(P<0.05).与Control组相比,HV组肺组织W/D比值、MPO活性、DAD评分、NF-κB、IL-8显著升高(P<0.05或P<0.01);与HV组相比,HV+LX组肺组织W/D比值、MPO活性、DAD评分及NF-κB和IL-8显著降低(P<0.05或P<0.01).结论 脂氧素在大鼠机械通气模型中可减少肺泡蛋白质的渗出,可抑制肺组织中NF-κB、IL-8的产生,减少中性粒细胞在肺泡内的浸润和黏附,从而减轻大容量机械通气造成的肺组织损伤.     

小窝蛋白-1和NF-κB在机械通气肺损伤大鼠肺组织中的表达

目的通过观察小窝蛋白-l(cav-1)及NF-κB p65、IL-8在大潮气量机械通气大鼠肺组织中的表达变化,探讨cav-1在通过对NF-κB信号转导通路的影响而导致对肺组织的损伤作用。方法将雄性SD大鼠随机分为三组:对照组、大潮气量通气0.5 h组(H-VT0.5h组)和大潮气量通气2 h组(H-VT2h组)。光镜下观察各组大鼠肺组织病理学改变;免疫组织化学染色法检测肺组织中cav-1的蛋白含量;反转录-聚合酶链反应(RT-PCR)检测NF-κB p65的m RNA表达;计算肺湿/干重比值(W/D);酶联免疫吸附试验(ELISA)测定支气管肺泡灌洗液(BALF)中IL-8的含量,并对cav-1及NF-κB p65进行相关性分析。结果 H-VT2h组肺组织中肺W/D比值、cav-1的蛋白表达、NF-κB p65 m RNA的表达水平及BALF中IL-8的含量均大于H-VT0.5h组,差异有统计学意义(均P<0.05);H-VT0.5h组肺组织中肺W/D比值、cav-1的蛋白表达、NF-κB p65 m RNA的表达水平以及BALF中IL-8的含量均大于对照组,但差异无统计学意义(均P>0.05)。相关性分析结果显示,各组大鼠肺组织cav-1蛋白表达水平与NF-κB p65 m RNA表达水平之间呈正相关(r=0.820,P<0.01)。结论 cav-1在机械通气导致肺损伤发生中可能起损伤作用。这种损伤作用可能与cav-1经过多种途径激活NF-κB炎症信号通路,使IL-8等细胞因子释放有关,最终导致炎症的加重和肺组织损伤。     

不同潮气量单肺通气后兔两侧肺损伤程度的比较

目的比较不同潮气量单肺通气后左右肺脏组织的损伤程度,探讨单肺通气的最佳潮气量。方法新西兰大白兔32只,随机分为对照组(A组),单侧肺机械通气(OLV)实验组(B组,C组,D组),每组8只。对照组潮气量(VT)=10ml/kg,呼吸频率(RR)=50次/min,双肺机械通气(TLV)3h;OLV实验组VT分别采用15ml/kg,10ml/kg,6ml/kg,OLV(左侧)2h后改TLV1h。结果 A组各时间点PaO2差异无统计学意义(P>0.05);与A组比较,在OLV开始后,B、C、D组的PaO2各个时间点均较A组低(P<0.05)。在恢复TLV后1h时,只有C组PaO2接近机械通气前水平。肺损伤评分A组左右侧相比较差异无统计学意义(P>0.05),另三组间比较表现为C组最低(P<0.05)。结论 OLV可以导致肺损伤,相对于15ml/kg组和6ml/kg组,10ml/kg潮气量组的肺组织损伤最轻。     

机械通气中呼吸频率与血液肿瘤坏死因子α和白细胞介素8水平的关系

目的:观察呼吸频率对呼吸机相关肺损伤外周血中,与急性肺损伤严重程度有关的炎症损伤性细胞因子肿瘤坏死因子α和白细胞介素8的影响。方法:实验于2004-08/12在解放军总医院呼吸科实验室进行。将16只新西兰大白兔随机分为两组,每组8只:低呼吸频率组,呼吸频率8次/min,潮气量50mL/kg;高呼吸频率组,呼吸频率40次/min,潮气量30mL/kg。两组均以容量控制通气,吸氧浓度(FiO2)=0.5,吸气时间(I)=25%,吸气暂停时间(P)=10%,稳定30min后,在0,30,60,90,120min抽动脉血2mL,放免法测定血浆中肿瘤坏死因子α、白细胞介素8水平。实验结束后放血处死动物,右肺用于肺湿重/干重比率测定。结果:16只兔进入结果分析。①肿瘤坏死因子α水平:随着通气时间延长,两组均显著升高(P<0.05)。在通气后30,60,90,120min,高通气频率组明显高于低通气频率组犤(2.78±0.54),(4.23±0.17),(5.57±0.28),(5.94±0.05)μg/L;(1.32±0.09),(1.40±0.08),(1.53±0.04),(2.36±0.26)μg/L,P<0.05犦。②白细胞介素8水平:随着通气时间延长,两组均显著升高(P<0.05)。在通气后30,60,90,120min,高通气频率组明显高于低通气频率组犤(2.43±0.17),(3.65±0.14),(4.01±0.08),(4.49±0.11)μg/L;(1.65±0.06),(1.98±0.11),(2.27±0.09),(2.44±0.04)μg/L,P<0.05犦。③高、低呼吸频率组肺组织湿重/干重比率分别为8.24±0.42,7.73±0.13。结论:呼吸频率可明显影响肺损伤兔的损伤严重程度,而且肿瘤坏死因子α和白细胞介素8增加可能是单纯容量性肺损伤加重的机制之一。     

TNF—α、IL—8在机械通气致肺损伤中的作用

目的探讨肿瘤坏死因子α(TNF-α)和白细胞介素8(IL-8)在机械通气致肺损伤中的可能作用。方法24只普通健康小猪随机等分为对照组、低潮气量组(A组)、正常潮气量组(B组)、大潮气量组(C组),采用持续给予小猪不同潮气量通气动物模型,利用放射免疫法、酶联免疫法(ELISA)和髓过氧化物酶(MPO)测定法,分别检测不同潮气量组通气1、3、7d后,血清和肺组织匀浆中TNF-α、IL-8及MPO含量的变化。结果A、B、C组血清、肺组织匀浆TNF-α、IL-8及MPO的含量较对照组升高(P＜0.05或P＜0.01),其中3d后,TNF-α达峰值;7d后IL-8及MPO达峰值,以A、C组明显。结论TNF-α、IL-8在机械通气致肺损伤中可能发挥重要作用。     

血管紧张素Ⅱ受体阻断剂对大鼠机械通气所致肺损伤的保护作用

目的 研究血管紧张素Ⅱ受体阻断剂洛沙坦对大鼠机械通气所致肺损伤（VILI）的保护作用及其机制。方法 40只健康SD大鼠随机均分成A、B、C、D四组：A组为对照组;B组为正常潮气量机械通气组,潮气量（VT）为10ml／kg;C组为大潮气量机械通气通气组,VT为40ml／kg;D组为大潮气量通气加洛沙坦处理组,VT为40ml／kg,D组大鼠实验前30min用血管紧张素Ⅱ受体（AT1型）特异性阻断剂洛沙坦（Losartan）溶液30mg／kg腹腔注射。B、C、D三组机械通气频率（P）均为80次／min,通气时间均为2h。实验完毕收集肺组织和肺泡灌洗液标本。光镜观察肺病理改变,逆转录聚合酶链式反应（RT-PCR）法检测A、B、C三组肺组织中血管紧张素原的表达水平,TUNEL法检测肺组织细胞凋亡情况,同时测定肺灌洗液总蛋白、白细胞计数、肺湿／干比以及肺组织髓过氧化物酶（IVIPO）的水平。结果 B组和A组各项指标差异无统计学意义;与A、B组相比,C组肺病理改变明显,肺细胞凋亡显著性增多,血管紧张素原的表达水平显著增高（P〈0．01）．肺湿／干比、总蛋白、白细胞计数、IVIPO等指标均显著性增高（P〈0．01）;与C组比较,D组肺病理改变明显减轻,肺细胞凋亡、肺湿／干比、总蛋白、白细胞计数、IVIPO等指标均显著性降低（P〈0．05或P〈0．01）。结论血管紧张素Ⅱ可能在VILI的致病机理中起着一定的作用,特异性阻断血管紧张素Ⅱ受体（AT1型）能显著减轻VILI时肺损伤和炎症反应的程度。     

吸入沙丁胺醇对呼吸衰竭患者容积标限压力控制通气时通气参数的影响

目的　探讨在容积标限压力控制 (VTPC)通气时吸入支气管扩张剂沙丁胺醇后对机械通气参数的影响。方法　 10例平均年龄为 (6 8± 5 )岁的呼吸衰竭患者均接受气管插管与机械通气支持治疗 ;采用Newport e5 0 0型呼吸机 ,并实施定容型通气 (VCV) 30 min,潮气量 (VT)为 8～ 10 ml/ kg;测定气道阻力 (Raw)和静态顺应性 (Cst)以及通气参数的变化 ,包括气道峰压 (PIP)、平台压 (Pplat)、充气时间 (Tinflate)、吸气峰流速(PIF)、呼气峰流速 (PEF)和平均吸气流速 (VT/ Tinflate)。随后转为 VTPC通气 30 m in,并同样记录上述参数。通过同轴吸入装置吸入沙丁胺醇 6 0 0 μg后重复 VCV和 VTPC通气 ,并记录上述通气参数。结果　 10例患者的 Cst为 (38.4± 2 .7) ml/ cm H2 O,Raw为 (2 0 .1± 2 .0 ) cm H2 O· L- 1 · s- 1 。VTPC时 PIP和 VT/ Tinflate较 VCV时显著降低 (P均 <0 .0 5 ) ,PIF则显著增高 ,两种通气时的 Pplat无显著性差异 ,分别为 (2 2 .1± 0 .9) cm H2 O和(2 3.0± 1.2 ) cm H2 O(P>0 .0 5 )。吸入沙丁胺醇后患者的 Raw均显著降低 ,而 Cst无明显变化 ,VCV时的 PIP有所降低 ,但 Pplat无变化 ;VTPC时的 PIP和 Pplat与吸入前比较无明显改变 ,但 PIF和 PEF出现显著增高 ,Tinflate则相应缩短 (P均 <0 .0 5     

俯卧位通气联合呼气末正压治疗急性呼吸窘迫综合征家猪的疗效研究

目的 探讨俯卧位通气联合呼气末正压(PEEP)治疗急性呼吸窘迫综合征(ARDS)的疗效及其机制.方法 12头家猪静脉注射油酸建立ARDS模型,分为仰卧位组和俯卧位组,均给予0(ZEEP)、10(PEEP10)、20 cm H2O(PEEP20,1 cm H2O=0.098 kPa)PEEP的机械通气15 min,监测家猪血流动力学、肺气体交换和呼吸力学指标;处死动物观察肺组织病理学变化.结果 俯卧位组ZEEP、PEEP10时氧合指数(PaO2/FiO2)明显优于仰卧位组[ZEEP:(234.00±72.55)mm Hg比(106.58±34.93)mm Hg,PEEP10:(342.97±60.15) mm Hg比(246.80±83.69)mm Hg,1 mm Hg=0.133 kPa,P均<0.05];PEEP20时两组PaO2/FiO2差异无统计学意义(P>0.05).PEEP10时两组肺复张容积(RV)差异无统计学意义(P>0.05);但PEEP20时俯卧位组RV显著高于仰卧位组[(378.55±101.80)ml比(302.95±34.31)ml,P<0.05].两组间心率(HR)、平均动脉压(MAP)、心排血指数(CI)、呼吸系统顺应性(Cst)及动脉血二氧化碳分压(PaCO2)差异均无统计学意义(P均>0.05);仰卧位组背侧肺组织的肺损伤总评分明显高于俯卧位组[(12.00±1.69)分比(6.03±1.56)分,P<0.05].结论 俯卧位通气联合合适的PEEP可改善ARDS家猪氧合,并且不影响血流动力学和呼吸力学,肺组织损伤的重新分布可能是其机制之一.     

The effects of pressure control versus volume control assisted ventilation on patient work of breathing in acute lung injury and acute respiratory distress syndrome

BACKGROUND: Patient work of breathing (WOB) during assisted ventilation is reduced when inspiratory flow (V(I)) from the ventilator exceeds patient flow demand. Patients in acute respiratory failure often have unstable breathing patterns and their requirements for V(I) may change from breath to breath. Volume control ventilation (VCV) traditionally incorporates a pre-set ventilator V(I) that remains constant even under conditions of changing patient flow demand. In contrast, pressure control ventilation (PCV) incorporates a variable decelerating flow wave form with a high ventilator V(I) as inspiration commences. We compared the effects of flow patterns on assisted WOB during VCV and PCV. METHODS: WOB was measured with a BICORE CP-100 monitor (incorporating a Campbell Diagram) in a prospective, randomized cross-over study of 18 mechanically ventilated adult patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Tidal volume, inspiratory time, and mean ventilator V(I) were constant in each mode. RESULTS: At comparable levels of respiratory drive and minute ventilation, patient WOB was significantly lower with PCV than with VCV (0.59 +/- 0.42 J/L vs 0.70 +/- 0.58 J/L, respectively, p < 0.05). Ventilator peak V(I) was significantly higher with PCV than with VCV (103.2 +/- 22.8 L/min vs 43.8 L/min, respectively, p < 0.01). CONCLUSIONS: In the setting of ALI and ARDS, PCV significantly reduced patient WOB relative to VCV. The decrease in patient WOB was attributed to the higher ventilator peak V(I) of PCV.     

The upper inflection point of the pressure-volume curve. Influence of methodology and of different modes of ventilation

OBJECTIVE: The pressure-volume (P/V) curve has been proposed as a tool to adjust the ventilatory settings in cases of acute respiratory distress syndrome (ARDS). The aim of this study was to test the influence of P/V tracing methodology on the presence and value of the upper inflection point (UIP). METHODS: In 13 medical ARDS patients, the interruption and the automated low flow inflation methods were compared while the patients were ventilated at conventional (10-12 ml/kg) and at low (5-6 ml/kg) tidal volume (Vt). Two levels of inspiratory flow and insufflation time were used (3 and 6 s). RESULTS: No significant difference in UIP was found between the static and the dynamic methods, whatever the flow used. At Vt 10-12 ml/kg, the static and dynamic UIPs were 22.4 +/- 4.4 cmH(2)O and 22.1 +/- 4.5 cmH(2)O ( p = 0.86), respectively; at Vt of 5-6 ml/kg, the static and dynamic UIPs were 26.6 +/- 4.1 cmH(2)O and 25.5 +/- 5 cmH(2)O ( p = 0.34), respectively. Significant differences in UIP were found, in the static and dynamic conditions, between the two levels of Vt ( p < 0.005): it was lower with the higher Vt, suggesting that UIP is dependent on previous tidal alveolar recruitment. CONCLUSION: Interruption and continuous flow techniques gave similar results, but the previous Vt influences the pressure value of the UIP.     

Choice of the parameters of artificial ventilation in patients with acute respiratory distress syndrome

The paper presents the results of use of two modes of controlled artificial ventilation (ALV) in adult patients with acute respiratory distress syndrome of various genesis: 1) ALV with its controlled volume, the descending pattern of inspiratory flow, the limitation of respiratory volume in the airways (RV, 6-8 ml/kg; Ptr.peak < 30 cm H2O), 2) ALV with its controlled volume, the orthogonal pattern of inspiratory flow (RV, 12-15 ml/kg, Ptr.peak > 35 cm H2O). It also shows the advantages and disadvantages of these respiratory procedures in this group of patients.     

异丙酚对急性呼吸窘迫综合征时肾Gq/11蛋白的干预作用

目的探讨异丙酚是否通过影响Gq/11蛋白的表达对肾脏起保护作用。方法采用尾静脉注射油酸(OA)法复制急性呼吸窘迫综合征(ARDS)大鼠模型。将健康雄性Wistar大鼠随机分为对照组(C组)、OA组和异丙酚预处理组(P组),并观察血压及相关酶的变化。用蛋白质免疫印迹法检测肾脏中Gq/11蛋白含量。结果P组Gq/11蛋白含量(124.68±19.38)%较C组(100.00±0)%增加了(24.68±19.38)%(P<0.01),但明显低于OA组(149.34±20.04)%(P<0.01)。P组肾组织血管紧张素转换酶(16.52±1.37)μmol·min-·g-1、乳酸脱氢酶(1.20±0.16)kU/g活性和丙二醛(1.51±0.35)μmol/g含量也均明显低于OA组分别为(17.56±1.02)μmol·min-1·g-1,(1.41±0.16)kU/g,(1.94±0.16)μmol/g,P均<0.01。结论预先注射异丙酚能降低Gq/11蛋白在肾脏中的含量,并减轻ARDS时肾损害的程度。     

Effects of dynamic ventilatory factors on ventilator-induced lung injury in acute respiratory distress syndrome dogs

BACKGROUND:

Mechanical ventilation is a double-edged sword to acute respiratory distress syndrome (ARDS) including lung injury, and systemic inflammatory response high tidal volumes are thought to increase mortality. The objective of this study is to evaluate the effects of dynamic ventilatory factors on ventilator induced lung injury in a dog model of ARDS induced by hydrochloric acid instillation under volume controlled ventilation and to investigate the relationship between the dynamic factors and ventilator-induced lung injuries (VILI) and to explore its potential mechanisms.

METHODS:

Thirty-six healthy dogs were randomly divided into a control group and an experimental group. Subjects in the experimental group were then further divided into four groups by different inspiratory stages of flow. Two mL of alveolar fluid was aspirated for detection of IL-8 and TNF-α. Lung tissue specimens were also extracted for total RNA, IL-8 by western blot and observed under an electronic microscope.

RESULTS:

IL-8 protein expression was significantly higher in group B than in groups A and D. Although the IL-8 protein expression was decreased in group C compared with group B, the difference was not statistically significant. The TNF-α ray degree of group B was significantly higher than that in the other groups (P<0.01), especially in group C (P>0.05). The alveolar volume of subjects in group B was significantly smaller, and cavity infiltration and cell autolysis were marked with a significant thicker alveolar septa, disorder of interval structures, and blurring of collagenous and elastic fiber structures. A large number of necrotic debris tissue was observed in group B.

CONCLUSION:

Mechanical ventilation with a large tidal volume, a high inspiratory flow and a high ventilation frequency can cause significant damage to lung tissue structure. It can significantly increase the expression of TNF-α and IL-8 as well as their mRNA expression. Furthermore, the results of our study showed that small tidal ventilation significantly reduces the release of pro-inflammatory media. This finding suggests that greater deterioration in lung injury during ARDS is associated with high inspiratory flow and high ventilation rate.KEY WORDS: Acute respiratory distress syndrome, Dynamic factors, Inspiratory flow, Ventilator-induced lung injury