家兔出血未控制性休克限制性液体复苏的实验研究
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摘要
目的：（1）探讨出血未控制性休克限制性液体复苏维持的理想血压水平；（2）维持此理想血压水平下，不会严重影响重要器官功能的最长时间。
方法：采用Wiggers改良法[8,9,10]制作出血未控制性休克模型，30只家兔随机分为5组：（1）正常对照组(NC组)：只进行插管等操作，不放血、不复苏；（2）不复苏组(NR组)：制模成功后不进行液体复苏；（3）N50组:制模成功后维持MAP在50mmHg；（4）N60组:制模成功后维持MAP在60mmHg；（5）N70组:制模成功后使MAP维持在70mmHg。通过监测继续出血量、输液量、存活时间、存活率、HCT、RBC、PLT、动脉血气分析（包括血乳酸、剩余碱、PO_2、PCO_2、pH值）、SOD、MDA等指标变化来比较不同MAP水平的复苏效果，并进一步推断维持的最长时间。
结果：
1.继续出血量随着维持MAP水平的升高而增加；N70组最高，NR组最少。NR组没有复苏，无补液量，其他各组随着维持的MAP水平升高而平均存活时间N60组最长为248.83±36.54min，其次是N70组202.00±31.02min，N50组112.67±35.16min,NR组最短为58.50±29.50min。各组间均差异有显著性。
2. HCT和RBC均随着复苏血压的升高而降低。复苏维持血压越高降低速度越快。各个时间点差异均有显著性。
3.休克后除NC组外各组乳酸均出现升高，N60组上升速度较慢，一直优于其他组，休克后60、120、150min前各时间点差异有显著性。剩余碱除NC组外均出现负值增加，休克后60min，N60和N70组优于N50和NR组，120min时间点各组间差异显著，N70组优于NC组外其他各组。
4. PO_2、PCO_2、pH值在休克后也出现改变，随着复苏时间的增加PO_2下降、PCO_2升高、PH值上升，N60组变化最为缓慢，优于其他组，而且180min前各指标基本维持在正常水平；其他组出现异常的时间点要早于N60组。
5.除Nc组外，其他组在休克后出现SOD降低、MDA值升高，但是N60组好于其他组，120min之后开始出现明显异常，差异有显著性。除了在NR组在休克0min出现明显AST升高外，ALT、Cr、Ur改变无统计学意义。
6.除了NC组外，其他组血小板数量在休克后立即出现大幅度下降，复苏后N60和N70组出现回升，之后再降低。N70组PLT数是高于其他各组，在180min后再次出现快速降低，而N60组在120mi就已经开始出现。N50和NR组PLT水平持续下降中，差异有显著性。
结论：
1.出血未控制性休克复苏维持MAP在60mmHg左右是比较理想的血压水平。
2.出血未控制性休克家兔，在无法控制出血前，给予限制性液体复苏，并维持MAP在60mmHg时，维持此低压水平不超过120min,一般不会引起重要脏器严重损害，预后相对较好。
Objective：
1.To search for the optimal mean arterial pressure (MAP) level during the fluidresuscitation for an uncontrolled shock.
2.Maintaining this ideal blood pressure levels，How long it will not seriously affectorgan function.
.Methods: Based on Wigger’s describtion, the animal models with uncontrolledhemorrhagic shock were established by femoral artery phlebotomy. Thirty rabbits wererandomly divided into five groups (each group, n=6):(1)Normal control group (NCgroup): intubation an other operations, no bleeding, no recovery;(2) Non-recoverygroup(NR group）control group; N50group:maintaining MAP at50mmHg; N60group:at60mmHg; N70group:at70mmHg. The arterial blood gas analysis (ABGA),including lactic acid, base excess, arterial oxygen tension (PaO_2), arterial carbondioxide tension (PaCO_2), hydrogen ion exponent (pH value), and et al, was performed atshock before,0,60,120,150,180and240minutes after shock, respectively.
Results:
1.The amount of continued bleeding with the maintenance of elevated MAP levelincreased;the highest in the N70group.NR group at least. No recovery in the NR group,there is no fluid volume，In other groups,the amount of fluid volume with themaintenance of elevated MAP level increased;the highest in the N70group.NR group atleast. N60group the average survival time of up to248.83±36.54min, followed by theN70group202.00±31.02min, N50group112.67±35.16min, the shortest of NR groupwas58.50±29.50min. Groups, the difference was significant.
2. HCT and RBC were reduced with the recovery of blood pressure increases. Each timepoint, the differences were statistically significant significant.
3. In addition to the NC group, other groups of lactic acid appeared increased, the N60group rose slower,it has been better than the other groups at the point of60,120,150minafter the shock,there was a significant difference. In addition to the NC group, baseexcess increased negative at60min, N60and N70group was better than the N50and theNR group,120min time point in each group were significantly different, the N70group was better than the other groups in addition to the NC group.
4. PO_2, PCO_2, pH value has changed after the shock, with the increase of the recoverytime,PO_2decreased, PCO_2increased, pH value lower.In addition to the NC group,mostslow changes in the N60group, better than the other groups, and180min before eachindexbasically maintained at normal levels; abnormal point in time earlier than the N60group in other groups.
5. In addition to the NC group, other groups in shock after SOD was lower, MDAincreased, but the N60group was better than the other groups,120min after the start toappear abnormal, the difference was significant.NR group AST increased at the pointof0min, ALT and Cr, Ur change was not statistically significant.
6. In addition to the NC group, other groups platelet count dropped significantlyimmediately after shock, after resuscitation, N60and N70groups rebound and thenlower.The number of PLT N70group is higher than other groups,180min afterrecurrence of rapid decrease, while the N60group has begun to emerge in120mi.N50and NR group PLT levels continue to decline, the difference was significant.
Conclusions:
1. During a limited fluid resuscitation for the rabbits with unconrntrolled hemorrhagicshock, maintaining MAP at60mmHg may be the ideal level of blood pressure。
2. Uncontrolled hemorrhagic shock in rabbits given the limited fluid resuscitation, andto maintain MAP at60mmHg when the time to maintain this level of blood pressuredoes not exceed120min, generally does not cause serious damage to vital organs,the prognosis is relatively good.
方法：采用Wiggers改良法[8,9,10]制作出血未控制性休克模型，30只家兔随机分为5组：（1）正常对照组(NC组)：只进行插管等操作，不放血、不复苏；（2）不复苏组(NR组)：制模成功后不进行液体复苏；（3）N50组:制模成功后维持MAP在50mmHg；（4）N60组:制模成功后维持MAP在60mmHg；（5）N70组:制模成功后使MAP维持在70mmHg。通过监测继续出血量、输液量、存活时间、存活率、HCT、RBC、PLT、动脉血气分析（包括血乳酸、剩余碱、PO_2、PCO_2、pH值）、SOD、MDA等指标变化来比较不同MAP水平的复苏效果，并进一步推断维持的最长时间。
结果：
1.继续出血量随着维持MAP水平的升高而增加；N70组最高，NR组最少。NR组没有复苏，无补液量，其他各组随着维持的MAP水平升高而平均存活时间N60组最长为248.83±36.54min，其次是N70组202.00±31.02min，N50组112.67±35.16min,NR组最短为58.50±29.50min。各组间均差异有显著性。
2. HCT和RBC均随着复苏血压的升高而降低。复苏维持血压越高降低速度越快。各个时间点差异均有显著性。
3.休克后除NC组外各组乳酸均出现升高，N60组上升速度较慢，一直优于其他组，休克后60、120、150min前各时间点差异有显著性。剩余碱除NC组外均出现负值增加，休克后60min，N60和N70组优于N50和NR组，120min时间点各组间差异显著，N70组优于NC组外其他各组。
4. PO_2、PCO_2、pH值在休克后也出现改变，随着复苏时间的增加PO_2下降、PCO_2升高、PH值上升，N60组变化最为缓慢，优于其他组，而且180min前各指标基本维持在正常水平；其他组出现异常的时间点要早于N60组。
5.除Nc组外，其他组在休克后出现SOD降低、MDA值升高，但是N60组好于其他组，120min之后开始出现明显异常，差异有显著性。除了在NR组在休克0min出现明显AST升高外，ALT、Cr、Ur改变无统计学意义。
6.除了NC组外，其他组血小板数量在休克后立即出现大幅度下降，复苏后N60和N70组出现回升，之后再降低。N70组PLT数是高于其他各组，在180min后再次出现快速降低，而N60组在120mi就已经开始出现。N50和NR组PLT水平持续下降中，差异有显著性。
结论：
1.出血未控制性休克复苏维持MAP在60mmHg左右是比较理想的血压水平。
2.出血未控制性休克家兔，在无法控制出血前，给予限制性液体复苏，并维持MAP在60mmHg时，维持此低压水平不超过120min,一般不会引起重要脏器严重损害，预后相对较好。
Objective：
1.To search for the optimal mean arterial pressure (MAP) level during the fluidresuscitation for an uncontrolled shock.
2.Maintaining this ideal blood pressure levels，How long it will not seriously affectorgan function.
.Methods: Based on Wigger’s describtion, the animal models with uncontrolledhemorrhagic shock were established by femoral artery phlebotomy. Thirty rabbits wererandomly divided into five groups (each group, n=6):(1)Normal control group (NCgroup): intubation an other operations, no bleeding, no recovery;(2) Non-recoverygroup(NR group）control group; N50group:maintaining MAP at50mmHg; N60group:at60mmHg; N70group:at70mmHg. The arterial blood gas analysis (ABGA),including lactic acid, base excess, arterial oxygen tension (PaO_2), arterial carbondioxide tension (PaCO_2), hydrogen ion exponent (pH value), and et al, was performed atshock before,0,60,120,150,180and240minutes after shock, respectively.
Results:
1.The amount of continued bleeding with the maintenance of elevated MAP levelincreased;the highest in the N70group.NR group at least. No recovery in the NR group,there is no fluid volume，In other groups,the amount of fluid volume with themaintenance of elevated MAP level increased;the highest in the N70group.NR group atleast. N60group the average survival time of up to248.83±36.54min, followed by theN70group202.00±31.02min, N50group112.67±35.16min, the shortest of NR groupwas58.50±29.50min. Groups, the difference was significant.
2. HCT and RBC were reduced with the recovery of blood pressure increases. Each timepoint, the differences were statistically significant significant.
3. In addition to the NC group, other groups of lactic acid appeared increased, the N60group rose slower,it has been better than the other groups at the point of60,120,150minafter the shock,there was a significant difference. In addition to the NC group, baseexcess increased negative at60min, N60and N70group was better than the N50and theNR group,120min time point in each group were significantly different, the N70group was better than the other groups in addition to the NC group.
4. PO_2, PCO_2, pH value has changed after the shock, with the increase of the recoverytime,PO_2decreased, PCO_2increased, pH value lower.In addition to the NC group,mostslow changes in the N60group, better than the other groups, and180min before eachindexbasically maintained at normal levels; abnormal point in time earlier than the N60group in other groups.
5. In addition to the NC group, other groups in shock after SOD was lower, MDAincreased, but the N60group was better than the other groups,120min after the start toappear abnormal, the difference was significant.NR group AST increased at the pointof0min, ALT and Cr, Ur change was not statistically significant.
6. In addition to the NC group, other groups platelet count dropped significantlyimmediately after shock, after resuscitation, N60and N70groups rebound and thenlower.The number of PLT N70group is higher than other groups,180min afterrecurrence of rapid decrease, while the N60group has begun to emerge in120mi.N50and NR group PLT levels continue to decline, the difference was significant.
Conclusions:
1. During a limited fluid resuscitation for the rabbits with unconrntrolled hemorrhagicshock, maintaining MAP at60mmHg may be the ideal level of blood pressure。
2. Uncontrolled hemorrhagic shock in rabbits given the limited fluid resuscitation, andto maintain MAP at60mmHg when the time to maintain this level of blood pressuredoes not exceed120min, generally does not cause serious damage to vital organs,the prognosis is relatively good.
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[61]Maegele M,Lefering R,Paffrath T.et al.Red-blood-cell to plasma ratios transfused duringmassive transfusion are associated with mortality in severe multiple injury: a retrospectiveanalysis from the Trauma Registry of the Deutsche Gesellschaft for Unfallchirurgie[J]. VoxSang,2008,Aug,95(2):112-9.Epub,2008,Jun,28.
[62]Frith D,Brohi K.The acute coagulopathy of trauma shock: clinicalrelevance[J].Surgeon,2010,Jun,8(3):159-63.Epub,2010,Feb,6.
[63]Brohi K,Singh J,Heron M.et al.Acute traumatic coagulopathy[J].J Trauma.2003,Jun,54(6):1127-30.
[64]Ganter MT,Pittet JF.New insights into acute coagulopathy in trauma patients[J].Best Pract ResClin Anaesthesiol,2010,Mar,24(1):15-25.
[65]Hess JR,Brohi K,Dutton RP.et al.The coagulopathy of trauma: a review of mechanisms[J].JTrauma,2008,Oct,65(4):748-54.
[1]刘大为,严静,邱海波,等.低血容量休克复苏指南(2007)[J].中国实用外科杂志,2007.8.27(8):581-7.
[2]朱捷,帅小军,何晓冉.高渗盐水对创伤失血性休克患者T细胞免疫的影响[J].中华急诊医学杂志,2009,18(4)376-79.
[3]Bulger EM,Jurkovich GJ,Nathens AB.et al.Hypertonic resuscitation of hypovolemic shock afterblunt trauma: a randomized controlled trial[J]. Arch Surg,2008,Feb,143(2):139-48; discussion149.
[4]Rolf Rossaint,Bertil Bouillon,Vladimir Cerny.et al.Management of bleeding following majortrauma: an updated European guideline[J].Critical Care,2010,14:R52.
[5]Pedrino GR, Rossi MV, Schoorlemmer GH.et al.Cardiovascular adjustments induced by hypertonicsaline in hemorrhagic rats:Involvement of carotid body chemoreceptors[J]. AutonNeurosci,2011,Feb,24,160(1-2):37-41. Epub,2010,Dec,10.
[6]Schroth M,Plank C,Meissner U,et al.Hypertonic-hyperoncotic solutions improve cardiac functionin children after open-heart surgery[J].Pediatrics,2006,118(1):e76-84.
[7]Elgjo GI,Mathew BP,Poli de Figueriedo LF.et al.Resuscitation with hypertonic saline dextranimproves cardiac function in vivo and ex vivo after burn injury insheep[J].Shock,1998,9(5):375-383.
[8]Frithiof R,Ramchandra R,Hood SG.et al.Hypertonic sodium resuscitation after hemorrhageimproves hemodynamic function by stimulating cardiac,but not renal,sympathetic nerveactivity[J].Am J Physiol Heart Circ Physiol,2011,Feb,300(2):H685-92. Epub2010Dec,10.
[9]秦薇,余艳红,王晨虹.等.限制性输液对失血性休克孕兔微循环灌注的影响[J].中华妇产科杂志,2010,10,45(10):775-80.
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[11]周彬,霍正禄,杨兴易.高渗盐羟乙基淀粉液对失血性休克犬中性粒细胞Fas表达的影响[J].中华急诊医学杂志,2006,1(15):31-33.
[12]Bulger EM,Cuschieri J,Warner K.et al.Hypertonic Resuscitation modulates the inflammatoryresponse in patients with traumatic hemorrhagic shock[J]. Ann Surq,2007,Apr,245(4):635-41.
[13]Isayama K,Murao Y,Saito F.et al.Effects of Hypertonic Saline on CD4(+)CD25(+)Foxp3(+)Regulatory T Cells After Hemorrhagic Shock in Relation to iNOS and Cytokines[J].J SurgRes,2012,Jan,172(1):137-45. Epub,2010,Aug,15.
[14]Rizoli SB,Rhind SG,Shek PN.et al.The immunomodulatory effects of hypertonic salineresuscitation in patients sustaining traumatic hemorrhagic shock: arandomized,controlled,double-blinded trial[J].Ann Surg,2006,Jan,243(1):47-57.
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[23]Battison C,Andrews PJ,Graham C.et al.Randomized controlled trial on the effect of a20%mannitol solution and a7.5%saline/6%dextran solution on increased intracranial pressure afterbrain injury[J].Crit Care Med,2005,Jan,33(1):196-202;discussion257-8.
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[1]刘大为,严静,邱海波,等.低血容量休克复苏指南(2007)[J].中国实用外科杂志,2007.8.27(8):581-7.
[2]朱捷,帅小军,何晓冉.高渗盐水对创伤失血性休克患者T细胞免疫的影响[J].中华急诊医学杂志,2009,18(4)376-79.
[3]Bulger EM,Jurkovich GJ,Nathens AB.et al.Hypertonic resuscitation of hypovolemic shock afterblunt trauma: a randomized controlled trial[J]. Arch Surg,2008,Feb,143(2):139-48; discussion149.
[4]Rolf Rossaint,Bertil Bouillon,Vladimir Cerny.et al.Management of bleeding following majortrauma: an updated European guideline[J].Critical Care,2010,14:R52.
[5]Pedrino GR, Rossi MV, Schoorlemmer GH.et al.Cardiovascular adjustments induced by hypertonicsaline in hemorrhagic rats:Involvement of carotid body chemoreceptors[J]. AutonNeurosci,2011,Feb,24,160(1-2):37-41. Epub,2010,Dec,10.
[6]Schroth M,Plank C,Meissner U,et al.Hypertonic-hyperoncotic solutions improve cardiac functionin children after open-heart surgery[J].Pediatrics,2006,118(1):e76-84.
[7]Elgjo GI,Mathew BP,Poli de Figueriedo LF.et al.Resuscitation with hypertonic saline dextranimproves cardiac function in vivo and ex vivo after burn injury insheep[J].Shock,1998,9(5):375-383.
[8]Frithiof R,Ramchandra R,Hood SG.et al.Hypertonic sodium resuscitation after hemorrhageimproves hemodynamic function by stimulating cardiac,but not renal,sympathetic nerveactivity[J].Am J Physiol Heart Circ Physiol,2011,Feb,300(2):H685-92. Epub2010Dec,10.
[9]秦薇,余艳红,王晨虹.等.限制性输液对失血性休克孕兔微循环灌注的影响[J].中华妇产科杂志,2010,10,45(10):775-80.
[10]Legrand M,Mik EG,Balestra GM.et al.Fluid resuscitation does not improve renal oxygenationduring hemorrhagic shock in rats[J]. Anesthesiology,2010,Jan,112(1):119-27.
[11]周彬,霍正禄,杨兴易.高渗盐羟乙基淀粉液对失血性休克犬中性粒细胞Fas表达的影响[J].中华急诊医学杂志,2006,1(15):31-33.
[12]Bulger EM,Cuschieri J,Warner K.et al.Hypertonic Resuscitation modulates the inflammatoryresponse in patients with traumatic hemorrhagic shock[J]. Ann Surq,2007,Apr,245(4):635-41.
[13]Isayama K,Murao Y,Saito F.et al.Effects of Hypertonic Saline on CD4(+)CD25(+)Foxp3(+)Regulatory T Cells After Hemorrhagic Shock in Relation to iNOS and Cytokines[J].J SurgRes,2012,Jan,172(1):137-45. Epub,2010,Aug,15.
[14]Rizoli SB,Rhind SG,Shek PN.et al.The immunomodulatory effects of hypertonic salineresuscitation in patients sustaining traumatic hemorrhagic shock: arandomized,controlled,double-blinded trial[J].Ann Surg,2006,Jan,243(1):47-57.
[15]Fernandes CI,Llimona F,Godoy LC.et al.Treatment of hemorrhagic shock with hypertonic salinesolution modulates the inflammatory response to live bacteria in lungs[J].Braz J Med BiolRes,2009,Oct,42(10):892-901.
[16]Murao Y,Hata M,Ohnishi K.et al.Hypertonic saline resuscitation reduces apoptosis and tissuedamage of the small intestine in a mouse model of hemorrhagicshock[J].Shock,2003,Jul,20(1):23-8.
[17]Lu YQ,Gu LH,Huang WD.et al.Effect of hypertonic saline resuscitation on heme oxygenase-1mRNA expression and apoptosis of the intestinal mucosa in a rat model of hemorrhagicshock[J].Chin Med J (Engl),2010,Jun,123(11):1453-8.
[18]Papia G,Burrows LL,Sinnadurai S.et al,Hypertonic saline resuscitation from hemorrhagic shockdoes not impair the neutrophil response to intraabdominalinfection[J].Surgery,2008,Nov,144(5):814-21.Epub.2008Sep,14.
[19]Gryth D,Rocksén D,Drobin D.et al.Effects of fluid resuscitation with hypertonic saline dextrane orRinger's acetate after nonhemorrhagic shock caused by pulmonary contusion[J].JTrauma,2010,Oct,69(4):741-8.
[20]Liu LM, Hu DY, Zhou XW.et al.HSD is a better resuscitation fluid for hemorrhagic shock withpulmonary edema at high altitude[J].Shock,2008,Dec,30(6):714-20.
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