宣白承气汤对急性肺损伤机械通气患者呼吸力学的影响
·30·
2010年8月第42卷第8期
JOURNALOFNEWCHINESEMEDICINEAugust2010Vol.42No.8
新中医
宣白承气汤对急性肺损伤机械通气患者呼吸力学的影响
张忠,乔秋杰,向素英,黄若兰,谢纬
深圳市中医院,广东深圳518033
[摘要]目的:研究宣白承气汤对急性肺损伤(ALI)机械通气患者呼吸力学的作用及其机制。方法:将符合要求的45例ALI患者随机分为治疗组23例和对照组22例,均给予常规治疗及机械通气,治疗组加用宣白承气汤,比较治疗前后气道峰压(PIP)、平台压(Pplat)、气道阻力(Raw)、氧合指数(PaO2/FiO2)、静态肺顺应性(Cst)及动态肺顺应性(Cdyn)等呼吸力学参数,胸片评分及血清肿瘤坏死因子α(TNF-α)、白介素-1β(IL-1β)和白介素-10(IL-10)等炎性因子。结果:治疗后治疗组患者PIP、Raw、Cdyn及胸片评分等均有改善,与对照组比较,差异均有显著性意义(P<0.05);而Pplat、Cst、PaO2/FiO2等改善更显著,明显优于对照组(P<0.01)。炎性指标方面,治疗后治疗组TNF-α、IL-1β水平较对照组明显下降(P<0.05);而IL-10较对照组明显上升(P<0.05)。结论:宣白承气汤对急性肺损伤患者呼吸力学有较好的改善作用,其机制可能与宣白承气汤调节促炎因子与抑炎因子之间的平衡有关。
[关键词]急性肺损伤;机械通气;宣白承气汤;呼吸力学;炎性因子[中图分类号]R563
[文献标识码]A
[文章编号]0256-7415(2010)08-0030-02
急性肺损伤(ALI)是以低氧血症为特征的急性起病的呼吸衰竭,急性呼吸窘迫综合征(ARDS)是病情进展的结果。如何在机械通气纠正顽固性缺氧的基础上,进一步改善患者的气道顺应性及呼吸动力,实现尽早脱机,减少其发展为ARDS的机会,仍是监护治疗的重要课题。本研究旨在观察宣白承气汤对应用机械通气的ALI患者呼吸力学的影响,为中医药治疗ALI提供思路。11.1
资料与方法病例来源
选择2006年3月~2009年6月于本院ICU
脉推注乌司他丁针剂每次40万U,每6小时1次;④维持水、电解质和酸碱平衡,给予必要的对症支持治疗。
治疗组在上述治疗的基础上给予宣白承气汤。处方:生石膏、瓜蒌皮各20g,生大黄9g,苦杏仁15g。由本院煎药室制成200mL煎剂,每天1剂,分早晚2次鼻饲。对照组同时给予温开水200mL,分早晚2次鼻饲。2组疗程均为7天。治疗过程中如病情发展为ARDS,或患者死亡,则研究中止,并作为无效统计。1.3
机械通气策略
2组患者均采用经口气管插管,气管导
管内径为男性8.0mm,女性7.5mm。使用MAQUETServo-i型呼吸机辅助通气,患者取平卧位,静脉注射咪唑安定以保持适当的镇静,Ramsay评分为2~3级[2],采用保护性机械通气策略,通气模式设为定容型,潮气量6~10mL/kg,吸气流速40~60L/分,吸气末暂停时间0.1~0.5秒,通气频率15~20次/分,呼吸末正压6~12cmH2O,吸氧浓度40%~60%,持续通气60分钟后,在患者生命体征及血流动力学稳定的情况下记录呼吸力学参数,每隔5分钟监测1次气道峰压(PIP)和平台压(Pplat),并计算气道阻力(Raw)、静态肺顺应性(Cst)及动态肺顺应性(Cdyn),共5次,取平均值作为统计数据。1.4
呼吸力学指标观测
观察治疗前(机械通气后60分
钟)、治疗7天时的氧合指数(PaO2/FiO2)、PIP、Pplat、Raw、Cst及Cdyn等,Cst(mL/cmH2O)=VT/(Pplat-PEEP);Cdyn(mL/cmH2O)=VT/(PIP-PEEP)[3]。
和呼吸内科住院的患者共45例,全部病例符合1994年美国和欧洲ARDS评审会议制订的ALI诊断标准[1],并需要有创机械通气治疗,将患者随机分为治疗组23例和对照组22例。治疗组男14例,女9例;年龄在28~69岁;其中脓毒症10例、腹部外伤5例、颅脑外伤4例、急性胰腺炎2例、误吸2例。对照组男15例,女7例;年龄在30~65岁;其中脓毒症12例、腹部外伤5例、颅脑外伤3例、急性胰腺炎1例、误吸1例。2组患者在性别、年龄、原发疾病、急性生理学评分系统(APACHEⅡ)评分等经统计学处理,差异均无显著性意义(P>0.05),具有可比性。1.2
治疗方法
2组患者均积极处理原发病,外伤患者及时
行手术治疗。所有患者给予常规治疗,包括:①必要的抗感染治疗,根据药敏选择和调整药物;②祛痰药物,静脉推注沐舒坦针剂每次45mg,每6小时1次;③抑制炎症反应药物,静
[收稿日期]2010-04-27
[作者简介]张忠(1970-),男,副主任医师,主要从事心血管和急危重症的临床、教学及科研工作。
2010年8月第42卷第8期
JOURNALOFNEWCHINESEMEDICINEAugust2010Vol.42No.8
新中医
·31·
1.5
胸部摄片
分别于治疗前(开始机械通气60分钟内)、
治疗7天时行床边胸部摄片了解肺部浸润情况,并给予评分。胸片评分标准[4]:0分,无肺泡浸润;1分,肺泡浸润局限于1个象限;2分,肺泡浸润局限于2个象限;3分,肺泡浸润局限于3个象限;4分,肺泡浸润局限于4个象限。1.6
炎性因子指标检测
分别于治疗前及治疗7天后清晨空
腹各抽取外周静脉血4mL,低温离心留血清,-80℃保存待测。采用放射免疫法测定肿瘤坏死因子α(TNF-α)、白介素-1β(IL-1β)和白介素-10(IL-10)等炎性因子。1.7统计学方法采用SPSS12.0统计学分析软件进行数据
处理,计量资料以(±s)表示,采用t检验。
2结果
2.1
2组治疗前后PIP、Pplat及Raw值比较
见表1。观察
期间治疗组1例,对照组3例发展为ARDS,均无死亡病例。2组治疗前呼吸力学指标比较均无差异性(P>0.05);治疗后治疗组患者PIP、Paw值下降程度较大,与对照组比较,差异均有显著性意义(P<0.05),Pplat值下降更显著,明显优于对照组(P<0.01)。
表12组治疗前后PIP、Pplat及Raw值比较(±s)
组别n
PIP(cmH2O)
Pplat(cmH2O)Raw(cmH2O/L/S)治疗组治疗前2335.42±1.9726.71±2.2618.11±2.81治疗后2221.55±2.08①15.29±1.80②
10.79±0.54①对照组
治疗前2236.49±1.7027.83±2.3518.93±3.48治疗后1923.89±2.13
20.24±1.97
13.86±0.90
与对照组治疗后比较,①P<0.05,②P<0.012.2
2组治疗前后PaO2/FiO2、Cst、Cdyn及胸片评分比较
见表2。2组治疗前氧合指数、肺顺应性及胸片评分比较均无差异性(P>0.05)。治疗后治疗组Cdyn和胸片评分的改善程度优于对照组(P<0.05),而PaO2/FiO2、Cst值的改善程度更加明显,与对照组比较,差异均有非常显著性意义(P<0.01)。表22组治疗前后PaO2/FiO2、Cst、Cdyn及胸片评分比较(±s)
组别nPaO2/FiO2(mmHg)Cst(mL/cmH2O)Cdyn(mL/cmH2O)胸片评分(分)治疗组治疗前23211.56±8.2736.71±12.8231.58±8.772.94±0.87
治疗后22302.10±6.91②52.68±10.13②47.19±10.12①1.25±0.55①
对照组
治疗前22215.99±7.4537.20±12.0932.04±7.853.01±0.61治疗后19
273.24±9.18
44.39±10.87
41.58±11.06
1.87±0.39
与对照组治疗后比较,①P<0.05,②P<0.012.3
2组治疗前后TNF-α、IL-1β及IL-10变化比较
见
表3。2组患者治疗前TNF-α、IL-1β及IL-10等炎性因子比较,差异均无显著性意义(P>0.05)。治疗后治疗组TNF-α、IL-1β水平下降程度优于对照组(P<0.05);而IL-10呈上升改变,且治疗组上升程度较对照组显著(P<0.05)。
表32组治疗前后TNF-α、IL-1β及IL-10变化比较(±s)pg/mL
组别n
TNF-α
IL-1βIL-10治疗组治疗前23520.15±28.70713.20±20.63495.10±34.65治疗后22457.85±29.04①661.50±24.60①547.72±38.14①
对照组
治疗前22514.68±26.51716.09±22.74483.06±30.90治疗后19481.34±23.97
689.32±23.11
520.21±33.26
与对照组治疗后比较,①P<0.053
讨论
ALI的病因及发病机制存在“肠-肝-肺轴”的假说,因而ALI并非单纯意义上的肺部疾病,而是失控的全身炎症反应在肺部的表现,上述发病机制表明胃肠道与肺之间有着内在的联系,这也符合“肺与大肠相表里”的中医学理论。当机体受致病因素打击,外邪入侵,机体正气受损,免疫力下降,肠道屏障功能亦随之下降,肠道菌群入血,内毒素释放,从而引发脓毒血症,即邪毒亢盛,此时以实热亢盛为主要表现,可见发热、大便秘结、腹胀等;若邪气太盛,正气不足以抗邪外出,邪毒壅滞于肺,灼伤气阴,煎熬血液,则见瘀血,血瘀则水停,瘀血、水邪阻滞则肺失宣降,可见肺间质渗出、水肿,肺泡透明膜形成,局灶性肺不张等,此时病以暴喘、结胸、腑实为主,进一步发展则内闭外脱甚至死亡。宣白承气汤出自《温病条辨》,是阳明温病“下之不通”五方之一,专治肺与大肠的同病证。生石膏与大黄合用,兼清肺胃肠腑之热,荡涤肠胃邪实积聚;苦杏仁与瓜蒌皮合用同走肺肠,止咳化痰,润肠降气。全方用药精当,仿麻杏石甘汤和承气汤之意,对于肺热痰壅兼胃肠邪实之候,不失为一张有参考意义的示范方。观察表明,宣白承气汤可通过相关途径抑制炎症反应,使促炎因子(TNF-α、IL-1β)和抑炎因子(IL-10)达到新的平衡,改善、延缓ALI一系列的病理变化进程,对机械通气患者呼吸力学有明显的改善作用。
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ZHANGMin(张敏),QIULing(邱玲),ZHANGJi(张吉)
Abstract:Objective:Toobservethetherapeuticeffectofacupuncturecombinedwithmoxa-boxmoxibustionforHuntfacialparalysis.Methods:Forty-eightqualifiedpatientswereequallyrandomizedintothetreatmentgroupandthecontrolgroup.Thetwogroupsreceivedacupuncture.Additionally,thetreatmentgroupwasgivenmoxa-boxmoxibustionontheauralregionoftheaffectedside.Therapeuticeffectwasevaluatedandthetimeforrelievingpainwascountedaftertreatment.Results:Thedifferencesofcurerateforperipheralfacialparalysisandherpeszosterweresignificantbetweenthetwogroups(P<0.05),indicatingthatthetreatmentgrouphadbettertherapeuticeffect.Theonsettimeforpainreliefwasshorterinthetreatmentgroupthanthatinthecontrolgroup(P<0.01),sodidtheaveragetimeforthepainrelief(P<0.05),indicatingthatthetreatmentgrouphadbetteranalgesiceffect.Conclusion:Acupuncturecombinedwithmoxa-boxmoxibustionexertscertaineffectforthetreatmentofHuntfacialparalysis.
(Originalarticleonpage102)EffectofElectroacupunctureonHippocampalNeurogenesisinEpilepsyRatsLIUJianhua(刘健华),FUWenbin(符文彬),XUZhenhua(徐振华),etal.
Abstract:Objective:Toobservethepossibleeffectofhippocampalneurogenesisonelectroacupuncture(EA)intreatingepilepsyrats.Methods:Epilepsyratsmodelswereinducedwithlithiumchloride-pilocarpine.Thefrequencyofspontaneousrecurrentseizures(SRS)wasobservedafterEAfor1,3and4week(s).Immunohistochemicalas-saywasusedtodetectthenumberofneoformativeneuronswith5-bromo-2-deoxyuri-dine(Brdu)positiveinhippocampaldentategyrus.Results:EarliestSRSoccurredinthesurvivalratsatepilepticstate3daysaftertheonsetofepilepsy.Fromthesecondweek,SRSwasfoundinthemodelgroupandEAgroup.AfterEAfor3and4weeks,thefrequencyofSRSwasreducedinEAgroup(P<0.05comparedwiththemodelgroup).ThenumberofBrdu-positiveneuronswasincreasedinthemodelgrouponeweekand3weeksaftertheonsetofepilepsy(P<0.01comparedwiththeblankgroup),anddecreasedtothelevelofblankgroupfromthefourthweek.OnthefirstweekofEA,thenumberofBrdu-positiveneuronswasdecreased,butthedifferencewasinsignificantascomparedwiththemodelgroup(P>0.05),andthenthedecreasewasobviousonthethirdweek(P<0.05).ThenumberofBrdu-positiveneuronsinEAgrouparrivedtothelevelinthemodelgroupandblankgrouponthefourthweekofEA.Conclusion:EAcaninhibitthehippocampalneurogenesisinthehippocampaldentategyrusofepilepsyrats,indicatingthathippocampalneurogenesisplaysanimportantroleinthetherapeuticeffectofEA.
(Originalarticleonpage117)TherapeuticMechanismofBushenTongluoPrescriptioninRegulatingSubchondralBoneRemodelingandinProtectingArticularCartilage
LIZhao(李钊),LIANGZujian(梁祖建),ZHANGBaidang(张百挡),etal.
Abstract:Objective:ToexplorethetherapeuticmechanismofBushenTongluoPre-scription(TBP)inregulatingsubchondralboneremodelingandinprotectingarticularcar-tilage.Methods:ThirtySPFSDratswererandomizedinto3groups:sham-operationgroup,modelgroupandTBPgroup.TheratmodelsofosteoarthritiswereinducedbymodifiedHulthmethod.Fourweeksaftertheoperation,TBPwasgiventotheratsinTBPgroupbygastricgavage,andtheratsinothertwogroupsweregiventhesamevolumeofnormalsaline.ContentsofproteoglycanandcollagentypeⅡinthearticularcartilageweredetectedwithimmunohistochemicalassay,andthemorphometryofthesubchondralbonewasanalyzedbyapplyingcriteriaestablishedbytheOsteoarthritisResearchSocietyInter-national(OARSI)8,12and16weeksaftertheoperation.Results:OARSIscoreinthesham-operationgroupandTBPgroupdifferedfromthatinthemodelgroup(P<0.05)8,12and16weeksaftertheoperation.ThelossofproteoglycanandcollagentypeⅡ,subchondralboneformationandsclerotinhardeningwereobviousinthemodelgroupcom-paredwiththoseinthesham-operationgroup.Inthemodelgroup,thebonetrabeculaareapercent,trabeculathichness,trabeculanumber,trabeculaseparation,andosteoclastnumberinpermillimeterdifferedfromthoseinthesham-operationgroupandTBPgroup(P<0.01).Thefluorescenceperimeterpercent,mineralizationsedimentationrateandboneformationwerelowerinthemodelgroupthanthoseinthesham-operationgroupandTBPgroup(P<0.01).Conclusion:Subchondralboneplaysanimportantroleinthedevelopmentofosteoarthritis,andTBPcanpreventchondroclasis,andcandelayandrelievechondropathyinosteoarthritispatientsbyregulatingthebiomechanicspropertyofsubchondralbone.
(Originalarticleonpage120)