液体复苏加山莨菪碱对烧伤兔心肌功能的影响

目的探讨山莨菪碱对烧伤兔心肌功能的影响。方法采用新西兰兔２５％Ⅲ度烫伤模型，分别于伤前，伤后即刻，１，３，５，７小时测定左心室内压峰值、左心室内压最大变化速率，并观察严重烧伤休克期液体复苏加山莨菪碱对上述指标的影响。结果严重烧伤后早期即发生心肌的收缩功能和舒张功能障碍，并呈进行性减退。单纯给予山莨菪碱或单纯输液治疗对兔严重烧伤后的心功能在短期内有支持作用，但治疗效果欠佳，且单纯山莨菪碱治疗组心功能下降早于单纯补液组。而在给予山莨菪碱同时进行液体复苏，可使心肌收缩性和舒张性在伤后７小时维持在同时相点的假烫组同一水平。结论提示在液体复苏的同时应用山莨菪碱可改善心肌功能，并有利于休克的恢复。     

液体复苏加山莨菪碱对烧伤兔心肌功能的影响

目的探讨山莨菪碱对烧伤兔心肌功能的影响。方法采用新西兰兔25％Ⅲ度烫伤模型,分别于伤前,伤后即刻,1,3,5,7小时测定左心室内压峰值、左心室内压最大变化速率,并观察严重烧伤休克期液体复苏加山莨菪碱对上述指标的影响。结果严重烧伤后早期即发生心肌的收缩功能和舒张功能障碍,并呈进行性减退。单纯给予山莨菪碱或单纯输液治疗对兔严重烧伤后的心功能在短期内有支持作用,但治疗效果欠佳,且单纯山莨菪碱治疗组心功能下降早于单纯补液组。而在给予山莨菪碱同时进行液体复苏。可使心肌收缩性和舒张性在伤后7小时维持在同时相点的假烫组同一水平。结论提示在液体复苏的同时应用山茛菪碱可改善心肌功能,并有利于休克的恢复。     

液体复苏加1－6－FDP对严重烧伤家兔心肌功能变化的研究

采用家兔２５％Ⅲ度烫伤模型，分别于伤前、伤后即刻、伤后１、３、５、７ｂ测定左心室内压峰值、左心室内压最大变化速率及血浆容量（不测伤后即刻值），并观察了液体复苏加１－６－ＦＤＰ对严重烧伤休克期家兔ＬＶＳＰ、ＬＶ±ｄｐ／ｄｔｍａｘ的影响，结果表明严重烧伤后心肌的收缩性和舒张性均立即受到抑制，并呈进行性减退，单纯的液体复苏并不能明显改善心肌的收缩性和舒张性；单用１－６－ＦＤＰ治疗可在伤后一定时间内对心功能有支持作用；而在液体复苏同时给予１－６－ＦＤＰ可使心肌的收缩性和舒张性得到明显改善，其与烧伤未治疗组和液体复苏组比较差异有非常显著性意义，提示在液体复苏的同时，应用１－６－ＦＤＰ，可改善心肌功能，有利于休克的复苏。     

液体复苏加1-6-FDP对严重烧伤家兔心肌功能变化的研究

采用家兔25％Ⅲ度烫伤模型,分别于伤前、伤后即刻、伤后1、3、5、7 h 测定左心室内压峰值、左心室内压最大变化速率及血浆容量(不测伤后即刻值),并观察了液体复苏加1-6-FDP 对严重烧伤休克期家兔 LVSP、LV±dp/dt max 的影响,结果表明严重烧伤后心肌的收缩性和舒张性均立即受到抑制,并呈进行性减退,单纯的液体复苏并不能明显改善心肌的收缩性和舒张性;单用1-6-FDP 治疗可在伤后一定时间内对心功能有支持作用;而在液体复苏同时给予1-6-FDP 可使心肌的收缩性和舒张性得到明显改善,其与烧伤未治疗组和液体复苏组比较差异有非常显著性意义,提示在液体复苏的同时.应用1-6-FDP,可改善心肌功能,有利于休克的复苏。     

伤后立即切痂对30% Ⅲ度烧伤大鼠心肌力学的影响

目的研究伤后立即切痂对大鼠心肌力学特别是左心室舒缩功能的影响。方法采用大鼠３０％ＴＢＳＡⅢ度烧伤模型，随机分为烧伤组、烧伤补液组和切痂组。切痂组伤后按Ｐａｒｋｌａｎｄ公式补液并立即切痂植以正常大鼠皮肤。颈动脉插管至左心室测量心肌力学参数。结果烧伤组心肌力学参数下降非常显著，烧伤补液组各点参数大多降低，但明显高于烧伤组，除左心室舒张末压（ＬＶＥＤＰ）外，切痂组心肌力学参数与烧伤补液组相近。伤后２４小时烧伤补液组心肌收缩功能显著低于切痂组。结论在有效复苏下，３０％Ⅲ度烧伤大鼠伤后立即实施切痂是可行且有益的     

伤后立即切痂对30%Ⅲ度烧伤大鼠心肌力学的影响

目的 研究伤后立即切痂对大鼠心肌力学特别是左心室舒缩功能的影响。方法 采用大鼠３０％ＴＢＳＡⅢ度烧伤模型，随机分为烧伤组、烧伤补液组和切痂组。切痂组伤后按Ｐａｒｋａｎｄ公式补液并立即切痂植以正常大鼠皮肤。颈动脉插管至左心室测量心肌力学参数。结果 烧伤组心肌力学参数下降非常显著，烧伤补液组各点参数大多降低，但明显高于烧伤组，除左心室舒张末压（ＬＶＥＤＰ）外，切痂组心肌力学参数与烧伤被液组相近。伤后２     

伤后立即切痂对30%Ⅲ度烧伤大鼠心肌力学的影响

目的研究伤后立即切痂对大鼠心肌力学特别是左心室舒缩功能的影响。方法采用大鼠30％TBSAⅢ度烧伤模型,随机分为烧伤组、烧伤补液组和切痂组。切痂组伤后按 Parkland 公式补液并立即切痂植以正常大鼠皮肤。颈动脉插管至左心室测量心肌力学参数。结果烧伤组心肌力学参数下降非常显著,烧伤补液组各点参数大多降低,但明显高于烧伤组,除左心室舒张末压(LVEDP)外,切痂组心肌力学参数与烧伤补液组相近。伤后24小时烧伤补液组心肌收缩功能显著低于切痂组。结论在有效复苏下,30％Ⅲ度烧伤大鼠伤后立即实施切痂是可行且有益的。     

严重烧伤早期心肌收缩性与钙转运功能变化

目的研究烧伤早期心肌肌浆网（ＳＲ）钙转运功能变化，探讨其在烧伤后心肌收缩功能下降发病中的作用。方法采用３０％ＴＢＳＡⅢ度烧伤大鼠模型，离体心脏灌流，测定伤前及伤后心肌室内压最大变化速率（±ｄｐ／ｄｔｍａｘ）变化，制备心肌肌浆网，应用微孔滤膜过滤技术测定心肌ＳＲ４５Ｃａ２＋转运功能改变。结果与对照组相比，烧伤组左心室±ｄｐ／ｄｔｍａｘ明显降低（Ｐ＜０．０１），心肌ＳＲＣａ２＋－ＡＴＰａｓｅ活性及ＳＲ４５Ｃａ２＋摄取初速度、摄取容量均明显降低（Ｐ＜０．０１），偶联率比对照值大幅度下降。结论烧伤后早期心肌肌浆网Ｃａ２＋转运功能严重障碍，其是烧伤后心肌收缩功能降低的重要因素之一。     

严重烧伤早期心肌收缩性与钙转运功能变化

目的研究烧伤早期心肌肌浆网(SR)钙转运功能变化,探讨其在烧伤后心肌收缩功能下降发病中的作用。方法采用30％TBSAⅢ度烧伤大鼠模型,离体心脏灌流,测定伤前及伤后心肌室内压最大变化速率(±dp/dtmax)变化,制备心肌肌浆网,应用微孔滤膜过滤技术测定心肌SR~(45)Ca~(2 )转运功能改变。结果与对照组相比,烧伤组左心室±dp/dtmax明显降低(P<0.01),心肌SRCa~(2 )-ATPase活性及SR~(45)Ca~(2 )摄取初速度、摄取容量均明显降低(P<0.01),偶联率比对照值大幅度下降。结论烧伤后早期心肌肌浆网Ca(2 )转运功能严重障碍,其是烧伤后心肌收缩功能降低的重要因素之一。     

烧伤休克时心脏对复苏治疗反应的差异

烧伤能损害高龄豚鼠心肌收缩功能。作者应用离体的幼年和老年豚鼠灌流心脏测定了左心室压(LVP)、最高左心室压(+dP/dt max)及最低左心室压(-dP/dtmax)等参数,证明老年豚鼠心脏的LVP、+dP/dt max及-dP/dt max均明显低于对照组。同时证明高龄豚鼠左心收缩功能不全不能被增加心率、细胞外钙浓度和心肌纤维长度以及补液复苏治疗所纠正。作者认为:严重烧伤使高龄鼠原已受损的心脏功能进一步降低,并影响了烧伤休克及液体复苏治疗的效果。     

Effect of aspiration pneumonia-induced sepsis on post-burn cardiac inflammation and function in mice

INTRODUCTION: Numerous studies have found that burn injury alters immune function, predisposing the subject to infectious complications. We developed a mouse model of burn injury complicated by either gram-positive or gram-negative infection and hypothesized that post-burn infection would exacerbate the myocardial cytokine responses and contractile dysfunction characteristic of either sepsis alone or burn alone. METHODS: Adult C57 BL6 mice were given burn injury over 40% of the total body surface area and conventional fluid resuscitation (lactated Ringer's solution, 4 mL/kg/% burn) followed on day 7 by intratracheal administration of 1 x 10(5) cfu of either Streptococcus pneumoniae or Klebsiella pneumoniae or saline. Mice received fluid resuscitation (2 mL of lactated Ringer's intraperitoneally) again after bacterial challenge. Cardiomyocyte cytokine secretion and the contractile function of isolated hearts (Langendorff perfusion) were examined in vitro 24 h after bacterial challenge. RESULTS: Infectious challenge seven days after burn injury exaggerated the inflammatory cytokine responses over those observed with either burn alone or gram-positive or gram-negative infection alone (tumor necrosis factor-alpha: sham, 72 +/- 9 pg/mL; burn alone, 176 +/- 6 pg/mL, Klebsiella pneumoniae alone, 337 +/- 8 pg/mL; Streptococcus pneumoniae alone, 184 +/- 2 pg/mL; burn + Klebsiella, 476 +/- 14 pg/mL; burn + Streptococcus, 351 +/- 6 pg/mL). Myocardial contractile depression was evident in the burn alone, infection alone, and burn plus infection groups, regardless of the organism selected to produce pneumonia-related sepsis. CONCLUSIONS: Gram-negative or gram-positive infection exacerbated the myocardial inflammation seen with burn alone or infection alone. The availability of a mouse model of burn injury complicated by pneumonia-related sepsis will allow use of genetically engineered mice to examine further the mechanisms by which burn injury increases susceptibility to infection.     

高张氯化钠右旋糖酐液在犬烧伤休克延迟复苏中的作用

目的 从血流动力学、心肌力学及代谢等方面探讨高张氯化钠右旋糖酐液（７．５％氯化钠＋６％右旋糖酐７０，ＨＳＤ）在烧伤休克延迟复苏中的作用。方法 采用犬３５％ＴＢＳＡⅢ度烧伤模型，伤后６ｈ分别用乳酸林格液及ＨＳＤ进行复苏，并以每ｈ尿量为１．０ｍｌ／ｋｇ及心输出量为伤前值的７０％￣８０％来调整输液速度瘃输液量，观察ＨＳＤ在复苏中容量负荷、左心室等容收缩期最大压力变化速度及左心室舒张期压力下降最大变化速度     

烧伤休克期有关补液公式的临床应用与评价

目的 评价第三军医大学烧伤休克期补液公式(简称三医大公式)在大面积烧伤患者休克防治中的应用.方法 选择2005-2007年笔者单位收治的热力烧伤患者(烧伤总面积大于或等于30%TBSA、伤后8 h内入院且无特殊疾患)共71例,分为成人组(46例)、小儿组(25例).患者入院后即按照三医大公式进行液体复苏治疗,同时监测尿量、心率、血压等指标,根据患者实际情况随时调整补液速度.记录并统计2组患者补液量、实际补液系数、尿量. 结果 71例患者均平稳度过休克期,未发生明显的因液体复苏引起的相关并发症.成人组伤后第1、2个24 h及小儿组伤后第2个24 h的实际补液量超过各自计划补液量的16%～38%.成人组第1、2个24 h的实际补液系数大于公式所要求的补液系数.2组患者第1个24 h尿量为1.1～1.2 mL·kg-1·h-1左右;第2个24 h成人组为(1.2±0.4)mL·kg-1·h-1,小儿组为(1.7±0.5)mL·kg-1·h-1. 结论 三医大公式是大面积烧伤患者休克期治疗的较好选择,在应用此公式时须强调进行个性化液体复苏治疗.     

p38丝裂原活化蛋白激酶信号转导通路在严重烧伤大鼠枯否细胞肿瘤坏死因子α和白细胞介素1β产生中的作用

目的 探讨p38丝裂原活化蛋白激酶(MAPK)信号转导通路在严重烧伤大鼠枯否细胞(KCs)促炎性细胞因子肿瘤坏死因子α(TNF-α)和白细胞介素1β(IL-1β)产生中的作用。方法 健康成年的雄性SD大鼠32只,随机分为：假烫组;假烫 SB203580组;烧伤对照组;烧伤 SB203580组,每组8只。假烫或烧伤24h后分离出肝脏KCs,培养18h后加入50ng／ml的LPS进行刺激,18h后取上清液,用酶联免疫吸附法(ELISA)测定TNF-α和IL-1β的含量,并收集KCs,实时逆转录聚合酶链反应检测KCs内TNF-α和IL-1β mRNA表达的改变,蛋白印迹(Western blot)法检测KCs中p38MAPK和JNK活性的变化。结果 烧伤大鼠分离出的KCs培养上清液中TNF-α和IL-1β含量、KCs中TNF-α和IL-1β mRNA的表达均较假烫组的明显增强,同时KCs中p38 MAPK活性和JNK活性升高,SB203580能显著抑制大鼠KCs上清液中TNF-α和IL-1β含量、KCs中TNF-α和IL-1β mRNA的表达和p38MAPK活性的升高,对JNK活性无影响。结论p38MAPK信号转导通路介导了严重烧伤大鼠KCs促炎性细胞因子TNF-α和IL-1β的产生。     

p38 mitogen-activated protein kinase inhibition attenuates burn-induced liver injury in rats

This study was made to evaluate the effect of SB203580, a specific p38 MAP kinase inhibitor, on burn-induced hepatic injury as well as the activation of nuclear factor (NF)-kappaB in severely burned rats. Sprague-Dawley rats were divided into three groups: (1) sham group, rats underwent sham burn; (2) burn group, rats given third-degree burns over 30% total body surface area (TBSA) and treated with vehicle plus lactated Ringer solution for resuscitation 4 ml/(kg% TBSA); and (3) burn plus SB203580 group, rats given burn injury and fluid resuscitation plus SB203580 (10 mg/kg i.v., 15 min and 12 h after burn). Hepatocellular injury (measured by serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT)) and hepatocellular function (determined by the indocyanine green dye retention rate (ICG R15)) were assessed at 24 h post-burn. Liver histologic changes were also analyzed. Burn trauma resulted in increased serum aminotransferases concentrations, decreased ICG R15, elevated serum tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta levels and hepatic TNF-alpha and IL-1beta mRNA expressions, and worsen histologic condition. The level of Nuclear Factor (kappa) inhibitor (IkappaBalpha) in liver was decreased and DNA-binding activity of Nuclear Factor-kappaB (NF-kappaB) was increased after thermal injury. p38 MAP kinase was more significantly activated in liver harvested from burn rats than from shams. SB203580 inhibited the activation of p38 MAP kinase, reduced the levels of TNF-alpha and IL-1beta, and prevented burn-mediated liver injury. Both the IkappaBalpha level and NF-kappaB activity in the liver following burns was not affected by administration with SB203580. These findings suggest that (1) p38 MAP kinase activation is one important aspect of the signaling event that may mediate the release of TNF-alpha and IL-1beta and contributes to burn-induced liver injury and (2) p38 MAP kinase does not influence the activation of NF-kappaB directly in the liver of severely burned rats.     

Role of p38 mitogen-activated protein kinase in Kupffer cell secretion of the proinflammatory cytokines after burn trauma

This study was designed to investigate the role of p38 mitogen-activated protein (MAP) kinase on Kupffer cells (KCs) secretion of proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta and hepatic injury following burn trauma. Sprague-Dawley rats were randomized into four groups: (1) sham burn rats given vehicle, (2) sham burn rats given the p38 MAP kinase inhibitor SB203580 (10mg/kg i.v., 15min and 12h after sham burn), (3) rats given a 30% total body surface area (TBSA) full-thickness burn and fluid resuscitation plus vehicle, and (4) burn rats given injury and fluid resuscitation plus SB203580. Rats from each group were killed at 24h post-burn to examine plasma aspartate transaminase (AST) and alanine transaminase (ALT) and KCs were isolated. The KCs secretion of TNF-alpha and IL-1beta and p38 MAP kinase activity (by Western blot analysis) were also examined. These studies showed by more significant activation of p38 MAP kinase in KCs harvested from burn rats than from shams. Burn trauma resulted in hepatic dysfunction and promoted KCs secretion of TNF-alpha and IL-1beta. SB203580 inhibited p38 MAP kinase activity, reduced KCs secretion of proinflammatory cytokines, and alleviated burn-mediated hepatic dysfunction. These data suggest p38 MAP kinase activation is one important aspect of the signaling event that may mediate the KCs secretion of proinflammatory cytokines TNF-alpha and IL-1beta following burn trauma.     

早期口服补液对犬50%总体表面积烧伤休克期血流动力学和组织灌流的影响

目的 研究早期口服补液对犬50%总体表面积(TBSA)烧伤休克期血流动力学和组织灌流的影响.方法 成年雄性Beagle犬18只,先期无菌手术行颈总动脉、颈外静脉、胃、空肠及膀胱置管,24 h后用凝固汽油燃烧法造成其颈、背和胸、腹部约50%TBSA Ⅲ.烧伤.随机分为不补液(NR)、口服补液(OR)和静脉补液(IR)三组,每组6只.伤后第1个24 h NR组无治疗,OR和IR组于伤后30 min开始按Parkland公式分别从胃管和静脉输注葡萄糖.电解质溶液,伤后24 h起各组犬均实施静脉补液.测定犬伤前(0 h)和伤后2、4、8、24、48和72 h非麻醉状态下的平均动脉压(MAP)、全身血管阻力(SVR)、心输出量(CO)、左室内压最大变化速率(dp/dtmax)、尿量以及胃黏膜CO2分压(PgCO2)和小肠黏膜血流量(IMBF),并记录伤后72 h死亡率.结果 与伤前相比,各组犬MAP、CO、dp/dtmax,、IMBF和尿量在伤后2 h均大幅降低(P<0.01),而SVR和PgCO2显著升高.两补液组上述指标伤后8 h开始恢复,72 h IR组除IMBF外均恢复至伤前水平,但OR组CO、SVR及胃肠组织灌流指标仍差于伤前水平(P<0.01).NR组上述指标持续恶化,伤后24 h内无尿并全部死亡.OR组血液动力学和内脏组织灌流指标显著优于NR组,但差于IR组.伤后72 h死亡率NR组为6/6、OR组3/6,而IR组为0/6.结论 50%TBSA烧伤后早期口服葡萄糖-电解质溶液复苏效果虽差于静脉补液,但相比不补液,能显著改善血流动力学指标和内脏组织灌流,减少早期死亡,有潜力成为战争或灾害时静脉液体复苏的替代方法.     

口服补液复苏对严重烧伤家兔心肌力学指标的改善作用

目的 了解口服补液复苏对严重烧伤家兔心脏功能的保护作用. 方法 150只家兔随机分为正常对照组(6只)、烧伤组(42只)、立即补液组(42只)、延迟补液组(30只)和延迟快速补液组(30只).正常对照组不致伤不补液.其余4组家兔均造成40%TBSAⅢ度烧伤,烧伤组不补液,余下3组伤后用灌胃的方式进行口服补液复苏.经家兔颈动脉左心室内置管,测量正常对照组及4组致伤家兔伤后2、6、8、12、24、36、48 h的平均动脉压(MAP)、左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)以及左心室压力最大上升/下降速率(LV±dp/dt max),另检测休克期尿量. 结果烧伤组家兔LVSP、LV±dp/dt max较正常对照组显著下降.立即补液组和延迟快速补液组上述指标在伤后24 h内高于烧伤组,其中立即补液组LV+dp/dt max在伤后8 h达峰值[(892±116)kPa/s,1 kPa=7.5 mm Hg],LV-dp/dt max在伤后6 h达峰值[(724±149)kPa/s];伤后8 h,延迟快速补液组LV±dp/dt max均达峰值.延迟补液组伤后各时相点LVSP、LV±dp/dt max与烧伤组接近.各组家兔MAP、伤后第1个24 h尿量的比较情况大致与以上指标相似.烧伤组与其余4组比较,各时相点LVEDP差异无统计学意义(P>0.05). 结论严重烧伤家兔伤后24 h内给予有效的口服补液,可改善心肌力学指标;延迟复苏的家兔按照延迟复苏补液公式预估补液量,才能进行有效复苏.     

Flüssigkeitstherapie und hämodynamisches Monitoring im Verbrennungsschock

Successful surgical and intensive care treatment of severely burned patients requires adequate prehospital management and fluid resuscitation adjusted to individual needs of the patient. Burn shock fluid resuscitation is now predominantly performed utilizing crystalloid solutions. Whenever possible, colloid solutions should not be given in the first 24 h after burn injury. The rate of administration of resuscitation fluids should maintain urine outputs between 0.5 ml/kg per h and 1 ml/kg per h and mean arterial pressures of >70 mmHg. Extended hemodynamic monitoring can provide valuable additional information, if burn resuscitation is not proceeding as planned or volume therapy guided by these typical vital signs is not attaining the desired effect. We recommend this in patients with TBSA burns of >30%. Inhalation injuries, pre-existing cardiopulmonary diseases, or TBSA burns of >50% definitely require extended hemodynamic monitoring during burn shock resuscitation. The Swan-Ganz catheter or less invasive transcardiopulmonary indicator dilution methods can be utilized to assess hemodynamic data.     

Ligustrazine attenuates acute myocardium injury after thermal trauma

This study was designed to investigate the effects of ligustrazine on burn-induced myocardiac injury as well as TNF-alpha levels in severely burned rats. Sprague-Dawley rats were divided into four groups: (1) sham group, rats who underwent sham burn; (2) fluid-resuscitated sham group (FRsham), rats who underwent sham burn, and lactated Ringer's solution for resuscitation; (3) control group, rats given third-degree burns over 30% total body surface area (TBSA) and lactated Ringer's solution for resuscitation; (4) ligustrazine group, rats given burn and lactated Ringer's solution with ligustrazine inside for resuscitation. Myocardial injury was assessed at 6h after burn by detecting serum levels of creatine kinase MB fraction (CK-MB) and lactate dehydrogenase (LDH), as well as water content, histological score, and ultrastructure change of cardiac tissue. In addition, myocardium ATP content was analyzed. Enzyme-linked immunosorbent assay (ELISA) was used to examine cardiac tumor necrosis factor-alpha (TNF-alpha) levels. The results showed that burn trauma resulted in the increasing serum LDH and CK-MB, elevated myocardial water content, aggravated myocardial histological and ultrastructural lesions, increased myocardium ATP, and serum TNF-alpha. Ligustrazine 10mg/kg iv markedly inhibited increases in serum CK-MB and LDH, reduced myocardial water content from 76.91+/-0.19% in control group to 75.40+/-0.57%, significantly decreased the histologic scores of myocardium, and mollified the ultrastructural damage in cardiac myocytes. Ligustrazine significantly attenuated elevations in serum TNF-alpha level and myocardial ATP quantity. Therefore, our results demonstrate that ligustrazine exhibits significant protective effects on burn-induced myocardial injury via inhibiting the release of TNF-alpha and improving utilization of ATP.