中华危重病急救医学
中華危重病急救醫學
중화위중병급구의학
Chinese Critical Care Medicine
2014年
12期
884-889
,共6页
宋俊杰%蒋敏%戚桂艳%谢宇颖%王怀泉%田永刚%曲晶东%张晓明%李海波
宋俊傑%蔣敏%慼桂豔%謝宇穎%王懷泉%田永剛%麯晶東%張曉明%李海波
송준걸%장민%척계염%사우영%왕부천%전영강%곡정동%장효명%리해파
潮气量%气道湿化%机械通气%炎症介质%气管纤毛
潮氣量%氣道濕化%機械通氣%炎癥介質%氣管纖毛
조기량%기도습화%궤계통기%염증개질%기관섬모
Tidal volume%Airway humidification%Mechanical ventilation%Inflammatory cytokine%Cilia
目的：探讨气道湿化对不同潮气量（VT）机械通气所致肺损伤的影响。方法将24只雄性日本大耳白兔按随机数字表法分为小VT组、大VT组、小VT湿化组、大VT湿化组4组，每组6只。所有动物均在气管切开插管后行机械通气6 h，小VT为8 mL/kg、大VT为16 mL/kg，吸入氧浓度（FiO2）为0.40，呼气末正压（PEEP）为0；湿化组通过加热型湿化器维持呼吸回路Y件处的温度在40℃左右。通气0、2、4、6 h行动脉血气分析〔pH值、动脉血氧分压（PaO2）和动脉血二氧化碳分压（PaCO2）〕和肺机械力学〔气道峰压（Ppeak）、气道阻力（Raw）、肺顺应性〕监测；采用酶联免疫吸附试验（ELISA）测定血浆及支气管肺泡灌洗液（BALF）中肿瘤坏死因子-α（TNF-α）和白细胞介素-8（IL-8）水平。机械通气后处死动物，计算肺组织湿/干质量（W/D）比值；光镜下观察肺组织病理学改变并进行评分，扫描电镜和透射电镜下观察气道纤毛及气道上皮改变。结果与小VT组比较，大VT组pH值明显升高，PaCO2明显降低，PaO2无明显变化，通气过程中Ppeak、Raw、肺顺应性均明显升高。小VT湿化组血气分析指标、肺机械力学指标与小VT组比较均无差异。与大VT组比较，大VT湿化组PaCO2明显降低，Ppeak明显升高，pH值、PaO2、Raw、肺顺应性均无明显差异。与小VT湿化组比较，大VT湿化组血气分析指标无明显差异，Ppeak、Raw、肺顺应性明显升高〔PaCO2（mmHg，1 mmHg＝0.133 kPa）2 h：27.96±4.64比36.08±2.11，4 h：28.62±2.93比34.55±5.50，6 h：29.33±2.14比35.01±5.53；Ppeak （cmH2O，1 cmH2O＝0.098 kPa）0 h：14.34±1.97比8.84±1.32，2 h：17.33±0.52比11.17±2.14，4 h：17.83±0.98比12.67±2.06，6 h：18.67±1.22比13.50±2.16；Raw（cmH2O）0 h：37.36±5.14比27.05±2.93，2 h：43.94±6.58比31.95±3.56，4 h：48.04±6.07比35.24±3.50，6 h：50.33±6.34比36.66±3.64；肺顺应性（mL/cmH2O）6 h：2.28±0.18比1.86±0.37，均P＜0.05〕。大VT组肺W/D比值较小VT组明显升高（6.17±2.14比3.50±1.52，P＜0.05）；而大VT湿化组肺W/D比值高于小VT湿化组，但差异无统计学意义（5.17±2.14比3.00±1.10，P＞0.05）。镜下观察显示：小VT组气道纤毛部分脱落，有倒伏、粘连，轻度稀疏；大VT组纤毛严重脱落，尚存的纤毛稀疏并且倒伏，细胞结构破坏，肺组织病理损伤评分较小VT组明显升高（分：6.17±2.14比3.50±1.52，P＜0.05）；小VT湿化组纤毛正常，细胞结构清晰，肺组织病理损伤评分与小VT组比较无差异（分：3.00±1.10比3.50±1.52，P＞0.05）；大VT湿化组纤毛明显稀疏，严重粘连、倒伏，细胞结构不清晰，肺组织病理损伤评分高于小VT湿化组，但差异无统计学意义（5.17±2.14比3.00±1.10，P＞0.05）。通气过程中各组血浆和BALF中炎症介质TNF-α、IL-8浓度未见明显变化，各组间也并未出现统计学差异。结论气道湿化降低了小VT及大VT机械通气所致的肺组织病理损害、气道纤毛损伤和气道细胞结构损害。大VT湿化时会出现明显的肺水肿。
目的：探討氣道濕化對不同潮氣量（VT）機械通氣所緻肺損傷的影響。方法將24隻雄性日本大耳白兔按隨機數字錶法分為小VT組、大VT組、小VT濕化組、大VT濕化組4組，每組6隻。所有動物均在氣管切開插管後行機械通氣6 h，小VT為8 mL/kg、大VT為16 mL/kg，吸入氧濃度（FiO2）為0.40，呼氣末正壓（PEEP）為0；濕化組通過加熱型濕化器維持呼吸迴路Y件處的溫度在40℃左右。通氣0、2、4、6 h行動脈血氣分析〔pH值、動脈血氧分壓（PaO2）和動脈血二氧化碳分壓（PaCO2）〕和肺機械力學〔氣道峰壓（Ppeak）、氣道阻力（Raw）、肺順應性〕鑑測；採用酶聯免疫吸附試驗（ELISA）測定血漿及支氣管肺泡灌洗液（BALF）中腫瘤壞死因子-α（TNF-α）和白細胞介素-8（IL-8）水平。機械通氣後處死動物，計算肺組織濕/榦質量（W/D）比值；光鏡下觀察肺組織病理學改變併進行評分，掃描電鏡和透射電鏡下觀察氣道纖毛及氣道上皮改變。結果與小VT組比較，大VT組pH值明顯升高，PaCO2明顯降低，PaO2無明顯變化，通氣過程中Ppeak、Raw、肺順應性均明顯升高。小VT濕化組血氣分析指標、肺機械力學指標與小VT組比較均無差異。與大VT組比較，大VT濕化組PaCO2明顯降低，Ppeak明顯升高，pH值、PaO2、Raw、肺順應性均無明顯差異。與小VT濕化組比較，大VT濕化組血氣分析指標無明顯差異，Ppeak、Raw、肺順應性明顯升高〔PaCO2（mmHg，1 mmHg＝0.133 kPa）2 h：27.96±4.64比36.08±2.11，4 h：28.62±2.93比34.55±5.50，6 h：29.33±2.14比35.01±5.53；Ppeak （cmH2O，1 cmH2O＝0.098 kPa）0 h：14.34±1.97比8.84±1.32，2 h：17.33±0.52比11.17±2.14，4 h：17.83±0.98比12.67±2.06，6 h：18.67±1.22比13.50±2.16；Raw（cmH2O）0 h：37.36±5.14比27.05±2.93，2 h：43.94±6.58比31.95±3.56，4 h：48.04±6.07比35.24±3.50，6 h：50.33±6.34比36.66±3.64；肺順應性（mL/cmH2O）6 h：2.28±0.18比1.86±0.37，均P＜0.05〕。大VT組肺W/D比值較小VT組明顯升高（6.17±2.14比3.50±1.52，P＜0.05）；而大VT濕化組肺W/D比值高于小VT濕化組，但差異無統計學意義（5.17±2.14比3.00±1.10，P＞0.05）。鏡下觀察顯示：小VT組氣道纖毛部分脫落，有倒伏、粘連，輕度稀疏；大VT組纖毛嚴重脫落，尚存的纖毛稀疏併且倒伏，細胞結構破壞，肺組織病理損傷評分較小VT組明顯升高（分：6.17±2.14比3.50±1.52，P＜0.05）；小VT濕化組纖毛正常，細胞結構清晰，肺組織病理損傷評分與小VT組比較無差異（分：3.00±1.10比3.50±1.52，P＞0.05）；大VT濕化組纖毛明顯稀疏，嚴重粘連、倒伏，細胞結構不清晰，肺組織病理損傷評分高于小VT濕化組，但差異無統計學意義（5.17±2.14比3.00±1.10，P＞0.05）。通氣過程中各組血漿和BALF中炎癥介質TNF-α、IL-8濃度未見明顯變化，各組間也併未齣現統計學差異。結論氣道濕化降低瞭小VT及大VT機械通氣所緻的肺組織病理損害、氣道纖毛損傷和氣道細胞結構損害。大VT濕化時會齣現明顯的肺水腫。
목적：탐토기도습화대불동조기량（VT）궤계통기소치폐손상적영향。방법장24지웅성일본대이백토안수궤수자표법분위소VT조、대VT조、소VT습화조、대VT습화조4조，매조6지。소유동물균재기관절개삽관후행궤계통기6 h，소VT위8 mL/kg、대VT위16 mL/kg，흡입양농도（FiO2）위0.40，호기말정압（PEEP）위0；습화조통과가열형습화기유지호흡회로Y건처적온도재40℃좌우。통기0、2、4、6 h행동맥혈기분석〔pH치、동맥혈양분압（PaO2）화동맥혈이양화탄분압（PaCO2）〕화폐궤계역학〔기도봉압（Ppeak）、기도조력（Raw）、폐순응성〕감측；채용매련면역흡부시험（ELISA）측정혈장급지기관폐포관세액（BALF）중종류배사인자-α（TNF-α）화백세포개소-8（IL-8）수평。궤계통기후처사동물，계산폐조직습/간질량（W/D）비치；광경하관찰폐조직병이학개변병진행평분，소묘전경화투사전경하관찰기도섬모급기도상피개변。결과여소VT조비교，대VT조pH치명현승고，PaCO2명현강저，PaO2무명현변화，통기과정중Ppeak、Raw、폐순응성균명현승고。소VT습화조혈기분석지표、폐궤계역학지표여소VT조비교균무차이。여대VT조비교，대VT습화조PaCO2명현강저，Ppeak명현승고，pH치、PaO2、Raw、폐순응성균무명현차이。여소VT습화조비교，대VT습화조혈기분석지표무명현차이，Ppeak、Raw、폐순응성명현승고〔PaCO2（mmHg，1 mmHg＝0.133 kPa）2 h：27.96±4.64비36.08±2.11，4 h：28.62±2.93비34.55±5.50，6 h：29.33±2.14비35.01±5.53；Ppeak （cmH2O，1 cmH2O＝0.098 kPa）0 h：14.34±1.97비8.84±1.32，2 h：17.33±0.52비11.17±2.14，4 h：17.83±0.98비12.67±2.06，6 h：18.67±1.22비13.50±2.16；Raw（cmH2O）0 h：37.36±5.14비27.05±2.93，2 h：43.94±6.58비31.95±3.56，4 h：48.04±6.07비35.24±3.50，6 h：50.33±6.34비36.66±3.64；폐순응성（mL/cmH2O）6 h：2.28±0.18비1.86±0.37，균P＜0.05〕。대VT조폐W/D비치교소VT조명현승고（6.17±2.14비3.50±1.52，P＜0.05）；이대VT습화조폐W/D비치고우소VT습화조，단차이무통계학의의（5.17±2.14비3.00±1.10，P＞0.05）。경하관찰현시：소VT조기도섬모부분탈락，유도복、점련，경도희소；대VT조섬모엄중탈락，상존적섬모희소병차도복，세포결구파배，폐조직병리손상평분교소VT조명현승고（분：6.17±2.14비3.50±1.52，P＜0.05）；소VT습화조섬모정상，세포결구청석，폐조직병리손상평분여소VT조비교무차이（분：3.00±1.10비3.50±1.52，P＞0.05）；대VT습화조섬모명현희소，엄중점련、도복，세포결구불청석，폐조직병리손상평분고우소VT습화조，단차이무통계학의의（5.17±2.14비3.00±1.10，P＞0.05）。통기과정중각조혈장화BALF중염증개질TNF-α、IL-8농도미견명현변화，각조간야병미출현통계학차이。결론기도습화강저료소VT급대VT궤계통기소치적폐조직병리손해、기도섬모손상화기도세포결구손해。대VT습화시회출현명현적폐수종。
Objective To explore the effect of airway humidification on lung injury as a result of mechanical ventilation with different tidal volume(VT). Methods Twenty-four male Japanese white rabbits were randomly divided into four groups:low VT with airway humidification group,high VT with airway humidification group,low VT and high VT group without humidification,with 6 rabbits in each group. Mechanical ventilation was started after intubation and lasted for 6 hours. Low VT denoted 8 mL/kg,while high VT was 16 mL/kg,fraction of inspired oxygen (FiO2)denoted 0.40,positive end-expiratory pressure(PEEP)was 0. Temperature at Y piece of circuit in airway humidification groups was monitored and controlled at 40℃. Arterial blood gas analysis,including pH value,arterial partial pressure of oxygen(PaO2),arterial partial pressure of carbon dioxide(PaCO2),lung mechanics indexes, including peak airway pressure(Ppeak)and airway resistance(Raw),and lung compliance was measured at 0,2,4, 6 hours of mechanical ventilation. The levels of tumor necrosis factor-α(TNF-α)and interleukin-8(IL-8)in plasma and bronchoalveolar lavage fluid(BALF)were determined by enzyme linked immunosorbent assay(ELISA). The animals were sacrificed at the end of mechanical ventilation. The wet to dry(W/D)ratio of lung tissues was calculated. Histopathologic changes in the lung tissueies were observed with microscope,and lung injury score was calculated. Scanning and transmission electron microscopies were used to examine the integrity of the airway cilia and the tracheal epithelium. Results Compared with low VT group,pH value in high VT group was significantly increased,PaCO2 was significantly lowered,and no difference in PaO2 was found. Ppeak,Raw,and lung compliance were significantly increased during mechanical ventilation. There were no significant differences in blood gas analysis and lung mechanics indexes between low VT with airway humidification group and low VT group. Compared with high VT group,PaCO2 in high VT with airway humidification group was significantly decreased,Ppeak raised obviously,and no difference in pH value,PaO2,Raw and pulmonary compliance was found. Compared with low VT with airway humidification group,no difference in blood gas analysis(PaCO2,mmHg,1 mmHg=0.133 kPa)was found,but Ppeak(cmH2O,1 cmH2O=0.098 kPa),Raw(cmH2O),and lung compliance(mL/cmH2O)were increased significantly in high VT with airway humidification group(PaCO2 at 2 hours:27.96±4.64 vs. 36.08±2.11,4 hours:28.62±2.93 vs. 34.55±5.50, 6 hours:29.33±2.14 vs. 35.01±5.53;Ppeak at 0 hour:14.34±1.97 vs. 8.84±1.32,2 hours:17.33±0.52 vs. 11.17±2.14,4 hours:17.83±0.98 vs. 12.67±2.06,6 hours:18.67±1.22 vs. 13.50±2.16;Raw at 0 hour:37.36±5.14 vs. 27.05±2.93,2 hours:43.94±6.58 vs. 31.95±3.56,4 hours:48.04±6.07 vs. 35.24±3.50, 6 hours:50.33±6.34 vs. 36.66±3.64;pulmonary compliance at 6 hours:2.28±0.18 vs. 1.86±0.37,all P<0.05). The lung W/D ratio in high VT group was significantly higher than that of the low VT group(6.17±2.14 vs. 3.50±1.52, P<0.05). W/D in high VT with airway humidification group was higher than that of low VT with airway humidification group but without statistically significant difference(5.17±2.14 vs. 3.00±1.10,P>0.05). Microscopic observation showed that cilia were partially detached,adhered and sparse in low VT group,while cilia in high VT group showed serious detachment and lodging. Remaining cilia were sparse,with lodging,and cellular structure was damaged. Lung tissue pathological injury score in the high VT group was significantly higher than that of low VT group(6.17±2.14 vs. 3.50±1.52,P<0.05). Cilia density and cellularity were normal in low VT with airway humidification group,and no difference in lung tissue pathological injury score was found compared with low VT group(3.00±1.10 vs. 3.50±1.52, P>0.05). Cilia were severely detached,adhered and lodging,and cellularity were not obvious in high VT with airway humidification group,and lung tissue pathological injury score was elevated significantly than that of the low VT with airway humidification group but without statistically significant difference(5.17±2.14 vs. 3.00±1.10,P>0.05). TNF-α and IL-8 concentrations showed no change in plasma and BALF in all groups during ventilation,and no significant difference was found among the groups. Conclusions Airway humidification can alleviate pathological lung injury,damage of cilia and cellular structure in trachea caused by mechanical ventilation with low and high VT. High VT with humidification can result in serious pulmonary edema.
