失血性休克后血管舒缩功能变化

目的研究失血性休克动物血管舒张收缩功能变化.方法Wistar大鼠戊巴妥钠ip麻醉,股动脉插管放血.15min内使MAP降至40mmHg,维持2h,完成休克模型,(S0组)继续保持该血压,维持2h(S2组)和4h(S4组).活杀大鼠,迅速取出胸主动脉VSM后,去除内皮,制成3mm宽血管环,悬于K-H液的浴槽中,37℃充入95%氧和5%CO2混合气.分别进行由NE、KCl、caffiene诱发的收缩实验及VSM环钙敏感性实验,数据经统计学处理.结果(1)休克后VSM环对NE的收缩反应在休克后2h开始下降,证明存在血管低反应性.(2)休克后蜕膜VSM环对Ca2+的收缩张力在休克后2h开始下降,说明休克后存在钙失敏及钙稳态的改变.(3)休克后VSM环对KCl收缩张力下降,说明休克后2h电压依赖性钙通道开放受阻.(4)休克后VSM环对PE及caffiene的收缩能力变化.前者休克后4h下降,后者休克后2h下降.说明胞内钙释放功能在休克后下降.因为PE及caffiene分别活化IP3敏感性及非敏感性钙池,证明二者在失血性休克后功能都有减退.结论严重失血性休克后存在血管低反应性,以及钙失敏现象,此时对血管活性药物的反应性下降,致使血压难以恢复.病程向难治性方向发展.失血性休克后血管低反应期血管平滑肌细胞内钙与钙通道变化     

内源性舒张因子在失血性休克中的变化

目的探讨内源性舒张因子一氧化氮（NO）与一氧化碳（CO）在失血性休克中的变化。方法按照Wigger’s改良法制作家猪失血性休克模型，失血性休克（H）组经股动脉快速放血使MAP降至40mmHg，然后复苏。对照（C）组处理同H组，但未失血。各组分别在休克前、休克末、复苏末、复苏后30、60、120、240min分别记录平均动脉压（MAP）、心率（HR）、中心静脉压（CVP）、肺动脉压（PAP）、肺动脉楔压（PCWP）、气道压（Peak）的变化，采血测定pH值、BE值、CO、NO及乳酸盐（Lae）水平。结果H组休克后MAP、PAP和CVP降低而HR升高，Peak、PCWP无显著变化。血浆NO水平在休克后逐渐升高，复苏后120min显著高于休克前和c组水平，此后一直维持较高水平，240rain时达到高峰。休克后CO水平逐渐增加，复苏后120min显著高于休克前，并高于c组，此后逐渐下降；Lac在失血后显著升高，休克末达峰值，显著高于休克前和c组，以后逐渐下降。pH值、BE值在休克后逐渐下降，与c组相比有显著差异。结论失血性休克后NO、CO水平增加，可能作为两种内源性保护因子起作用。     

酚妥拉明对失血性休克家兔微循环血流动力学的影响

本研究旨在探讨酚妥拉明对失血性休克微循环血液灌流的作用.两组家兔——生理盐水对照组(n=7)和酚妥拉明治疗组(n=8),麻醉后放血至血压为5.33～6.00kPa以造成重度失血性休克.维持60min后将5mg酚妥拉明加入25ml生理盐水中静脉滴注(对照组仅滴注等量生理盐水),同时将放出的全部血液回输.观察休克及用药前后平均动脉血压、心率和肠系膜微循环变化.用显微电视录像静像步进技术测定毛细血管口径、血流速度及血流量.酚妥拉明滴往后,心率略加快,血压明显下降,血流速度和血流量显著降低,毛细血管口径两组间无明显差异.表明休克时酚妥拉明单独应用可使血压严重下降,从而加重肠系膜毛细血管的血流障碍.     

体外反搏对失血性休克犬大脑和皮肤微血管血流灌注的作用

应用激光多普勒测定微血管血流灌注技术，观察体外反搏提高灌注压力对失血性休克犬大脑皮层及皮肤微血管血流灌注的作用。结果显示，体外反搏可明显提高休克犬主动脉平均压力，增加休克犬大脑皮层及皮肤微血管血流灌注。在回输失血复苏后，对照组和反搏组主动脉平均压力恢复接近失血前水平，但反搏组微血管灌注的回升却明显高于对照组。结果提示体外反搏在犬失血性休克期预处理能改善其微循环障碍，有利于复苏期微血管的灌注     

失血性休克及复苏后内源性内毒素的变化及其意义

失血性休克及复苏后内源性内毒素的变化及其意义田昆仑蒋建新刁有芳陈惠孙刘韧刘萍（第三军医大学野战外科研究所，重庆６３００４２）创伤和外科手术中常合并失血性休克，且常伴内毒素（ＥＴ）移位，而ＥＴ移位与休克预后有密切联系，观察ＥＴ移位具有重要的临床意义。本...     

失血性休克患者血浆神经肽Y的含量变化

采用放射免疫分析法测定了３０例健康人、３１例轻度休克及３０例中度休克患者血浆神经肽Ｙ的含量。结果显示，轻度休克患者血浆ＮＰＹ含量明显高于正常对照组（ｐ〈０．０１）；中度休克患者血浆ＮＰＹ含量明显高于正常对照组（ｐ〈０．００１），也明显高于轻度休克组（ｐ〈０．０１）。血浆神经肽Ｙ含量增高与失血性休克的严重程度密切相关，提示神经肽Ｙ在休克的发病机理中可能起重要作用。     

川芎嗪对失血性休克家兔肠系膜毛细血管血流动力学的影响

家兔１６只，随机分为生理盐水对照组和川芎嗪治疗组，麻醉后造成失血性休克，用显微电视录像静像步进技术测定川芎嗪对小肠系膜毛细血管内径、血流速度及血流量的作用。结果提示，川芎嗪比对照组可加快失血性休克家兔小肠系膜毛细血管血流速度、改善肠系膜微循环血流灌注，但对毛细血管口径无明显作用。     

海水浸泡失血性休克大鼠血液动力学的变化

目的探讨21℃海水浸泡失血性休克大鼠时血液动力学的变化规律及其同平原失血性休克大鼠血液动力学变化的比较.方法Wistar大鼠20只,随机分为平原失血性休克组和海水浸泡失血性休克组.右颈总动脉插管至左心室,运用四道生理记录仪监测血液动力学指标;失血性休克模型快速放血至50mmHg,维持低血压30min.平原失血性休克组在21℃室温下观察和测定血液动力学,海水浸泡失血性休克组浸入21℃模拟海水中(海盐浓度为2.535%),监测动物入水后10、30、60、180、300min时及平原失血性休克组相应时相点的血液动力学指标.结果海水浸泡失血性休克组动物心率显著下降,从伤前时(433±40)teats/min,降至入水5h时的(120±80)teats/min,而平原失血性休克组动物5h时的心率(288±14)teats/min,是海水浸泡失血性休克组的2.4倍,差别非常显著(P＜0.01);海水浸泡失血性休克组动物浸泡各时相点LVSP、±dp/dtmax均较伤前显著下降,并随着浸泡时间的延长而下降更加明显,浸泡5h时LVSP降为伤前的40%、平原失血性休克组同时相值的63%;浸泡5h时+dp/dtmax从伤前10.50±1.41降至3.20±1.24,-dp/dtmax从伤前7.53±1.42降为1.70±1.11,分别为平原失血性休克组5h时LVSP、±dp/dtmax值的56.5%、59.2%、59.4%.海水浸泡失血性休克组动物入海水早期血压明显升高,30min后很快下降,并随着时间的增加下降越明显,浸泡5h时血压值仅为平原失血性休克组同时相点的57%.结论21℃海水浸泡失血性休克动物血液动力学状态明显恶化,动物心肌电兴奋性、心肌收缩力、心肌顺应性均下降,伤情显著重于平原失血性休克动物,因此在治疗时要更加注意心功能状况和输液速度,防止心力衰竭.     

失血性休克大鼠肠淋巴管压力的变化

目的 :探讨肠淋巴循环在失血性休克发生、发展和转归中的作用。方法 :应用肠淋巴管插管术 ,观察大鼠休克及补液过程中肠淋巴管压力的变化。结果 :休克初期 ,组间及组内的肠淋巴管压力均无显著性变化 (P >0 .0 5) ,休克期肠淋巴管压力比休克前及对照组显著降低 (P<0 .0 5～ 0 .0 1) ,回输血液及生理盐水 ,肠淋巴管压力迅速恢复且急骤升高 ,自补液 10min起 ,肠淋巴管压力明显高于实验前和对照组 (P <0 .0 5～ 0 .0 1)。血压虽有回升趋势但未完全恢复到休克前水平。停止输液后 ,肠淋巴管压力虽有所降低但仍高于实验前 (P <0 .0 5～ 0 .0 1) ,实验组输液后期淋巴管压力和血压之间呈直线相关 (r =0 .978,P <0 .0 1,y =0 .2 0 6x)。 结论 :失血性休克及补血补液时肠淋巴管压力的变化对休克的发展和康复具有重要的意义     

失血性休克再灌注后血浆内皮素的变化及磷酯酶A2阻断剂？…

家兔出血性休克再灌注（Ｓ／Ｒ）后，放名分析发现血浆内皮素逐渐升高，同失血前比较第６ｈ有显著差异（Ｐ〈０．０５），假手术组没有改变。磷脂酶Ａ２阻断剂氯喹、磷酸萘喹和抗氧化剂黄芪酮于失血后再灌注前使用可抑制Ｓ／Ｒ后２ｈ内血浆内皮素增高，后两者可更明显降低Ｓ／Ｒ后３０ｍｉｎ的内皮素水平，与的血前比较差异非常显著（Ｐ〈０．０１）。同时，ＨＣＯ３＾－和碱贮备（ＳＢＣ）显著降低，上述三种药物治疗显著增加ＨＣＯ     

Selective brain cooling achieves peripheral organs protection in hemorrhagic shock resuscitation via preserving the integrity of the brain-gut axis

Background: Although whole-body cooling has been reported to improve the ischemic/reperfusion injury in hemorrhagic shock (HS) resuscitation, it is limited by its adverse reactions following therapeutic hypothermia. HS affects the experimental and clinical bowel disorders via activation of the brain-gut axis. It is unknown whether selective brain cooling achieves beneficial effects in HS resuscitation via preserving the integrity of the brain-gut axis.Methods: Male Sprague-Dawley rats were bled to hypovolemic HS and resuscitated with blood transfusion followed by retrograde jugular vein flush (RJVF) with 4 °C or 36 °C normal saline. The mean arterial blood pressure, cerebral blood flow, and brain and core temperature were measured. The integrity of intestinal tight junction proteins and permeability, blood pro-inflammatory cytokines, and multiple organs damage score were determined.Results: Following blood transfusion resuscitation, HS rats displayed gut barrier disruption, increased blood levels of pro-inflammatory cytokines, and peripheral vital organ injuries. Intrajugular-based infusion cooled the brain robustly with a minimal effect on body temperature. This brain cooling significantly reduced the HS resuscitation-induced gut disruption, systemic inflammation, and peripheral vital organ injuries in rats.Conclusion: Resuscitation with selective brain cooling achieves peripheral vital organs protection in hemorrhagic shock resuscitation via preserving the integrity of the brain-gut axis.     

不同复苏压力对颅脑创伤合并非控制性失血性休克大鼠血流动力学及存活率的影响

目的探讨颅脑创伤合并非控制性失血性休克大鼠彻底止血前的理想复苏压力。方法制作大鼠颅脑创伤合并非控制性失血性休克模型,观察彻底止血前不同复苏压力(50 mmHg、60 mmHg、70 mmHg、80 mmHg和90 mmHg)对输液量、失血量、血流动力学、大脑灌注以及动物存活率的影响。结果不同复苏压力对颅脑创伤合并非控制性失血性休克的失血量有明显的影响,随着复苏压力的增加,大鼠的失血量、输液量逐渐增加,当复苏压力大于80 mmHg时,其失血量和输液量显著高于70 mmHg。当复苏压力小于70 mmHg时,随着复苏压力增加,脑含水量和血流量逐渐增加,70 mmHg复苏组脑含水量接近假手术组,而80 mmHg和90 mmHg组的血流量反而下降。血压维持在50 mmHg、60 mmHg、70 mmHg动物的存活时间和存活率明显高于常压(80 mmHg和90 mmHg)复苏组;50 mmHg、60 mmHg、70 mmHg组的血流动力学指标明显得到改善。结论对于颅脑创伤合并非控制性出血性休克,最理想的复苏压力是70 mmHg,它能改善血流动力学,降低脑水肿,提高动物存活率。     

Energy metabolism in the rat brain in the course of traumatic shock

The concentration of high-energy phosphates (ATP, creatine phosphate), the total content of adenyl nucleotides, and the energy potential of the brain cells did not change significantly in experimental animals after trauma to the soft tissues of the thigh, until the terminal phase. The intensity of glycolysis was increased. In the terminal phase anaerobic processes predominated somewhat over aerobic. The absence of changes in the concentration of high-energy phosphates in the rat brain in traumatic shock is probably associated with centralization of the circulation and it is evidence that no critical exhaustion of energy takes place in the brain.I. I. Dzhanelidze Leningrad Emergency Aid Scientific-Research Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR V. S. Il'in.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 78, No. 11, pp. 27–29, November, 1974.     

Morphologic changes in the pancreas in hemorrhagic shock and in the postresuscitation period

Laboratory of Pathomorphology, N. V. Sklifisovskii Moscow Emergency Aid Research Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR N. E. Permyakov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 108, No. 9, pp. 362–365, September, 1989.     

Changes in phospholipid composition of synaptic membranes in medulla oblongata and frontal lobes of the cerebral hemispheres in cats with hemorrhagic shock

We studied phospholipid composition of brain synaptic membranes isolated from cats with severe hemorrhagic shock. Changes in the medulla oblongata were most pronounced and manifested in decreased content of phosphatidylcholine. Changes in the phospholipid composition of synaptic membranes in the frontal lobes included an increase in phosphatidylinositol content and reduced content of phosphatidylserine. Accumulation of phosphatidylethanolamine in synaptic membranes was found in both the medulla oblongata and frontal lobes. These data help to understand the mechanisms underlying exhaustion of compensatory reserves in brain cells during severe hemorrhagic shock.     

Use of phosphatidylcholine liposomes for correction of mitochondrial phospholipid composition in the medulla oblongata and frontal lobes in hemorrhagic shock

Phosphatidylcholine liposomes normalize phosphatidylcholine and lysophospholipid levels in mitochondrial membranes of the medulla oblongata of cats with hemorrhagic shock. In the frontal lobes of brain hemispheres of liposome-treated cats, phospholipid levels in the mitochondria and their membranes are close to the norm, with the exception of phosphatidylserine and lysophosphatidylserine: their contents in the inner mitochondrial membranes remain below the control. It is concluded that phosphatidylcholine liposomes exert protect brain mitochondrial membranes in hemorrhagic shock. Translated fromByulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 123, No. 4, pp. 374–377, April, 1997     

休克肺发病学实验研究—肠道因素在休克肺过程中的作用

在网状内皮系统功能抑制的基础上,失血性休克可恒定地引起白细胞由肝脾释放,入肺扣押,并有肺系数明显增大和相应的肺结构损伤。这些现象可被隔离灌流肠道循环而全部消除;又可用内毒素补偿而使其完全重新再现。“肝脾释放”与“肺扣押”,“肺扣押”与肺系数增大,均呈明显正相关;而且肺系数增大与肺结构改变也是相符合的。     

环孢素A对严重创伤失血性休克大鼠的治疗作用

目的观察环孢素A(CsA)对创伤失血性休克大鼠的治疗作用。方法采用144只健康成年SD大鼠,分为正常对照组、休克对照组、乳酸林格氏液(LR)复苏组、CsA 1 mg/kg、5 mg/kg和10 mg/kg组。建立创伤失血性休克模型后,观察不同剂量CsA治疗对休克动物的存活时间和24 h存活率的影响,同时通过股动脉和左心室插管测定血流动力学指标,观察CsA对大鼠平均动脉血压(MAP)、左心室收缩压(LVSP)、左心室舒张末压(LVEDP)、左心室压力最大上升/下降速率(±dp/dtmax)和心率(HR)的影响。结果 CsA(5 mg/kg和10 mg/kg)可明显提高创伤失血性休克大鼠的存活时间和24 h存活率。休克后大鼠血流动力学指标包括MAP、LVSP、±dp/dtmax和HR都显著降低,LR复苏可使各项指标有所回升,但显著低于正常对照组;CsA(5 mg/kg和10 mg/kg)可明显升高LVSP和±dp/dtmax,在复苏2 h时明显高于LR组,并接近正常水平。结论 CsA显示出较好的抗创伤失血性休克作用,其中以5 mg/kg和10 mg/kg的给药剂量效果明显。