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.     

犬烧伤休克延迟复苏的实验研究

目的探讨应用林格液进行烧伤休克延迟复苏的效果.方法12只犬随机分为对照组(S组,6只)和治疗组(LR组,6只).LR组采用35%TBSAⅢ度烧伤模型,伤后6h以乳酸林格液进行复苏,并以尿量为1.0ml@kg-1@h-1及心输出量为伤前值的70%～80%来调整输液速度及输入量,观察其在伤后第一个24h复苏中的容量负荷、平均动脉压(MAP)、左心室收缩压(LVSP)、左室内压最大上升/下降速率(±dp/dtmax)、心脏排血指数(CI)、氧供给(DO2)及氧消耗(VO2)等的变化.结果乳酸林格液在烧伤休克延迟复苏后第一个24h的复苏中,每1%烧伤面积的输液量为(887±1.02)ml/kg,比采用Parkland公式复苏多1.2倍,其中在复苏后4h内的输液量为(3.63±0.99)ml/kg,为总入量的41%;MAP、LVSP、±dp/dtmax、CI、DO2及VO2等指标在复苏后2h即达到或接近对照组水平.结论乳酸林格液在烧伤休克延迟复苏中,比早期复苏需要更多的液体量才能满足需求,而血流动力学、心肌功能及氧动力学等在复苏后2h即有明显改善.     

延迟复苏对烧伤休克犬氧代谢的影响

目的探讨在烧伤休克延迟复苏情况下,快速补液对烧伤犬氧代谢的影响。方法建立40%TBSAⅢ度烫伤犬模型,将24只伤犬随机分为对照组、延迟均匀复苏组和延迟快速复苏组,每组8只。观察犬伤前及伤后2、6、8、12、24、36、48h氧供(DO2)、氧耗(VO2)、氧摄取率(O2ext)及血液中碱缺失(BD)和乳酸(LA)含量的变化。结果烧伤后各组犬DO2均显著下降,明显低于伤前值(P<0.01),而O2ext均大幅增加,明显高于伤前值(P<0.01)。伤后8h延迟快速复苏组DO2为(7.35±0.21)L·min-1·m-2,明显高于延迟均匀复苏组(5.32±0.96)L·min-1·m-2(P<0.01);其VO2(2.02±0.58)L·min-1·m-2也明显高于延迟均匀复苏组(1.71±0.38)L·min-1·m-2(P<0.01);但O2ext有所下降,延迟快速复苏组为(27.7±5.9)%,明显低于延迟均匀复苏组(32.2±3.9)%(P<0.01)。烧伤后各组犬BD均大幅降低并明显低于伤前(P<0.01),但复苏后逐渐升高,伤后8h延迟快速复苏组为(-6.5±0.7)mmol/L,显著高于延迟均匀复苏组(-9.3±1.4)mmol/L(P<0.01)。伤后各组犬LA均大幅升高,明显高于伤前(P<0.01),复苏后逐渐降低,伤后8h延迟快速复苏组LA为(2.30±0.20)mmol/L,显著低于延迟均匀复苏组(2.67±0.30)mmol/L(P<0.01)。结论快速补液可以显著改善烧伤犬组织的氧代谢状况,有益于烧伤休克的延迟复苏。     

兔烧伤后应用冬眠药物对肠道细菌易位的影响

烧伤后肠道细菌移位的研究已有很多报导,我们观察了兔烧伤后在液体复苏同时应用具有抑制神经内分泌过度反应的冬眠药物对肠道细菌移位的影响。材料和方法新西兰兔共50只雌雄不拘,体重2.5～3kg。随机分为冬眠药物组和对照组,每组各25只动物。兔背部脱毛在乙醚吸入麻醉下以85℃热水烫20秒造成15%体表面积的Ⅲ度烫伤(经切片证实)。两组动物均于伤后立即腹腔内注入生理盐水按3ml·kg~(-1)·BSA%给予复苏,伤后第2天补液量减半,第3天不输液。冬眠组在给予液体复苏后立即给予冬眠药物(度冷丁100mg、     

卡巴胆碱对烧伤休克犬口服补液时胃肠功能和循环指标的影响

目的：研究拟胆碱药卡巴胆碱对烧伤休克口服补液犬血循环指标和胃肠功能的影响。方法：健康雄性杂种犬24只,采用凝固汽油燃烧法制成30%TBSAⅢ度烧伤模型。随机分为不补液（NR）组、口服葡萄糖-电解质溶液（ORS液）组和口服葡萄糖电解质液＋卡巴胆碱（ORS/CAR）组,分别于伤前和伤后3、6、9、24、48h测定平均动脉压（MAP）、胃黏膜内pH值（pHi）、肠腔内压力（IP）、血浆D-乳酸含量、血浆二胺氧化酶（DAO）活性及24、48 h尿量等指标,同时记录伤后呕吐量。结果：烧伤后ORS组和ORS/CAR组犬MAP及48 h尿量在各时间点差异均无显著性（P均〉0.05）,但均高于NR组（P均〈0.05）;烧伤后NR组胃pHi低于两补液组（P〈0.05）,并且ORS组胃phi低于ORS/CAR组（P〈0.05）;烧伤后各组IP、DAO和D-乳酸均升高,其中ORS组IP和DAO始终高于ORS/CAR组（P〈0.05）;ORS组D-乳酸仅在伤后48h与ORS/CAR组有差异（P〈0.05）。结论：卡巴胆碱能显著改善烧伤休克口服补液时的胃肠功能和循环指标,提高烧伤休克口服液体复苏的疗效。     

烧伤休克延迟补液对肝,肾的影响

烧伤休克延迟补液会对机体造成进一步损伤。作者研究了烧伤大鼠在不补液、立即补液和延迟补液三种复苏条件下的肝、肾损伤情况。结果显示，烧伤早期肝、肾中可产生多量的超氧阴离子并发生脂质过氧化反应，对脏器造成不同程度的损伤，延迟补液组和不补液员伤更为明显。实验提示，立即补液对肝、肾仅有部分保护作用，严重烧伤早期的液体复苏应辅以氧自由基清除剂。     

严重烧伤大鼠早期外周血中性粒细胞CD11b/CD18分子的动态变化

为探讨烧伤后早期外周血中性粒细胞(PMN)膜上 CD11b/CD18分子的动态变化,采用大鼠30%TBSAⅢ度烧伤模型,伤后随机分为立即复苏组和延迟复苏组,于伤前及伤后12小时内的不同时间取血作流式细胞仪分析。结果表明:两组大鼠于伤后30分钟起 PMN CD11b/CD18表达就明显增加;立即复苏组于伤后4小时达到峰值;延迟复苏组在伤后1小时和8小时各有一个峰值,并比立即复苏组增高。认为烧伤后粘附分子 CD11b/CD18的变化可能与炎性介质、细胞因子、血流动力学改变引起的PMN 切应力的变化及缺血再灌注等密切相关。     

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.     

严重烧伤大鼠早期外周血中怀粒细胞CD11b／CD18分子的动态…

为探讨烧伤后早期外周血中性粒细胞（ＰＭＮ）膜上ＣＤ１１ｂ／ＣＤ１８分子的动态变化，采用大鼠３０％ＴＢＳＡⅢ烧伤模型，伤后随机分为立即复苏组和延迟复苏组，于伤前及伤后１２小时内的不同时间取血作流式细胞仪分析。结果表明，两组大鼠于伤后３０分钟起ＰＭＮ ＣＤ１１ｂ／ＣＤ１８表达就明显增加，立即复苏组于伤后４小时达到峰值；延迟复苏组在伤后１小时和８小时各有一个峰值，并比立即复苏组增高。认为烧伤后粘附分子Ｃ     

丙酮酸腹膜透析液对大鼠失血性休克静脉液体复苏后腹腔脏器的保护作用

目的：研究丙酮酸腹腔透析液对大鼠失血性休克静脉液体复苏后腹腔脏器的保护作用。方法：雄性SD大鼠40只,随机分为4组（n=10）。大鼠按全身血容量的45％经股动脉放血制作失血性休克模型。单纯静脉复苏组（VR组）于休克1h后回输失血及2倍失血量的乳酸钠林格液行静脉复苏,其余3组在上述静脉复苏基础上,分别腹腔注射生理盐水（DPR组）、乳酸钠透析液（L组）、丙酮酸钠透析液（P组）20ml行腹腔复苏,时间30min。分别于休克前（O时）及休克后60（静脉复苏前）、180（腹腔复苏后1h）、360rain（腹腔复苏后4h）用PICCO心肺容量监测仪监测大鼠平均动脉压（MAP）;激光多普勒血流仪测定休克后180min和360min肝、肾和小肠黏膜血流量;生化法测定休克前及休克后180、360min血丙氨酸转氨酶（ALT）、二胺氧化酶（DAO）活性和肌酐（cr）水平;干／湿比重法测定休克后180、360min肝、肾、肠各组织含水率。结果：失血性休克后各组MAP骤降至（35±5）mmHg;休克后60min时,各组大鼠MAP无明显差异（P〉0．05）。腹腔复苏后,与VR组比较,L和P组均能显著提高失血性休克大鼠MAP（P〈0．05）,降低血ALT、Cr和DAO水平,减轻肝、肾、肠组织含水率,提高腹腔脏器血流量（P〈0．05或P〈0．01）,在失血后360min时,P组的上述变化较其余复苏组更为显著。结论：丙酮酸腹腔透析液对大鼠失血性休克静脉液体复苏后腹腔脏器具有保护作用。     

烧伤延迟复苏与细胞集落刺激因子

为探讨严重烧伤延迟复苏血清粒细胞集落刺激因子（Ｇ－ＣＳＦ）的变化规律及其与感染发生，发展，预后的关系，采用大鼠３０％ＴＢＳＡⅢ度烧伤模型，动态了观察了大鼠在立即复苏与延迟复苏两种条件下，外周血白细胞数量，血清（Ｇ－ＣＳＦ）和肿瘤坏死因子－α（ＴＮＦ－α）含量，中性粒细胞吞噬功能；采用大鼠３０％ＴＢＳＡⅡ度烧伤延迟复苏合并早期创面感染模型，动态观察应用重组粒细胞－巨噬细胞集落刺激因子（ｒｈＧＭ－ＣＳ     

A pilot study on early versus delayed hypertonic saline dextran resuscitation in a porcine model of near-lethal liver injury: early hemodynamic response and short-term survival

BACKGROUND: We studied the effects of early versus delayed fluid resuscitation on hemodynamic response and short-term survival in a porcine model of severe hepatic injury associated with hemorrhagic shock. MATERIALS AND METHODS: Eighteen anesthetized swine were randomized after standardized liver injury into two groups: early resuscitation (ER, n = 9) and delayed resuscitation (DR, n = 9). The ER and DR groups were resuscitated with hypertonic saline dextran (HSD) 20 min and 40 min after the injury, respectively. Mean arterial pressure (MAP), cardiac output (CO), and arterial blood gases were measured in addition to vascular blood flow rates in the aorta, hepatic artery and portal vein. The duration of follow-up was 100 min. RESULTS: MAP decreased from 112 +/- 4 to 23 +/- 2 mmHg (P < 0.05) during 20 min after the injury. Bolus infusion of HSD significantly elevated MAP, CO, and flow rates in the aorta, portal vein and common hepatic artery in both groups. Portal vein flow remained relatively high during the shock. Intra-abdominal bleeding (ER, 701 +/- 42 mL; DR 757 +/- 78 mL) and the mortality rate (ER 44%; DR 33%) did not differ between the groups 100 min after injury (P > 0.05). Aortic flow, portal vein flow, common hepatic artery flow, MAP, CO, PaO(2), PaCO(2), base deficit, pH, hemoglobin measurements, and the volume of blood shed into the intraperitoneal cavity did not affect survival in the Cox regression analysis. CONCLUSIONS: Early versus delayed fluid infusion with HSD resulted in a comparable hemodynamic response and survival 100 min after injury. No rebleeding was observed.     

延迟快速复苏对烧伤休克循环影响的临床研究

目的探讨在烧伤延迟复苏情况下,如何迅速纠正休克.方法通过对20例烧伤面积大于40%TBSA、因延迟复苏导致休克的患者,进行延迟快速复苏.观察休克期液体出入量、动咏压(BP)、肺动脉压(PAP)、肺动脉楔状压(PAWP)、中心静脉压(CVP)、心输出量(CO)、肺血管阻力(PVR)、外周血管阻力(SVR)、氧供应(DO2)、氧消耗(VO2)、氧摄取率(O2ext)、乳酸(LA)及碱缺失(BD)等血流动力学和氧代谢指标的变化.结果快速补液后2h内输入液体占“第一个24h公式计算量”的(38.8±6.1)%,如果加上院外补液量则占“第一个24h公式计算量”的(48.3±5.0)%.第一个24h实际补入量占“第一个24h公式计算量”的(131.4±14.3)%;第二个24h实际补入量占“第二个24h公式计算量”的(103.2±7.2)%.快速补液后,尿量大幅增加,CO显著升高,DO2增强,SVR、LA、BD大幅下降,PVR虽大幅升高,但PAWP、PAP和CVP并未超过正常.结论在严密血流动力学监护下,烧伤后延迟复苏初期加快补液速度是可行且有益的,烧伤休克的延迟复苏需要显著增加补液量.指导休克延迟快速复苏应以监护心输出量及PAP、PAWP、CVP等血流动力学指标为主,辅以血中LA、BD水平及尿量变化等临床指标的监测.     

Pentoxifylline restores intestinal microvascular blood flow during resuscitated hemorrhagic shock

We studied the intestinal microvascular blood flow responses to hemorrhage and resuscitation with pentoxifylline by in vivo video microscopy. Male Sprague-Dawley rats were hemorrhaged to 50% of baseline mean arterial pressure for 45 minutes and then blindly randomized to receive pentoxifylline (25 mg/kg bolus + 0.2 mg/kg/minute) or an equivalent volume of saline plus return of shed blood and an additional bled volume of Ringer's lactate solution. Hemorrhage caused intestinal microvascular blood flow to decrease to 10% to 15% of baseline values. In the control group, resuscitation restored cardiac output and mean arterial pressure to baseline values, but intestinal microvascular blood flow remained at 30% of baseline values. In contrast, addition of pentoxifylline to the resuscitation regimen resulted in an immediate hyperemic response with an increase in intestinal microvascular blood flow to significantly greater than baseline values followed by return to baseline. Arteriolar dilation was not responsible for the improvement in flow implicating improved flow dynamics between erythrocytes, granulocytes, and vascular endothelia within the microcirculation. We conclude that addition of pentoxifylline to resuscitation from hemorrhagic shock restores intestinal microvascular blood flow.     

The role of oxygen-free radical in the apoptosis of enterocytes in scalded rats after delayed resuscitation

BACKGROUND: This study aimed to evaluate the relation between apoptosis of enterocytes and oxygen-free radical injury in scalded rats with delayed resuscitation as well as the role of antioxidants in the prevention of enterocyte apoptosis. METHODS: For this study, 150 male Wistar rats were divided randomly into four groups representing early resuscitation (ER), delayed resuscitation (DR), N-acetylcysteine (NAC) treatment, and allopurinol (Allo) treatment. The animals were subjected to a 30% total body surface area, full-thickness scald. Fluid therapy was started 6 hours after the injury in the DR and treatment groups. Apoptosis of enterocytes was identified by DNA fragmentation (ap%), DNA agarose gel electrophoresis, and terminal deoxynucleotidyl transferace (TdT)-mediated dUPT-biotin nick end labeling (TUNEL). The contents of malondialdehyde (MDA), total sulfhydryl (TSH), and nonprotein sulfhydryl (NPSH) and the activity of xanthine oxidase in intestinal mucosa were determined after the burn in the four groups. RESULTS: Apoptosis of enterocytes increased significantly in all the groups. The animals in the DR group showed an earlier and greater increase in ap% than the animals in the ER group. Similar results were seen for electrophoresis, TUNEL assay, and levels of MDA, xanthine oxidase (XO), TSH, and NPSH. Treatment with NAC was associated with a decrease in ap% and MDA, but not XO, as compared with the levels in the DR group, whereas treatment with Allo was associated with a decrease in MDA and XO, but not ap%. Delayed resuscitation was associated with significant decreases in TSH and NPSH, as compared with the levels in the ER group, whereas both the NAC and Allo groups had significantly higher levels of TSH and NPSH than the DR group. CONCLUSIONS: Significant apoptosis of enterocytes was induced by oxidative stress in the intestinal mucosa after a burn in rats. The findings show that NAC blunted intestinal apoptosis induced by oxygen-free radical, which was generated in the process of ischemia-reperfusion injury after a burn because of delayed resuscitation.     

Effects of two fluid resuscitations on the bacterial translocation and inflammatory response of small intestine in rats with hemorrhagic shock

Objective： To investigate the effects of two fluid resuscitations on the bacterial translocation and the inflammatory factors of small intestine in rats with hemorrhagic shock. Methods： Fifty SD healthy male rats were randomly divided into 5 groups （ n = 10 per group） ： Group A （ Sham group）, Group B （ Ringer＇ s solution for 1 h ）, Group C （Ringer＇ s solution for 24 h ）, Group D （ hydroxyethyl starch for 1 h ） and Group E （（ hydroxyethyl starch for 24 h）. A model of rats with hemorrhagic shock was established. The bacterial translocation in liver, content of tumor necrosis factor-α （TNF-α） and changes of myeloperoxidase enzyme （MPO） activities in small intestine were pathologically investigated after these two fluid resuscitations, respectively. Results ： The bacterial translocation and the expression of TNF-α in the small intestine were detected at 1 h and 24 h after fluid resuscitation. There were significant increase in the number of translocated bacteria, TNF-α and MPO activities in Group C compared with Group B, significant decrease in Group E compared with Group D and in Group B compared with Group D. The number of translocated bacteria and TNF-α expression significantly decreased in Group E as compared with Group C. Conclusions： The bacterial translocation and the expression of TNF-α in the small intestine exist 24 h after fluid resuscitation. 6 % hydroxyethyl starch can improve the intestinal mucosa barrier function better than the Ringer＇ s solution.     

延迟复苏对烫伤大鼠肠道淋巴细胞凋亡率的影响

目的：探讨延迟复苏对烫伤大鼠小肠Peyer氏结淋巴细胞（PPL）、固有层淋巴细胞（LPL）和上皮内淋巴细胞（IEL）凋亡率的影响。方法：Wistar大鼠30只,分为假伤对照组、立即复苏组（ER）和延迟复苏组（DR）。建立30%体表面积Ⅲ度烫伤合并延迟复苏模型。按Davies法分离、收集上述3种淋巴细胞,采用DNA片段百分率（ap%）反映其伤后细胞凋亡百分率变化。采用DNA凝胶电泳、TUNEL法和电镜观察3种淋巴细胞凋亡特征性改变。结果：两组PPL、LPL、IEL伤后ap%均显著高于伤前（P〈0.01）;伤后6h、12h,DR组PPLap%显著高于ER组（P〈0.05或P〈0.01）,其中LPL伤后12hap%高达56.26%。伤后12hDR组LPL、IELap%显著高于ER组（P〈0.01）。伤后6hLPL、IEL基因组DNA电泳均可见凋亡特征性梯形条带;伤后12hTUNEL法和电镜均观察到3种淋巴细胞典型的凋亡形态学改变。结论：烫伤延迟复苏后细胞凋亡是肠道淋巴细胞数量急剧减少的主要原因;可能是烫伤后肠道免疫功能抑制的重要机制之一。     

快速输液对烫伤后延迟复苏休克犬循环的影响

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The effect of hypertonic saline resuscitation on bacterial translocation after hemorrhagic shock in rats

Translocation of enteric bacteria occurs in rats after hemorrhagic shock. A proposed mechanism involves intestinal mucosal injury by hypoperfusion. Recent work suggests that moderate hypovolemia causes gut arteriolar constriction, which is ameliorated by hypertonic saline resuscitation. Bacterial translocation should, therefore, be reduced when hypertonic saline (HS) is used as the resuscitative fluid. Seventy-eight Sprague-Dawley rats were anesthetized and subjected to 30 minutes of hemorrhagic shock (systolic blood pressure 30 to 50 mm Hg) through a modified Wigger's model. Resuscitation was performed with either shed blood (B), 3% HS + 1/2B (1:1), or with 7.5% HS + 1/2B (1:1). Spleen, liver, and mesenteric lymph nodes were sent for quantitative culture 24 hours later. Translocation occurred if enteric organisms were cultured from at least one organ. Statistical analysis used the Fisher exact test. Compared to autotransfusion, hemodilutional resuscitation from hemorrhagic shock with hypertonic saline resulted in a significant reduction in bacterial translocation (p values were 0.03 and 0.04 for 3% and 7.5% hypertonic saline, respectively). The reduction in translocation after hypertonic saline resuscitation may be the consequence of microcirculatory alterations preventing gut hypoperfusion.