静脉复苏辅助腹腔注射高渗液对感染性休克大鼠的治疗效果

目的 探讨静脉复苏辅助腹腔注射高渗液对感染性休克大鼠的治疗作用.方法 感染性休克模型SD雄性大鼠36只,随机均分为三组,分别行单纯静脉复苏(A组)、静脉复苏辅助腹腔注射生理盐水(B组)和腹腔注射高渗液(C组).静脉复苏采用复方乳酸钠25 ml/kg快速静脉输注30 min,随后B组腹腔注入生理盐水100 ml/kg,C组腹腔注入等量2.5％葡萄糖低钙腹膜透析液.观测大鼠血流动力学变化,测定复苏前后TNF-α与IL-6的含量及复苏后2h动脉血气.复苏后20 h观察大鼠存活情况并解削观察其内脏改变.结果 静脉复苏结束至复苏后2h,C组MAP无明显变化,A、B组MAP逐渐下降,复苏后2hC组MAP显著高于A、B组(P＜0.05).复苏后2h,C组pH、HCO-3、BE、BEcef值明显高于A、B组,乳酸浓度明显低于A、B组(P＜0.05或P＜0.01).复苏前0.5h、复苏后1、2h三组血清TNF-α和IL-6含量均明显高于基础值(P＜0.01).复苏后1、2hC组血清TNF-α、IL-6含量明显低于A、B组(P＜0.05或P＜0.01).复苏后20 h,A组有7只(58％)大鼠存活,B组有9只(75％),C组有10只(83％),三组存活率差异无统计学意义.结论 静脉复苏辅助腹腔注射高渗液对感染性休克大鼠多项复苏指标的恢复能够产生积极的影响,从而改善感染性休克大鼠的复苏治疗效果.     

生脉复合4%琥珀酰明胶对失血性休克大鼠血流动力学和血液流变学的影响

目的 探讨生脉复合4%琥珀酰明胶对失血性休克大鼠血流动力学和血液流变学的影响.方法 30只SD大鼠随机分为三组,每组10只.使用颈动脉失血-回输的方法制备失血性休克大鼠模型,维持MAP 40 mm Hg,30 min后复苏.A组依次按10 ml/kg颈动脉回输生脉注射液和20 ml/kg颈动脉回输4%琥珀酰明胶,B组按30 ml/kg颈动脉回输4%琥珀酰明胶;C组不给药作为对照.记录三组血流动力学和血液流变学变化.结果 A组和B组复苏后各时间点MAP和HR均恢复到接近休克前水平,复苏后30 min,血粘度指标均低于C组(P＜0.05).A组复苏后30 min血粘度指标低于B组(P＜0.05).结论 生脉复合4%琥珀酰明胶能明显改善失血性休克大鼠微循环障碍,降低血粘度.     

丙泊酚和芬太尼预处理减轻急性失血性休克兔心肌损伤的观察

目的 观察丙泊酚和芬太尼预处理对急性失血性休克家兔心肌缺血损伤的影响.方法 24只家兔随机均分为丙泊酚预处理组(P组)、芬太尼预处理组(F组)和对照组(C组).按Wigger's改良法制作家兔失血性休克模型.放血前各组分别给予等容量丙泊酚5 mg/kg、芬太尼25 μg/kg和生理盐水.放血使MAP降至约40 mmHg.持续监测MAP、左室压(LVP)、左室收缩压最大上升和下降速率(±dp/dtmax).放血前、放血后60 min和90 min抽血测定血清心肌肌钙蛋白Ⅰ(cTnI)浓度,实验结束时取心尖部组织行电镜检查.结果 各组放血后MAP、LVP、±dp/dtmax均明显下降,但P组和F组明显高于C组(P＜0.05或P＜0.01).cTnI在放血后60 min和90 min与放血前比较均明显增高(P＜0.01),P组和F组增高程度低于C组(P＜0.01),P组和F组之间差异无统计学意义.电镜检查发现P组和F组心肌损伤较C组减轻.结论 丙泊酚和芬太尼预处理均能减轻家兔急性失血性休克后的心肌损伤.     

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。     

醋酸钠林格氏液对犬失血性休克复苏过程中血流动力学及血乳酸的影响

目的 比较醋酸钠林格氏液(AR)、乳酸林格氏液(LR)和生理盐水(NS)对失血性休克犬碱剩余(BE)、乳酸(LAC)水平及其血液动力学的影响.方法 将健康成年雄性犬15条随机分为3组:AR组、LR组和NS组,用放血法复制失血性休克模型.分别于放血前、复苏前和复苏后5、30、60 min检测血流动力学参数、动脉血气和血乳酸值.结果 平均动脉压(MAP)恢复至休克前的水平,AR组[(41.10±2.18) ml/kg、(28.15±0.29) min]较LR组[(54.17±2.97) ml/kg、(43.26±0.87) min]、NS组[(59.61±2.88) ml/kg、(48.19±1.23) min]所需输液量更少、时间更短,差异有统计学意义(P＜0.05);复苏30 min后,MAP AR组[(99.25±12.13) mmHg(1mmHg=0.133 kPa)]较LR组[(84.25±11.87)mm Hg]、NS组[(81.25±13.26) mm Hg]明显升高,且AR组较其他组血液pH值、BE及LAC水平显著改善,差异有统计学意义(P＜0.05).结论 醋酸钠林格液比乳酸林格氏液和生理盐水更适合失血性休克犬的早期紧急液体复苏治疗.     

卡托普利在家兔主动脉阻断手术中对对脊髓损伤的保护作用

目的研究卡托普利在家兔肾上主动脉阻断手术中对脊髓损伤的保护作用及其机理.方法家兔24只,随机分为假手术组(A组)、缺血组(B组)和卡托普利组(C组).肾上阻断腹主动脉30min后松开,C组于阻断前10min静注卡托普利0.5mg@kg-1,继以0.15mg@kg-1@h-1持续输注至松开前10min.连续监测颈总动脉(BPi)和股动脉(BP2)平均动脉压,记录阻断前10min、阻断后5min、20min、30min以及松开后5min、60min、180min的BP1和BP2值,松开后3h观察胸10和腰3水平脊髓形态学变化,并测定脊髓组织丙二醛(MDA)含量.结果①B组动物阻断后的BP1显著高于阻断前(P＜0.05或0.01),C组阻断后BP1较阻断前无显著变化;B组松开后5、60、180min的血压均明显低于阻断前,C组松开后60、180min的血压比B组明显升高(P＜0.05).②B组脊髓MDA含量明显高于A组(P＜0.01),C组与A组无显著性差异,但明显低于B组(P＜0.05).③B组脊髓病理变化较重,可见大量神经元坏死,C组偶有神经元坏死.结论在家兔肾上主动脉阻断手术中使用卡托普利对脊髓损伤有较好保护作用,其机制与抗过氧化反应及缓解血液动力学波动有关.     

高渗氯化钠高氧液对失血性休克家兔血乳酸和动脉血气的影响

目的:观察高渗氯化钠高氧液对失血性休克家兔动脉血气和血乳酸值的影响，评价其对失血性休克的早期救治效果。方法:制备高渗氯化钠溶液(HS)、生理盐水高氧液（NSO）和高渗氯化钠高氧液(HSO)。30只雄性家兔制备失血性休克模型［于10min内使平均动脉压（MAP）降至40mmHg（1mmHg＝0.133kPa），维持60min］，随机分为NSO，HS，HSO组3个治疗组。分别按6mL/kg剂量5min内静脉输入NSO,HS和HSO。记录休克前后及给药后心率（HR）、呼吸（RR）、MAP及尿滴（UD），测定休克前、休克60min，给药后30，60，120min时血乳酸（BL）和动脉血气值。最后观察尸肺，测定肺系数。结果:HS和HSO组均显著地改善MAP，HR和UD，降低BL，改善代谢性酸中毒,肺系数明显低于NSO组。HSO与NSO及HS比较，能更显著地降低血BL，提高动脉血氧饱和度（SaO2）和动脉血氧分压（PaO2）。结论:HSO较HS和NSO能更显著地降低血BL,提高SaO2和PaO2，对失血性休克的早期救治具有较高的使用价值。     

腹腔扩容术对猪休克复苏后腹腔高压症心脏的影响

目的 观察腹腔扩容术对腹腔高压症(IAH)心脏影响.方法 建立失血性休克、门静脉不全阻断复苏后猪IAH模型,随机分腹腔扩容组(n=4)及假手术组(n=4),分别观察心率、平均动脉压(MAP)、缩短分数(FS)和射血分数(EF),测心脏干湿比及苏木素-伊红(HE)染色结果结果 与休克前比,IAH后2 h心率加快(154次/min比123次/min),MAP下降[110.0 mm Hg(1 mm Hg =0.133 kPa)比127.5 mm Hg],FS下降(29.8％比40.4％),EF下降(55.5％比72.0％)(P＜0.05).与IAH后2h比,腹腔扩容组手术后8h及12h较假手术组心率减慢(124次/min比156次/min,120次/min比156次/min)( P＜0.05) 腹腔扩容组22 h后与IAH后2h比,EF上升(P ＜0.05).结论 腹腔扩容术可显著改善本IAH模型的心率及EF.     

失血性休克对猪一氧化氮与内皮素的影响

目的 探讨内源性一氧化氮（NO）与内皮素（ET）在失血性休克中的变化及其意义。方法 14头体重为14～17kg的健康雄性家猪,随机均分为失血性休克组（H组）和对照组（C组）。H组按照Wigger’s改良法制作失血性休克模型,经股动脉快速放血使MAP降至40mmHg,维持90min,然后回输血液及等量的复方氯化钠。C组处理同H组,但未放血。各组分别在休克前、休克末、复苏末、复苏后30、60、120、240min记录MAP、HR、CVP、肺动脉压（PAP）、肺动脉楔压（PCWP）的变化,同时测定血浆NO与ET水平以及动脉血乳酸盐浓度（Lac）的变化。结果 H组休克末MAP、PAP和CVP降低而HR升高,PCWP无显著变化。血浆NO水平在休克后逐渐升高,复苏后60min显著高于休克前和C组水平（P〈0．05）,此后一直维持较高水平,240min时达到高峰;休克后ET水平显著增加,并显著高于C组及休克前（P〈0．05）,复苏后逐渐下降。结论 失血性休克后血浆NO、ET水平增加,在失血性休克的病理生理过程可有一定意义。     

山莨菪碱对失血性休克兔小肠微循环血量及血液酸碱度的影响

目的观察山莨菪碱对失血性休克兔小肠微循环血流量及血液酸碱度变化情况。方法大白兔16只随机分为2组,分别是山莨菪碱治疗组(S组,n=8)和生理盐水对照组(C组,n =8)。复制兔重度失血性休克及复苏的动物模型,在休克期间分别予等容量的山莨菪碱注射液和生理盐水治疗,复苏60 min。观察放血前、放血后10、30、60 min小肠黏膜微循环血流量、动脉平均血压、中心静脉压。在放血前、放血后10、30、60 min取颈动脉、肠系膜上静脉血液少量进行血气分析。结果放血后两组动物休克期小肠黏膜微循环血流量均比放血前明显降低(P<0.05);回输血液后S组动物小肠微循环血流量恢复,与放血前比较差异无统计学意义(P>0.05);C组动物在再灌注10、30、60 min时的微循环血流量明显低于放血前(P<0.05)。在再灌注60 min时S组的颈动脉血pH值、BE值高于C组(P<0.05);而对肠系膜上静脉血,S组在再灌注30、60 min时的pH值高于C组,在再灌注10、30、60 min时的BE值高于C组(P<0.05)。结论山莨菪碱能改善失血性休克时肠黏膜微循环,有利于更快清除肠微循环蓄积的酸性物质。     

限制性液体复苏对失血性休克大鼠网状内皮系统的影响

目的探讨限制性液体复苏对失血性休克大鼠网状内皮系统的影响。方法60只SD大鼠制成未控制性重度失血性休克模型,随机分成对照组、NF组(无液体复苏组)、NS40组(限制性液体复苏组)和NS80组(常规大量液体复苏组),检测和比较休克复苏后各组存活大鼠肝脏枯否细胞和腹腔巨噬细胞的吞噬功能。结果重度失血性休克大鼠失血后150min存活率NF组、NS40组和NS80组比对照组明显提高,NS40组较NS80组显著改善(P0.05);NS40组大鼠肝脏枯否细胞和腹腔巨噬细胞的吞噬功能较NS80组明显改善(P0.05)。结论限制性液体复苏可以显著改善失血性休克大鼠的网状内皮系统的吞噬功能,提高大鼠的免疫功能,降低死亡率。     

不同液体腹腔复苏对失血性休克大鼠肠道炎性反应的影响

目的 探讨不同液体腹腔复苏对失血性休克大鼠肠道炎性反应的影响.方法 清洁级健康雄性SD大鼠50只,体重200～250 g,随机分为5组(n=10):假手术组(S组)仅行手术操作,不制备失血性休克模型;采用股动脉置管放血法制备大鼠失血性休克模型,常规静脉复苏组(CVR组)失血性休克1 h后,经左侧股静脉匀速回输自体血及相当于2倍失血量的生理盐水行常规静脉复苏;不同液体腹腔复苏组(DPR1～3组)行常规静脉复苏,同时分别腹腔输注生理盐水、6%羟乙基淀粉130/0.4、2.5%腹膜透析液20 ml行腹腔复苏.输注时间均为30 min.右颈总动脉连接多功能监测仪持续监测平均动脉压;于复苏后2 h时股动脉采血,测定乳酸浓度,取小肠组织检测髓过氧化物酶(MPO)活性,采用免疫组化法检测小肠组织肿瘤坏死因子α(TNF-α)表达水平,光镜下观察小肠黏膜组织形态,计算小肠黏膜上皮损伤指数.结果 与S组比较,其余各组大鼠复苏后平均动脉压差异无统计学意义(P>0.05),动脉血乳酸浓度、小肠组织MPO活性、TNF-α表达水平及小肠黏膜上皮损伤指数升高(P<0.05或0.01);与CVR组比较,DPR3组动脉血乳酸浓度、小肠组织MPO活性、TNF-α表达水平及小肠黏膜上皮损伤指数降低(P<0.05).结论 采用2.5%腹膜透析液20 ml行腹腔复苏可有效抑制肠道炎性反应,从而对失血性休克大鼠产生保护作用.     

A novel method of peritoneal resuscitation improves organ perfusion after hemorrhagic shock

BACKGROUND: After resuscitation from hemorrhagic shock, intestinal microvessels constrict leading to impairment of blood flow. This occurs despite restoration and maintenance of central hemodynamics. Our recent studies have demonstrated that topical and continuous exposure of the gut microvasculature to a clinical solution (Delflex; Fresenius Medical Care), as a technique of direct peritoneal resuscitation (DPR), reverses the postresuscitation vasoconstriction and hypoperfusion to a sustained dilation and hyperperfusion. We hypothesize that initiation of DPR simultaneously with resuscitation from hemorrhagic shock enhance organ blood flow to all tissues surrounding the peritoneal cavity as well as distant organs. METHODS: Male Sprague-Dawley rats were anesthetized, intubated and cannulated for monitoring of hemodynamics and for withdrawal of blood. Rats were hemorrhaged to 50% of mean blood pressure for 60 minutes prior to resuscitation with shed blood plus 2 volumes of saline. Animals were randomized for intraperitoneal therapy with 30 mL saline (group 1, n = 9), or Delflex (group 2, n = 9). Whole organ blood flow was measured by colorimetric microsphere technique with phantom organ at baseline, after completion of resuscitation, and at 120 minutes postresuscitation. Replenishment of the dwelling intraperitoneal saline or Delflex was performed in (group 3, n = 8), and (group 4, n = 8), respectively at 90 minutes postresuscitation, and a single whole organ blood flow was performed at 120 minutes postresuscitation. RESULTS: Direct peritoneal resuscitation caused a significant increase in blood flow to the jejunum (35%), ileum (33%), spleen (48%), and pancreas (57%), whereas a marked increase in blood flow was detected in the lung (111%), psoas major muscle (115%), and diaphragm (132%), as compared with the saline treated animals in group 1. At 120 minutes postresuscitation, organ blood flow returned to the prehemorrhagic shock baseline level in all organs irrespective of peritoneal therapy. Replenishment of the intraperitoneal solution in group 3 and 4, enhanced blood flow to the liver, kidneys, and diaphragm. CONCLUSIONS: Direct peritoneal resuscitation enhanced blood flow to organs incited in the pathogenesis of multiple organ failure that follows hemorrhagic shock.     

四种不同复合液对急性颅内高压伴失血性休克兔复苏的效果及其机制

目的 探讨4种不同复合液体对急性颅内高压伴失血性休克兔复苏的效果及机制.方法 家兔24只,随机分为甘露醇羟乙基淀粉组( MT+ HS)组、甘露醇低分子右旋糖酐组(MT+HD)组、7.5％高渗氯化钠羟乙基淀粉组(HSH)组、7.5％高渗氯化钠低分子右旋糖酐组(HSD)组,每组6只,采用硬膜外球囊注水和动脉放血的方法复制急性颅内高压伴失血性休克模型,分别于8个不同时点采集平均动脉压(MAP)、中心静脉压(CVP)、颅内压(ICP)、脑灌注压(CPP)数据.结果 4组复合液均能提高MAP,HSH组在复苏后20 min达到峰值,反应速度最快,提高MAP的平均幅度分别为(29.4±2.1)、(27.9±3.4)、(41.0±2.2)、(40.6±1.6) mm Hg(1 mm Hg =0.133 kPa),提高幅度差异有统计学意义(P＜0.05);4组复合液提高CVP值的幅度均接近于(3.0±1.4) cm H2O(1 cm H2O =0.098 kPa),提高幅度差异无统计学意义(P＞0.05);4组复合液均能在不同时段将ICP值降至基础值水平(7.3±1.6) mmHg,将CPP值升至基础值水平(69.6±6.8)mm Hg,峰值水平差异无统计学意义(P＞0.05).结论 4组复合液均有纠正休克和降低颅内压的效果,HSH维持效用的时间最持久,复苏效果最明显.     

Splanchnic blood flow response to intraaortic balloon pump assist of hemorrhagic shock

Hemorrhagic shock results in marked changes in splanchnic arterial blood flow. We studied the effects of intraaortic balloon pump assist (IABP) upon splanchnic blood flow during sustained hemorrhagic shock and following volume resuscitation. Hemorrhagic shock was induced (mean blood pressure = 30 mm Hg) for 120 min in 20 dogs. Controls (n = 11) underwent resuscitation with shed blood and lactated Ringers solution only. In the study group (n = 9), IABP was begun after 60 min of hemorrhagic shock and continued throughout a 90-min period after resuscitation. Hemodynamic parameters were assessed and splanchnic blood flow was estimated (radioactive microsphere technique) at baseline, through 120 min of sustained hypotension, and during the resuscitation period. Splanchnic blood flow was significantly reduced in both the control and the IABP groups during the period of hemorrhagic shock. Interestingly, the IABP group was found to have a return to preshock splanchnic viscera perfusion without the hyperemic reperfusion phenomenon seen in control animals resuscitated with shed blood and Ringers lactate alone. IABP assist of hemorrhagic shock appears to improve vasomotor control of splanchnic blood flow in this experimental preparation of shock. This may result in less reperfusion injury to the splanchnic viscera during the resuscitation of severe hemorrhagic shock.     

高渗氯化钠羟乙基淀粉复合液对失血性休克肺的保护作用

目的观察用高渗氯化钠羟乙基淀粉复合液(7.5%氯化钠 6%羟乙基淀粉200/0.5,HHS)小容量复苏对失血性休克后肺损伤的影响。方法雄性SD大鼠随机分为五组:正常对照组(CON组,n=6):不放血不补液;其他大鼠通过放血使MAP降至45mmHg并维持120min,然后分为:休克组(SH组,n=6),不补液复苏;HHS组(n=8),用HHS5ml/kg静脉滴注;7.5%氯化钠高渗溶液组(HTS组,n=6),用7.5%NaCl5ml/kg静脉滴注;复方乳酸钠组(LR组,n=7),用3倍失血量的复方乳酸钠静脉滴注。观察休克2h末、补液结束即刻、15、30、60、120、180min时MAP、CVP的变化,测定补液结束2、24h存活动物的氧合指数和肺水含量、肺髓过氧化物酶(MPO)水平、肺损伤评分。结果在补液结束120、180min,HTS组MAP、CVP低于HHS和LR组(P<0.05);在补液结束24h,HHS组氧合指数、肺水含量、肺MPO水平、肺损伤评分优于HTS和LR组(P<0.05)。结论用HHS小容量复苏失血性休克,维持血流动力学稳定时间更长;对肺组织的保护作用优于7.5%氯化钠高渗溶液或复方乳酸钠。     

失血性休克兔复苏的多因素分析

目的 评价两种高渗液体、两种液体温度和两种复苏目标血压对失血性休克兔的复苏效果,寻找合理的复苏方案.方法 采用随机分组三因素两水平析因设计,实验因素为高渗液体种类(因素A)、液体温度(因素B)和复苏目标血压(因素C),A_1和A_2分别为7.5%NaCl(HS)和7.2%NaCl+6%右旋糖酐40混合液(HSD),B_1和B_2分别为常温(23℃)和高温(45℃),C_1和C_2分别为平均动脉压(MAP)60 mm Hg和MAP 80 mm Hg.按各因素不同水平排列组合,40只成年雄性家兔随机分为8组(n=5):A_1B_1C_1组、A_1B_1C_2组、A_1B_2C_1组、A_1B_2C_2组、A_2B_1C_1组、A_2B_1C_2组、A_2B_2C_1组和A_2B_2C_2组.采用Wiggers改良法建立失血性休克模型,模型建立成功后立即进行液体复苏,分别在建立模型前(基础状态)、失血性休克模型建立成功时、液体复苏1、2、3 h时采集动脉血样,进行血气分析,测定全血乳酸浓度、血清肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)浓度,监测小肠系膜微循环和直肠温度.结果 行HSD复苏动物的动脉血二氧化碳分压(PaO_2)高于行HS复苏的动物,行常温HSD复苏动物的PaO_2高于行常温HS复苏的动物(P<0.05);行常温HSD复苏动物的全血乳酸浓度低于行常温HS复苏的动物(P<0.05);行HSD复苏动物的血清TNF-α和IL-6浓度低于行HS复苏的动物(P<0.05).行常温液体复苏动物的血清TNF-α浓度低于行高温液体复苏的动物(P<0.05);因素C对上述各指标的影响均无统计学意义(P>0.05),与各因素间无交互作用.各因素对小肠系膜微循环的影响无统计学意义(P>0.05).行高温液体复苏动物的直肠温度下降速度明显减慢(P<0.05).结论 失血性休克兔HSD的复苏效果优于HS,常温液体的复苏效果优于高温液体,液体种类与液体温度间存在交互作用,虽然两种复苏目标血压对复苏效果无影响,但常温HSD复苏维持MAP60 mm Hg是较为合理的方案.     

Direct peritoneal resuscitation from hemorrhagic shock: effect of time delay in therapy initiation

BACKGROUND: After conventional resuscitation from hemorrhagic shock, splanchnic microvessels progressively constrict, leading to impairment of blood flow. This occurs despite restoration and maintenance of central hemodynamics. The authors' recent studies have demonstrated that topical and continuous ex vivo exposure of the gut microvasculature to a glucose-based clinical peritoneal dialysis solution (Delflex), as a technique of direct peritoneal resuscitation (DPR), can prevent these postresuscitation events when initiated simultaneously with conventional resuscitation. This study aimed to determine whether DPR applied after conventional resuscitation reverses the established postresuscitation intestinal vasoconstriction and hypoperfusion. METHODS: Male Sprague-Dawley rats were bled to 50% of baseline mean arterial pressure and resuscitated intravenously over 30 minutes with the shed blood returned plus two times the shed blood volume of saline. Initiation of ex vivo, topical DPR was delayed to 2 hours (group 1, n = 8), or to 4 hours (group 2, n = 8), respectively, after conventional resuscitation. Intravital microscopy and Doppler velocimetry were used to measure terminal ileal microvascular diameters of inflow A1 and premucosal A3 (proximal pA3, distal dA3) arterioles and blood flow in the A1 arteriole, respectively. Maximum arteriolar dilation capacity was obtained from the topical application, in the tissue bath, of the endothelium-independent nitric oxide-donor sodium nitroprusside (10M). RESULTS: Hemorrhagic shock caused a selective vasoconstriction of A1 (-24.1% +/- 2.15%) arterioles from baseline, which was not seen in A3 vessels. This caused A1 blood flow to drop by -68.6% of the prehemorrhage value. Conventional resuscitation restored and maintained hemodynamics in all the animals without additional fluid therapy. In contrast, there was a generalized and progressive postresuscitation vasoconstriction of A1 (-21.7%), pA3 (-18.5%), and dA3 (-18.7%) vessels. The average postresuscitation A1 blood flow was -49.5% of the prehemorrhage value, indicating a persistent postresuscitation hypoperfusion. Direct peritoneal resuscitation reversed the postresuscitation vasoconstriction by 40.9% and enhanced A1 blood flow by 112.9% of the respective postresuscitation values. CONCLUSIONS: Delayed DPR reverses the gut postresuscitation vasoconstriction and hypoperfusion regardless of the initiation time. This occurs without adverse effects on hemodynamics. Direct peritoneal resuscitation-mediated enhancement of tissue perfusion results from the local effects from the vasoactive components of the Delflex solution, which are hyperosmolality, lactate buffer anion, and, to a lesser extent, low pH. The molecular mechanism of this vasodilation effect needs further investigation.