甲强龙对出血性休克大白鼠的影响

目的研究甲强龙(甲泼尼龙)对出血性休克大白鼠的影响并探讨其机制.方法大白鼠经动脉放血,造成失血性休克模型,随后用自体血和生理盐水从静脉回输,进行复苏.复苏前大白鼠随机分成三组假休克组,休克组和甲强龙治疗组.结果复苏后72 h,休克组的生存率降至20%,而甲强龙治疗组的生存率达80%,差异显著(P＜0.01).复苏后18h器官病理取材,H-E染色,光镜下显示休克组大白鼠的心、肺、肾、肝组织出现不同程度水肿、细胞变性、间质炎性细胞浸润等.甲强龙治疗组大白鼠的上述脏器的病理改变明显减轻.复苏后18 h,CK、Cr、ALT、AST、ALKP检测,休克组明显升高,而甲强龙治疗组只有轻度增高,差异非常显著(P＜0.01).复苏后2 h,肝脏枯否细胞用LPS刺激后,休克组的细胞内Ca2+浓度和TNF-α产量明显增高,而甲强龙治疗组轻度增高,差异显著(P＜0.01).结论甲强龙可以通过抑制kupffer细胞内Ca2+升高和激活,阻止TNF-α的过度产生,降低机体系统性炎症反应程度,最终减轻出血性休克大白鼠脏器的损伤和降低死亡率.     

糖皮质激素对出血性休克大鼠生存率的影响及对脏器的保护作用

目的研究糖皮质激素甲强龙和氢考对出血性休克大鼠生存率的影响,并探讨其机制。方法80只Wistar大鼠随机分成假休克组、休克组、甲强龙治疗组和氢考治疗组。经动脉放血建立大鼠出血性休克模型,随后采用自体血和生理盐水静脉回输进行复苏。结果复苏后72h,休克组大鼠的生存率明显低于甲强龙治疗组和氢考治疗组(P<0.01和P<0.05)。复苏后18h器官病理取材,光镜下显示休克组大鼠的心、肺、肾、肝组织出现不同程度水肿、细胞变性、间质炎性细胞浸润等,甲强龙治疗组和氢考治疗组大鼠上述脏器的病理改变明显减轻。复苏后2h,肝脏Kupffer细胞经脂多糖刺激后,休克组细胞内Ca2 浓度和肿瘤坏死因子α含量明显增高,而甲强龙治疗组和氢考治疗组轻度增高,差异显著(P<0.01)。结论甲强龙和氢考可以通过抑制Kupffer细胞内Ca2 升高和激活、阻止肿瘤坏死因子α的过度产生来降低机体全身炎性反应程度,最终减轻出血性休克大鼠脏器的损伤并降低死亡率。     

创伤性休克复苏后脏器缺血/再灌注损伤的实验研究

目的 观察创伤性休克复苏后大白鼠脏器缺血/再灌注损伤的病理学改变和特征.方法 Wistar大鼠用铁块从固定高度垂直落下砸击左侧大腿并同时放血来建立大白鼠创伤性休克模型,随后用自体血和生理盐水进行复苏,复苏前大鼠分成两组:对照组和休克组.结果 24小时后休克组中各脏器组织的病理变化明显:间质细胞增多,组织内大量炎性细胞浸润,毛细血管扩张、充血,微血管内可见微血栓形成,细胞肿胀、变性和坏死;病理损伤评分均显著重于对照组(P＜0.05).结论 创伤性休克复苏后组织脏器存在明显的病理变化,动物实验证实,创伤性休克复苏后脏器缺血/再灌注损伤向多器官功能障碍综合征(MODS)转变存在病理学特征和基础.     

雷米芬太尼与苏芬太尼对失血性休克鼠肺内中性粒细胞聚集激活的对比研究

目的 :观察失血性休克大鼠血中丙二醛 (MDA)、超氧化物歧化酶 (SOD)含量及肺内髓过氧化物酶(MPO)活性的变化 ,探讨雷米芬太尼和苏芬太尼对失血性休克大鼠炎性 /应激反应的影响。方法 :健康SD大鼠 72只 ,雌雄不拘 ,体重 2 5 0～ 30 0 g ,建立改良Wigger失血性休克模型 ,股动脉放血使平均动脉压降至 (5 .33± 0 .6 6 )kPa,维持 180min ;随机分为三组 :对照组、雷米芬太尼组、苏芬太尼组 ,后两组分别在复苏开始时静脉持续输注雷米芬太尼 0 .5 μg/ (kg·min)或苏芬太尼 0 .0 5 μg/ (kg·min)。在休克前、休克、复苏 2h、复苏 4h ,观察上述指标的变化。每组每个时间点的动物数为 6只。结果 :动物休克时血中MDA含量升高 ,在对照组和苏芬太尼组 ,MDA含量持续升高 ;复苏 2h和 4h的含量约为休克前、休克时的 1.8～ 2倍 (P <0 .0 5 )。静脉输注雷米芬太尼 ,血中MDA含量升高不明显 ,复苏各时间点与休克前相比均无显著性差异 (P >0 .0 5 )。复苏 2h、4h ,雷米芬太尼组与对照组和苏芬太尼组相比 ,差异显著 (P <0 .0 5 )。血中总SOD、肺内MPO的变化与MDA相似 ,复苏 2h、4h雷米芬太尼组与对照组和苏芬太尼组相比 ,有显著性差异 (P <0 .0 5 )。结论 :MDA、总SOD和MPO是反映肺内中性粒细胞聚集、激活的敏感指标。等效剂     

低压复苏治疗未控制性出血性休克的作用

目的:通过检测血内皮素和乳酸的动态变化,探讨低压复苏治疗未控制性出血性休克的作用.方法: 建立未控制性出血性休克模型,分为低压复苏组和传统复苏组;假休克组作对照组.于休克初期、休克末期、充分复苏结束后和观察期末测定血乳酸和内皮素浓度.结果:(1)低压复苏组和传统复苏组乳酸和内皮素水平较假休克组各时间点明显增高,差异有统计学意义(P＜0.05),休克末达到最高水平.(2)休克初期传统复苏组和低压复苏组乳酸和内皮素差异无统计学意义(P＞0.05),其他时间段传统复苏组比低压复苏组均明显增高,差异有统计学意义(P0＜.05);低压复苏组乳酸和内皮素复苏后下降趋势更明显.结论:低压复苏比传统复苏有更低血乳酸和内皮素水平,而且复苏后下降趋势更明显.提示低压复苏的方法能改善微循环和减轻酸中毒,复苏的效果和预后更好.     

高渗氯化钠羟乙基淀粉溶液对大鼠非控制出血性休克复苏的保护作用

目的探讨高渗氯化钠羟乙基淀粉溶液(hypertonic sodium chloride hydroxyethyl starch 40,HHS)对大鼠非控制出血性休克(uncontrolled hemorrhagic shock,UHS)复苏的保护作用。方法采用修订的Capone等方法制备创伤UHS模型。用随机数字表法将30只SD大鼠随机分为3组:正常对照组(NC组)、生理盐水复苏组(NS组)、高渗氯化钠羟乙基淀粉溶液复苏组(HHS组)。NS组及HHS组大鼠经动脉放血,使血压降至40 mmHg,然后在距鼠尾根部1/4处断尾,造成活动性出血。分别给予生理盐水和HHS输注,使平均动脉压(MAP)维持在50 mmHg。复苏1 h后,两复苏组均给予手术止血、回输血液及给予足量的液体输注,保持MAP 90 mmHg,充分复苏2 h后,将大鼠放回笼内观察。分别于伤后0、30、90、210 min观察大鼠的心率(HR);血气指标包括pH、碱剩余(BE)、乳酸(LAC)、动脉血氧分压(PaO2);凝血功能指标包括凝血酶原时间(PT)、部分凝血活酶时间(APTT);各脏器功能指标包括磷酸肌酶激酶同工酶(CKMB)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、肌酐(Cr)以及出血量、输液量、存活率。结果大鼠休克后的HR显著下降,复苏后HHS组与NS组HR明显升高(P<0.05);休克大鼠的pH、BE、PaO2下降,LAC明显升高,复苏后与NS组比较,HHS组的pH、BE、PaO2增高,LAC显著下降(P<0.05);休克大鼠的PT、APTT明显延长(P<0.05),复苏后HHS组PT、APTT均短于NS组(P<0.05);休克后大鼠的CKMB、ALT、AST、Cr明显增高,复苏后,HHS组大鼠的CKMB、ALT、AST、Cr低于NS组(P<0.05);同时与NS组比较,HHS组大鼠活动性出血量和出血急救期输液量明显减少,且24 h及72 h存活率显著增高(P<0.05)。结论 HHS对UHS大鼠早期有较好的复苏效果。     

不同复苏液体对"二次打击"致多器官功能障碍综合征的影响

目的:探讨不同复苏液体对"失血性休克 内毒素"二次打击致大鼠多器官功能障碍综合征(MODS)的影响。方法:SD大鼠90只,随机分为正常对照组、乳酸林格液复苏组和高渗盐水复苏组3组,每组各30只。先采用通过颈动脉插管放血的方法复制大鼠失血性休克的动物模型,维持平均动脉压(MAP)在35~40mmHg1h后进行液体复苏,乳酸林格液复苏组用乳酸林格液复苏,高渗盐水复苏组用7.5%高渗盐水复苏。复苏成功后30min腹腔注入内毒素复制大鼠MODS模型,分别在注射内毒素后24h和36h取血和收集相关标本,观察各组大鼠主要器官功能指标、MODS发生率以及死亡率的变化。结果:乳酸林格液复苏组、高渗盐水复苏组2组氧分压(PaO2)、谷丙转氨酶(ALT)、尿素氮(BUN)和肌酸激酶(CK)等主要器官功能指标在24h和36h均高于正常对照组,差异有统计学意义(P<0.01)。同时高渗盐水复苏组PaO2、ALT、BUN和CK在24h和36h(除PaO2)高于乳酸林格液复苏组,差异有统计学意义(P<0.01)。MODS发生率高渗盐水复苏组为20.8%,较乳酸林格液组(41.7%)明显降低(P<0.05)。高渗盐水复苏组大鼠48h内死亡率为14.2%,较乳酸林格液复苏组(28.6%)明显降低(P<0.05)。48~72h高渗盐水复苏组大鼠死亡率为21.4%,明显低于乳酸林格液复苏组(35.7%),差异有统计学意义(P<0.05)。结论:7.5%高渗盐水复苏失血性休克可明显减轻失血性休克复苏后大鼠再次予以内毒素打击时所引起的重要脏器功能损害,并且可明显降低MODS的发生率和死亡率。     

复苏压力对大鼠未控制出血性休克早期复苏效果的影响

目的比较不同的复苏压力对大鼠未控制出血性休克（uncontrolled hemorrhagic shock,UHS）早期复苏效果的影响。方法采用脾脏损伤的未控制出血性休克模型。48只SD大鼠根据早期复苏压力的不同分为6组：不复苏组（对照）和40、50、60、70、80mmHg复苏组,每组8只。伤后平均动脉压（mean arterial pressure,MAP）降至40mmHg时开始低压复苏,用乳酸林格液加羟乙基淀粉（2：1比例）复苏,使MAP维持在各组设定的水平,持续1h,对照组此期不输注任何液体,然后结扎脾动脉止血,各组均行充分复苏2h。记录各组血流动力学、失血量、血细胞比容、血气、肝功及存活时间。结果60、70、80mmHg复苏组的出血量显著高于另3组（P〈0．05）,50mmHg复苏组的存活时间显著长于对照组和80mmHg复苏组（P〈0．05）。40mmHg复苏组和80mmHg复苏组的血流动力学指标显著低于50、60、70mmHg复苏组（P〈0．05）。70、80mmHg复苏组的酸中毒显著轻于40mmHg复苏组（P〈0．05）。40～60mmHg复苏组的血细胞比容显著高于80mmHg复苏组（P〈0．05）。40mmHg复苏组的肝功指标显著高于50、60、70mmHg复苏组（P〈0．05）。结论未控制出血性休克的早期复苏中,血压过高会增加出血量,缩短存活时问;血压过低则抑制心功能,加重肝功能损害。血压在50～60mmHg较为合适。     

腹腔复苏对失血性休克家兔肝脏功能的影响

目的 观察腹腔复苏对失血性休克家兔肝脏功能的影响。方法 21 只雄性家兔随机分为3组,正常对照组 (A组) 、常规静脉复苏组（B组）、腹腔复苏组（C组）。B组与C组于10min 内使MAP降至40mmHg。通过放血或回输血液维持40mmHg 水平60min后,在20min内静脉回输放出的血液和两倍于放血量的复方乳酸钠进行液体复苏,并于血液和液体复苏的同时,C组腹腔内注射120mL临床用透析液,而A组和B组腹腔注入等量生理盐水对照。观察休克前、休克后60min、液体复苏后60min和180 min的ALT和AST活性。复苏3h后,取肝组织测定干湿重比、MDA、SOD,观察形态学变化。结果 C组ALT和AST值均低于B组( P<0.05 ),MDA与SOD活性分别低于和高于B组 (P<0.05)。C组组织的干湿重比值高于B组(P<0.05);B组形态学损伤较C组更明显。并且与正常对照组组相比结果相近。结论 腹腔复苏对失血性休克家兔足量液体复苏后的肝脏功能可能有改善作用。 [关键词] 失血性休克 ;腹腔复苏;肝脏功能     

不同液体复苏对脑组织核因子-κB和肿瘤坏死因子-α表达的影响

目的 探讨不同液体复苏对脑组织核因子κB（NF-κB）和肿瘤坏死因子-α（TNF-α）表达的影响。方法 采用大鼠股动脉放血休克模型，实验组大鼠休克1h后分别用2倍出血量的6％羟乙基淀粉（贺斯）、1倍出血量的贺斯加1／2出血量的自体血、3倍出血量的复方氯化钠液（林格液）、2倍出血量的林格液加1／2出血量的自体血和全部白体血复苏30min，假手术组大鼠无休克、无复苏。取脑组织经苏木精伊红染色观察其病理改变；采用免疫组织化学法检测脑组织中NF-κB和TNF-α的表达。结果 除假手术组外，各实验组脑组织均有不同程度的水肿和炎性细胞浸润等早期炎症表现，且实验组脑组织NF-κB和TNF—α表达较假手术组显著增加（P〈0．01）。实验组大鼠分别经1倍出血量的贺斯加1／2出血量的自体血、2倍出血量的林格液加1／2出血量的自体血、3倍出血量的林格液复苏后，NF-κB和TNF-a的表达明显低于2倍出血量的贺斯和全部自体血复苏组（P〈0．05或P〈0．01）。各组NF-κB与TNF-α变化具有显著正相关（r=0．805，P〈0．01）。结论 出血性休克复苏早期，采用常规量的贺斯加1／2出血量的白体血、2倍出血量的林格液加1／2出血量的白体血或3倍出血量的林格液复苏可降低脑组织NF-κB和TNF—α的表达，从而减轻出血性休克液体复苏后的脑损伤。     

Distribution of endotoxins in tissues and circulation and its effects following hemorrhagic shock

OBJECTIVE: To systemically investigate 1) distribution of endogenous endotoxin (ET) in tissues and circulation; 2) its relationship with shock duration and organ damage; and 3) its possible mechanism after hemorrhagic shock. METHODS: To further elucidate the intrinsic relationship between endogenous endotoxin translocation and hemorrhagic shock, the present study systematically investigated the distribution of endogenous ET into the liver, lungs, kidneys and circulation, and the relationship between ET levels and the corresponding organ dysfunction with limulus amebocyte lysate (LAL) chromogenic assay following hemorrhagic shock in rats. RESULTS: It was found that ET levels in hepatic homogenate markedly increased (P = 0.09) 1.5 hours following shock compared with that in the sham group. After resuscitation, ET levels in hepatic, pulmonary and renal tissues were all significantly elevated. The levels kept increasing with the prolonged experimental time, and reached as high as 3.88 +/- 0.95 EU (endotoxin unit)/g in the livers, 2.53 +/- 1.46 EU/g in the lungs and 2.51 +/- 0.89 EU/g in the kidneys 12 hours after shock. ET levels in plasma reached a peak of 1.13 +/- 0.42 EU/ml at 1 hour following resuscitation, then rapidly decreased to the sham levels 3 hours following resuscitation. There was a close relationship between endotoxin translocation and shock duration. Correlation analysis further indicated that the changes in glutamic-pyruvic transaminase (GPT), blood urea nitrogen (BUN) in plasma and angiotensin I-converting exzyme (ACE) in pulmonary homogenate were significantly and positively correlated with the ET levels in the liver, kidneys and lungs after hemorrhagic shock. CONCLUSIONS: Hemorrhagic shock can induce obvious endogenous ET translocation, which is closely related to the shock duration. Although only transient endotoxemia occurs after hemorrhagic shock, ET can massively accumulate in tissues (liver, lungs and kidneys), and may play an important role in the development of shock.     

Effects of glycine and methylprednisolone on hemorrhagic shock in rats

Background Methylprednisolone (MP), a synthetic glucocorticosteroid, has been broadly studied in experiments on endotoxin-induced shock and septic shock. This study was designed to ascertain whether glycine and MP can protect against organ injury and death caused by hemorrhagic shock, and to elucidate the underlying mechanisms of these protective effects in rats.Method To establish a shock model, Wistar rats were bled to maintain mean arterial pressure at 30-50 mmHg for 1 hour and subsequently resuscitated with the shed blood and normal saline. Just prior to resuscitation, the rats were randomly assigned to four groups: sham group (operation performed without inducing shock), shock group, shock+glycine group (glycine injected at the beginning of resuscitation) and shock+MP group (MP injected at the beginning of resuscitation).Results ① Seventy-two hours after resuscitation, the survival rate of rats from the shock group had decreased to 20%, while the survival rates of rats from the shock+glycine and shock+MP groups were 77.8% and 80%, respectively. The difference was significant (P&lt;0.05). ② Eighteen hours after resuscitation, pathological alterations in the organs of the rats were apparent. In rats from the shock group, edema, interstitial leukocyte infiltration, and cellular degeneration occurred in the liver, lungs, kidneys, and heart. Glycine and MP reduced these pathological changes significantly. ③ Eighteen hours after resuscitation, the levels of creatine phosphokinase, transaminases, and creatine were elevated significantly in rats from the shock group, indicating injury to the heart, liver, and kidneys, while these levels were elevated only slightly in the shock+glycine and shock+MP groups. The differences were significant (P&lt;0.01). ④ There were significant increases in intracellular calcium and production of tumor necrosis factor (TNF-α) by isolated Kupffer cells stimulated by endotoxin after hemorrhagic shock. These changes were completely prevented by glycine and MP (P&lt;0.01). Conclusion Glycine and MP reduce organ injury and mortality caused by hemorrhagic shock by preventing increase of intracellular calcium levels in Kupffer cell, suppressing Kupffer cell activation, decreasing the production of TNF-α by Kupffer cells, and blocking systemic inflammatory responses.     

高容量血液滤过防治MODS过程中内毒素受体及炎性细胞因子的变化及意义

目的：探讨高容量血液滤过（high volume hemofiltration,HVHF）防治多器官功能障碍综合征（multiple organ dysfunction syndrome,MODS）过程中内毒素（LPS）受体及炎性细胞因子的变化及其关系。方法：建立二次打击（失血性休克＋再灌注损伤＋内毒素复合因素）猪MODS模型。19只猪随机分为MODS组（M组,9只）及HVHF组（HF组,10只）。M组为模型组,HF组在建模后实施高容量血液滤过,观察7 d后处死动物。流式细胞仪检测外周血单核细胞CD14、TLR4的表达变化,ELISA法检测血浆及滤液中TNFα、IL-10、IL-6浓度,并观察抗炎/促炎因子的比率变化。结果：HF组MODS发生率为2/10,死亡率为2/10,显著低于M组（P〈0.01）。M组CD14、TLR4的表达在LPS注射后维持在较高水平;HF组CD14、TLR4的表达在滤过前同M组相似,但滤过后逐渐降低,各时间点与M组相比差异有统计学意义。滤过治疗开始后,TNFα、IL-10浓度开始下降,且明显低于治疗前水平,并维持在一个比较稳定的浓度,治疗后各时间点与M组相比差异有统计学意义;IL-6在治疗后虽有轻度上升,但治疗后各时间点较M组水平仍有显著下降;HF组IL-10/TNFα比率随治疗时间的延长保持在比较稳定的状态。结论：HVHF能有效降低血浆细胞因子水平,使得抗炎和促炎两方面趋于动态平衡;并可通过此途径下调CD14、TLR4受体的表达水平。     

失血性休克合并内毒素血症兔肺cAMP反应元件结合蛋白表达和活性的变化

目的探讨失血性休克合并内毒素血症诱发急性肺损伤（ALI）兔肺cAMP反应元件结合蛋白（CREB）表达和活性的变化。方法采用家兔失血性休克合并内毒素血症诱发肺损伤模型,36只家兔随机分为：造模后2h组,造模后12h组和对照组。分析动脉血氧分压（PaO2）、肺湿重／干重（W／D）和肺组织病理学改变,用酶联免疫吸附法（ELISA）检测肺组织匀浆肿瘤坏死因子（TNF）-α含量,Western印迹检测肺组织CREB蛋白的表达,凝胶电泳迁移率（EMSA）法检测CREB／DNA结合活性：结果病理学显示造模后12h组肺泡结构破坏,肺泡壁和肺间质内有大量中性粒细胞浸润和较多红细胞渗出,造模后2h组病变轻微。造模后12h组PaO2显著低于对照组（55．0±11．0 mmHg vs 92．9±14．6mmHg;P〈0．01）,W／D高于对照组（5．5±1．1 vs 3．5±0．8;P〈0．01）,而造模后2h组与对照组比较变化不明显;造模后12h组肺组织匀浆中TNF-α含量显著高于对照组（491．6±59．2pg／m vs 159．3±44．9pg／ml;P〈0．01）,而造模后2h组与对照组比较变化不明显。造模后2h组和12h组肺组织CREB蛋白的表达量均显著高于对照组（0．874±0．182,0．775±0．258 vs 0．483±0．199;P〈0．01）,造模后2h组和12h组CREB／DNA结合活性也显著高于对照组（355±79,330±108vs185±68;P〈0．01）。结论失血性休克合并内毒素血症促进了肺组织CREB的表达和活化,CREB可能通过促进炎症因子的表达而参与了急性肺损伤的炎症反应过程。     

血管黏附蛋白1在大鼠重症失血性休克中的表达

目的 观察重症失血性休克及复苏过程中大鼠小肠及血清中血管黏附蛋白1(VAP-1)的表达和活性变化,探讨抑制其功能对休克预后的影响.方法 将实验大鼠随机分为假手术组、休克组、休克复苏组、复苏对照组和复苏实验组,每组10只.建立重症失血性休克及复苏大鼠模型,采用蛋白质印迹和real-time RT-PCR法检测假手术组、休克组、休克复苏组休克前、休克1h、复苏1h时小肠组织中VAP-1表达及其编码基因含量,ELISA法检测血清中VAP-1含量及其活性.复苏实验组加用20 mg/kg 2-溴乙胺,复苏对照组加用1 mL/kg生理盐水,比较两组复苏后的血压、复苏24 h后小肠黏膜损伤情况(Chiu's评分)和小肠黏膜上皮细胞凋亡情况(TUNEL),并比较大鼠24 h生存率.结果 重症失血性休克组大鼠小肠组织VAP-1蛋白水平以及其编码基因mRNA水平、血清中VAP-1含量及其活性均较假手术组升高(均P＜0.05),复苏后上述各值均有所下降,但仍高于假手术组.相对于生理盐水对照组,休克复苏后1h和24 h使用20 mg/kg2-溴乙胺的复苏实验组大鼠血压升高(P值分别为0.010和0.039),且复苏实验组Chiu's评分及肠黏膜上皮细胞凋亡指数均低于生理盐水复苏对照组(P值分别为o.022和0.002),休克大鼠24 h生存率也高于复苏对照组(90％vs 60％).结论 重症失血性休克能使大鼠VAP-1的表达、活性增高,而液体复苏能减轻这种增高;抑制其活性能改善重症失血性休克及复苏后的低血压以及小肠黏膜的损伤和细胞凋亡,提高大鼠24 h生存率.     

灵光注射液对失血性休克大鼠胃肠粘膜的保护作用

目的　观察灵光注射液 (复方樟柳碱 )对失血性休克再灌注大鼠胃肠粘膜损伤的影响。方法　将 5 6只雄性Wistar大鼠随机分 4组 ,分别设为假休克组 (8只 )、模型组 (16只 )、灵光注射液低剂量组 (16只 )和高剂量组(16只 ) ,除假休克组外 ,大鼠均经历 4kPa ,70min的失血性休克 ,在休克复苏后 6h和 12h各组分别处死半数动物 ,观察大鼠肠道菌移位情况、病理组织学和超微结构变化。结果　灵光注射液对大鼠失血性休克再灌注引起的肠道细菌移位和胃肠粘膜形态损伤有明显的保护作用 ,其治疗机制可能与改善微循环、清除氧自由基作用有关     

连续性血液透析滤过在多器官功能障碍综合症试验犬应用管理与效果观察

目的观察连续性血液透析滤过(CVVHDF)治疗在多器官功能障碍综合症(MODS)试验犬的治疗效果,探讨CVVHDFD管理措施在治疗MODS的效果,为临床患者CVVHDF的治疗管理提供依据。方法 15只Beagle犬采用失血性休克+复苏灌注+内毒素血症建立MODS模型,随机分为CVVHDF组(n=8)和MODS组(n=7)。内毒素注射完毕后CVVHDF组接受CVVHDF治疗12 h;MODS组未接受CVVHDF治疗。CVVHDF组实施系统管理,观察要点:观察CVVHDF治疗过程中试验犬生命指征的变化和重要脏器功能变化,实施心电监测,呼吸机辅助呼吸,保证机器正常运转,维持体外循环通道畅通,准确按时留取。结果 CVVHDF组8只试验犬的连续12 h的治疗均顺利完成,各主要器官功能明显改善,平均动脉压基本保持在正常水平,尤其在6、3、9、及12h时间点显著高于MODS组,差异均有统计学意义(P<0.01)。PaCO2逐渐升高与MODS组在3、6、9及12 h比较,差异均有统计学意义(P<0.01)。结论连续性血液透析滤过能明显改善内毒素诱导的低血压,提高动脉血氧分压;能改善主要脏器功能,稳定内环境。有效的CVVHDF管理措施,可以保证治疗的顺利完成,达到治疗预期目标。     

Study on delay two-phase multiple organ dysfunction syndrome

OBJECTIVE: To study the injury factors, pathogenic process and clinical features of delay two-phase multiple organ dysfunction syndrome (MODS) in severe burned patients and to replicate a standardized animal model that would accurately imitate the clinical features of MODS. METHODS: Forty-five human patients with burn size larger than 30% total body surface area (TBSA) were analyzed. All of them underwent severe burn shock in early stage and sepsis in late stage. Thirty-two goats were randomly divided into three groups: 1) hemorrhagic shock (group H, n = 6); 2) endotoxemia (group E, n = 6); and 3) hemorrhagic shock plus endotoxemia (group M, n = 20). Hemorrhagic shock was produced according to the method of Wigger (6.7 kPa for an hour, 1 kPa = 7.5 mmHg). Endotoxin (E. coli O111 B4) was given via the portal vein 24 hours after the resuscitation of hemorrhagic shock, in a dose of 30 ng/kg/min for 5 consecutive days. During the observation period of 10 days, all animals were hemodynamically monitored, given standard metabolic support and due cardiac and pulmonary support according to human intensive care. RESULTS: All the patients showed burn shock at 1-3 days and hyperdynamic circulation, hypermetabolism and systemic inflammatory responses over two weeks post-injury. Thirteen cases were found to develop MODS according to the prevailing diagnostic criteria, and 10 of them died with a mortality of 77%. Eighteen animals died in group M with a mortality of 90%, 12 of the 18 developed MODS, with overall incidence of 60%. Most animals in group M showed changes similar to that observed in human cases. The experimentation proved that in the pathogenic process of MODS, there was a two-hit phenomenon in the dvelopment of the syndrome. To prevent the development of MODS, it therefore was imperative to blunt the first hit or the second hit, so that an excessive inflammatory response was alleviated. This postulation has been verified in the treatment of extensive burns. Two patients with burn extent reaching 100% TBSA survived with only mild acute respiratory distress syndrome (ARDS) and renal dysfunction after comprehensive treatment of burn shock, including adequate fluid resuscitation, drugs to remove oxygen free radicals, rapid restoration of pHi, and early extensive excision of burn eschars. CONCLUSION: Both in human patients or animal experimentation, the typical delay two-phase MODS is shown to be produced by two successive insults in the forms of hypovolemic shock and sepsis. This postulation is helpful in formulating the prevention and treatment modality of MODS.     

连续性血液透析滤过在多器官功能障碍综合征犬中的器官支持作用

目的:探讨连续性血液透析滤过(CVVHDF)对多器官功能障碍综合征(MODS)犬的多器官支持治疗作用。方法:15只雄性Beagle犬,采用失血性休克 复苏灌注 内毒素血症复制MODS模型,随机分为CVVH-DF组(n=8)和MODS组(n=7),CVVHDF组在内毒素注射完毕后给予CVVHDF治疗12 h,MODS组不给予CVVHDF治疗。观察两组动物体温、血压、心率、全血白细胞计数和各器官的功能指标变化。结果:体温、血压、心率、全血白细胞计数指标在CVVHDF治疗后均明显好转;CVVHDF组治疗过程中,平均动脉压(MAP)基本保持在正常水平,尤其在T5、T6及T7时间点显著高于MODS组(P<0.01);PaO2逐渐升高,与MODS组在T4、T5、T6及T7时间点相比差异有统计学意义(P<0.05);血清肌酐(Cr)、血尿素氮(BUN)水平与MODS组在T4、T5、T6及T7时间点相比显著降低(P<0.05);结论:CVVHDF对MODS不但有肾代替作用,而且有呼吸、循环、酸碱和电解质内环境的平衡等多器官支持、治疗作用。