机械通气对改良腹腔高压液体动物模型腹腔压力-容量关系的影响
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摘要
目的探讨机械通气对腹腔高压液体动物模型腹腔压力-容量关系的影响。方法以12只实验猪为研究对象,采用随机数字表法随机分为A组(机械通气组)和B组(非机械通气组),各6只。两组均采用全身麻醉,A组行气管插管后接机械通气,模式为容量控制通气(VCV),设定潮气量(VT) 10 ml/kg,呼吸频率16次/min,吸入氧浓度(Fi O_2) 0. 40,高呼气末正压通气(PEEP) 5 cm H_2O(1 cm H_2O=0. 098 k Pa)。按照水囊法制作腹腔高压液体动物模型,每注入生理盐水10 ml,测压1次,记录腹腔内注入总液体量,同步记录腹腔压力(IAP),绘制腹腔压力-增容量曲线,并在IAP为0,10,20,30,40,50 cm H_2O时(0是指腹腔压力升高的0界点)记录注液量。腹内压维持在35 cm H_2O,观察4 h后处死实验动物,切取心脏、肺脏,用10%甲醛溶液固定24 h后常规石蜡包埋,切片,苏木精-伊红(HE)染色,生物光学显微镜下观察。结果 12只家猪均制模成功,无一发生气压伤和死亡。A组腹腔压力-增容量曲线为不规则的"S"形双函数曲线,IAP在22 cm H_2O为节点,IAP<22 cm H_2O,IAP与增容量存在线性相关关系(r~2=0. 78,P <0. 05),IAP> 22 cm H_2O,IAP与增容量存在线性相关关系(r~2=0. 96,P <0. 01); B组腹腔压力-增容量曲线为单函数曲线,IAP与增容量存在正相关关系(r~2=0. 87,P <0. 01)。A组在IAP为0,10,20,30,40,50 cm H_2O时注液量[(2 018. 22±108. 66) ml,(2 032. 60±114. 42) ml,(2 038. 54±112. 60) ml,(2 080. 88±118. 44) ml,(2 162. 38±118. 86) ml,(2 310. 78±124. 20) ml]均低于B组[(2 890. 40±164. 50) ml,(3 000. 58±176. 22) ml,(3 060. 24±178. 24),(3 098. 50±183. 40) ml,(3 120. 00±184. 20) ml,(3 145. 80±188. 60) ml],均差异有统计学意义(t=4. 42,4. 61,4. 85,4. 66,4. 37,5. 35;均P <0. 01)。心脏标本病理检查:A组心脏心肌纤维玻璃样变性,横纹明显减少,部分心肌纤维萎缩; B组心脏心肌纤维部分萎缩,部分肥大,心肌纤维玻璃样变性,心肌间动脉扩张充血。肺脏病理检查:A组肺脏可见大小不一的肺泡腔,部分肺泡融合,肺泡腔扩张,肺组织间可见出血、慢性炎细胞浸润及炎性渗出,细支气管周围平滑肌增生; B组肺脏肺泡融合,形成较大的肺泡囊,肺泡内皮细胞中度增生,可见心衰细胞,间质淋巴管扩张,管内充满淋巴液,支气管动脉扩张充血,管腔内大量红细胞聚集。结论腹腔高压可引起心脏和肺脏出现明显的细胞学损伤,机械通气使腹腔间隔室综合征(ACS)发生代偿的空间缩小,腹腔压力与容积关系曲线发生改变,并对心和肺损伤起到一定程度的保护作用。
Objective To explore the effect of mechanical ventilation on the pressure-volume relationship of abdominal cavity via making an improved abdominal hypertension liquid animal model by means of water bag superposition pressurization. Methods 12 experimental pigs were randomly divided into group A( mechanical ventilation group) and group B( non mechanical ventilation group),6 pigs in each group. Both groups were anesthetized under general anesthesia. In group A,ventilator was used to assist breathing after tracheal intubation. The breathing mode was volume controlled ventilation( VCV),tidal volume( VT) 10 ml/kg,breathing rate 16 times/min,inhaled oxygen concentration( Fi O_2) 0. 40,positive end expiratory pressure( PEEP) 5 cm H_2O( 1 cm H_2O = 0. 098 k Pa). The abdominal hypertensive fluid models of group A and group B were made according to the operation procedure of the abdominal hypertensive fluid model made by the water sac method,the abdominal hypertensive fluid models of group A and group B were injected with normal saline through the drainage pipe of the drainage bag,the abdominal pressure was measured once every 10 ml,the total fluid volume was recorded,the abdominal pressure was recorded synchronously,and the abdominal pressure increase curve was drawn. The volume of fluid injection was recorded when the abdominal pressure was 0,10,20,30,40,50 cm H_2O( 0 refers to the zero point of abdominal pressure rise).The intraabdominal pressure was maintained at 35 cm H_2O( 25. 74 mm Hg). After 4 hours of observation,the experimental animals were killed,the hearts and lungs were harvested and fixed with 10%formaldehyde solution for 24 hours. The samples were embedded in paraffin and stained with HE.Results All 12 pigs were successfully moulded without barometric injury or death. In group A,the abdominal pressure-volume increase curve was an irregular "S"hyperfunction curve. The turning point of abdominal pressure 22 cm H_2O,there was a positive correlation between the abdominal pressure and volume increase when the abdominal pressure was less than 22 cm H_2O( r~2= 0. 78,P <0. 05),and the abdominal pressure was positively correlated with the volume increase when the abdominal pressure was more than 22 cm H_2O( r~2= 0. 96,P <0. 01). In group B showed that there was a positive correlation between abdominal pressure and volume increase( r~2= 0. 87,P <0. 01). While the intraperitoneal pressures of group A were 0,10,20,30,40,50 cm H_2O,the amounts of fluid of group A [( 2 018. 22 ± 108. 66) ml,( 2 032. 60 ± 114. 42) ml,( 2 038. 54±112. 60) ml,( 2 080. 88± 118. 44) ml,( 2 162. 38± 118. 86) ml,( 2 310. 78±124. 20) ml] were significantly lower than those of group B [( 2 890. 40 ± 164. 50) ml,( 3 000. 58± 176. 22) ml,( 3 060. 24 ±178. 24) ml,( 3 098. 50 ± 183. 40) ml,( 3 120. 00 ± 184. 20) ml,( 3 145. 80± 188. 60) ml ],there were statistical significances( t = 4. 42,4. 61,4. 85,4. 66,4. 37,5. 35,all P < 0. 01). Cardiological examination: in group A,myocardial fibers with hyaline degeneration,reduced transverse striation model,and partial atrophy of myocardial fibers could be seen. In group B,partial atrophy and hypertrophy of cardiac myocardial fibers,hyaline degeneration of myocardial fibers,dilatation and congestion of myocardial arteries could be seen.Lung pathology examination: in group A,alveolar lumen of different sizes can be seen in the lungs. There was part alveolar fusion,alveolar cavity dilatation,bleeding,chronic inflammatory cell infiltration and inflammatory exudation between lung tissues,smooth muscle proliferation around bronchioles. In group B,the pulmonary alveoli fused to form larger alveolar sacs,alveolar endothelial cells moderately proliferated,heart failure cells could be seen,interstitial lymphatic vessels dilated,lymphatic vessels were filled with lymph,bronchial artery dilated and congested,and a large number of red blood cells accumulated in the lumen.Conclusion Abdominal hypertension can cause significant cytological damage to the heart and lungs.Mechanical ventilation can reduce the compensatory space of abdominal compartment syndrome( ACS),change the relationship between abdominal pressure and volume,and protect the heart and lung to a certain extent.
Objective To explore the effect of mechanical ventilation on the pressure-volume relationship of abdominal cavity via making an improved abdominal hypertension liquid animal model by means of water bag superposition pressurization. Methods 12 experimental pigs were randomly divided into group A( mechanical ventilation group) and group B( non mechanical ventilation group),6 pigs in each group. Both groups were anesthetized under general anesthesia. In group A,ventilator was used to assist breathing after tracheal intubation. The breathing mode was volume controlled ventilation( VCV),tidal volume( VT) 10 ml/kg,breathing rate 16 times/min,inhaled oxygen concentration( Fi O_2) 0. 40,positive end expiratory pressure( PEEP) 5 cm H_2O( 1 cm H_2O = 0. 098 k Pa). The abdominal hypertensive fluid models of group A and group B were made according to the operation procedure of the abdominal hypertensive fluid model made by the water sac method,the abdominal hypertensive fluid models of group A and group B were injected with normal saline through the drainage pipe of the drainage bag,the abdominal pressure was measured once every 10 ml,the total fluid volume was recorded,the abdominal pressure was recorded synchronously,and the abdominal pressure increase curve was drawn. The volume of fluid injection was recorded when the abdominal pressure was 0,10,20,30,40,50 cm H_2O( 0 refers to the zero point of abdominal pressure rise).The intraabdominal pressure was maintained at 35 cm H_2O( 25. 74 mm Hg). After 4 hours of observation,the experimental animals were killed,the hearts and lungs were harvested and fixed with 10%formaldehyde solution for 24 hours. The samples were embedded in paraffin and stained with HE.Results All 12 pigs were successfully moulded without barometric injury or death. In group A,the abdominal pressure-volume increase curve was an irregular "S"hyperfunction curve. The turning point of abdominal pressure 22 cm H_2O,there was a positive correlation between the abdominal pressure and volume increase when the abdominal pressure was less than 22 cm H_2O( r~2= 0. 78,P <0. 05),and the abdominal pressure was positively correlated with the volume increase when the abdominal pressure was more than 22 cm H_2O( r~2= 0. 96,P <0. 01). In group B showed that there was a positive correlation between abdominal pressure and volume increase( r~2= 0. 87,P <0. 01). While the intraperitoneal pressures of group A were 0,10,20,30,40,50 cm H_2O,the amounts of fluid of group A [( 2 018. 22 ± 108. 66) ml,( 2 032. 60 ± 114. 42) ml,( 2 038. 54±112. 60) ml,( 2 080. 88± 118. 44) ml,( 2 162. 38± 118. 86) ml,( 2 310. 78±124. 20) ml] were significantly lower than those of group B [( 2 890. 40 ± 164. 50) ml,( 3 000. 58± 176. 22) ml,( 3 060. 24 ±178. 24) ml,( 3 098. 50 ± 183. 40) ml,( 3 120. 00 ± 184. 20) ml,( 3 145. 80± 188. 60) ml ],there were statistical significances( t = 4. 42,4. 61,4. 85,4. 66,4. 37,5. 35,all P < 0. 01). Cardiological examination: in group A,myocardial fibers with hyaline degeneration,reduced transverse striation model,and partial atrophy of myocardial fibers could be seen. In group B,partial atrophy and hypertrophy of cardiac myocardial fibers,hyaline degeneration of myocardial fibers,dilatation and congestion of myocardial arteries could be seen.Lung pathology examination: in group A,alveolar lumen of different sizes can be seen in the lungs. There was part alveolar fusion,alveolar cavity dilatation,bleeding,chronic inflammatory cell infiltration and inflammatory exudation between lung tissues,smooth muscle proliferation around bronchioles. In group B,the pulmonary alveoli fused to form larger alveolar sacs,alveolar endothelial cells moderately proliferated,heart failure cells could be seen,interstitial lymphatic vessels dilated,lymphatic vessels were filled with lymph,bronchial artery dilated and congested,and a large number of red blood cells accumulated in the lumen.Conclusion Abdominal hypertension can cause significant cytological damage to the heart and lungs.Mechanical ventilation can reduce the compensatory space of abdominal compartment syndrome( ACS),change the relationship between abdominal pressure and volume,and protect the heart and lung to a certain extent.
引文
[1]王丽,谢镒鞠,唐小唪,等.创伤失血性休克后腹腔高压对心肺基础监测指标的影响[J].第三军医大学学报,2013,35(20):2159-2163.
[2]刘道城,谭浩,张连阳,等.腹腔扩容术对猪休克复苏后腹腔高压症心脏的影响[J].中华实验外科杂志,2012,29(8):1447-1449.
[3]王宏业,安峰,杨秀义,等.腹腔置管减压治疗恶性腹水源性腹腔间隔室综合征29例临床观察[J].中华胃肠外科杂志,2010,13(4):273-275.
[4]李育明,周秋香,江伟伟,等.呼气末正压滴定方式对急性呼吸窘迫综合征伴腹腔高压患者呼吸功能的影响研究[J].现代生物医学进展,2017,17(18):3583-3587.
[5]王宏业,尉继伟,杨靖,等.改良腹腔高压水囊动物模型肝、肾病理改变[J].中国实用医刊,2015,42(4):63-65.
[6]王宏业,尉继伟,杨靖,等.甲状腺激素、肿瘤坏死因子在腹腔置管减压治疗恶性腹水源性腹腔间隔室综合征前后的表达[J].中华内分泌外科杂志,2013(4):342-344.
[7]Kirkpatrick AW,Roberts DJ,De Waele J,等.世界腹腔间隙学会腹内高压和腹腔间隙综合征2013版专家共识与诊疗指南[J].中华外科杂志,2015,53(3):173-175.
[8]葛慧青,徐培峰,陆志华,等.腹内高压对机械通气兔膈肌细胞凋亡和超微结构的影响[J].中华急诊医学杂志,2012,21(8):851-854.
[9]罗建宇,王晓源,蒋文芳,等.呼气末正压在急性呼吸窘迫综合征合并腹腔高压患者中的应用研究[J].中国呼吸与危重监护杂志,2015,14(3):282-285.
[10]曹建春,张东萍,李乃卿,等.腹腔压升高规律的研究[J].医学研究杂志,2008,37(6):46-49.
[11]王宏业,尉继伟.羊水囊叠加加压法腹腔高压动物模型的建立[J/CD].中华临床医师杂志(电子版),2017,11(23):2450-2453.
[12]Malbrain ML,Wilmer A.The polycompartment syndrome:towards an understanding of the interactions between different compartments[J].Intensive Care Med,2007,33(11):1869-1872.
[13]严姝瑛,陈远卓,彭沪,等.腹腔高压对急性肺损伤猪呼吸系统的影响[J].同济大学学报(医学版),2012,33(6):68-71.
[14]李涛,段军,张庆,等.腹腔高压对呼吸力学及血流动力学的影响[J].内科急危重症杂志,2015,21(3):192-194.
[15]王黎卫,陈鹏,王锦栋.腹腔高压下每搏输出量变异度对脓毒血症患者容量反应预测[J/CD].中华危重病医学杂志(电子版),2016,9(4):271-275.
[16]杨斌,吴志雄,宋晓华.腹腔高压病理生理研究进展[J].老年医学与保健,2016,22(5):320-322.
[17]张宏光,刘东,张连阳.腹腔高压症对中枢神经系统影响的研究进展[J/CD].中华普通外科学文献(电子版),2014,8(2):139-142.
[18]程君涛,肖光夏,张诚华,等.改良腹内高压动物模型制作及动脉血气分析[J].第三军医大学学报,2005,27(21):2189-2190.
[19]陈勇,王宏业.腹腔间隔室综合症白细胞介素-6和10变化规律的实验研究[J].中国医师进修杂志,2018,41(11):1012-1015.
[20]Rezende-Neto JB,Moore EE,Masuno T,et al.The abdominal compartment syndrome as a second insult during systemic neutrophil priming provokes multiple organ injury[J].Shock,2003,20(4):303-308.
[2]刘道城,谭浩,张连阳,等.腹腔扩容术对猪休克复苏后腹腔高压症心脏的影响[J].中华实验外科杂志,2012,29(8):1447-1449.
[3]王宏业,安峰,杨秀义,等.腹腔置管减压治疗恶性腹水源性腹腔间隔室综合征29例临床观察[J].中华胃肠外科杂志,2010,13(4):273-275.
[4]李育明,周秋香,江伟伟,等.呼气末正压滴定方式对急性呼吸窘迫综合征伴腹腔高压患者呼吸功能的影响研究[J].现代生物医学进展,2017,17(18):3583-3587.
[5]王宏业,尉继伟,杨靖,等.改良腹腔高压水囊动物模型肝、肾病理改变[J].中国实用医刊,2015,42(4):63-65.
[6]王宏业,尉继伟,杨靖,等.甲状腺激素、肿瘤坏死因子在腹腔置管减压治疗恶性腹水源性腹腔间隔室综合征前后的表达[J].中华内分泌外科杂志,2013(4):342-344.
[7]Kirkpatrick AW,Roberts DJ,De Waele J,等.世界腹腔间隙学会腹内高压和腹腔间隙综合征2013版专家共识与诊疗指南[J].中华外科杂志,2015,53(3):173-175.
[8]葛慧青,徐培峰,陆志华,等.腹内高压对机械通气兔膈肌细胞凋亡和超微结构的影响[J].中华急诊医学杂志,2012,21(8):851-854.
[9]罗建宇,王晓源,蒋文芳,等.呼气末正压在急性呼吸窘迫综合征合并腹腔高压患者中的应用研究[J].中国呼吸与危重监护杂志,2015,14(3):282-285.
[10]曹建春,张东萍,李乃卿,等.腹腔压升高规律的研究[J].医学研究杂志,2008,37(6):46-49.
[11]王宏业,尉继伟.羊水囊叠加加压法腹腔高压动物模型的建立[J/CD].中华临床医师杂志(电子版),2017,11(23):2450-2453.
[12]Malbrain ML,Wilmer A.The polycompartment syndrome:towards an understanding of the interactions between different compartments[J].Intensive Care Med,2007,33(11):1869-1872.
[13]严姝瑛,陈远卓,彭沪,等.腹腔高压对急性肺损伤猪呼吸系统的影响[J].同济大学学报(医学版),2012,33(6):68-71.
[14]李涛,段军,张庆,等.腹腔高压对呼吸力学及血流动力学的影响[J].内科急危重症杂志,2015,21(3):192-194.
[15]王黎卫,陈鹏,王锦栋.腹腔高压下每搏输出量变异度对脓毒血症患者容量反应预测[J/CD].中华危重病医学杂志(电子版),2016,9(4):271-275.
[16]杨斌,吴志雄,宋晓华.腹腔高压病理生理研究进展[J].老年医学与保健,2016,22(5):320-322.
[17]张宏光,刘东,张连阳.腹腔高压症对中枢神经系统影响的研究进展[J/CD].中华普通外科学文献(电子版),2014,8(2):139-142.
[18]程君涛,肖光夏,张诚华,等.改良腹内高压动物模型制作及动脉血气分析[J].第三军医大学学报,2005,27(21):2189-2190.
[19]陈勇,王宏业.腹腔间隔室综合症白细胞介素-6和10变化规律的实验研究[J].中国医师进修杂志,2018,41(11):1012-1015.
[20]Rezende-Neto JB,Moore EE,Masuno T,et al.The abdominal compartment syndrome as a second insult during systemic neutrophil priming provokes multiple organ injury[J].Shock,2003,20(4):303-308.