高渗盐胶体对失血性休克大鼠小肠黏膜形态的影响

目的:研究小容量高渗盐羟乙基淀粉液(HSH)复苏失血性休克大鼠时肠黏膜形态的变化和血清NO浓度变化.方法:SD大鼠麻醉后放血致平均动脉压40mmHg±5mmHg,维持30min,SD大鼠随机分成3组:(1)高渗盐羟乙基淀粉复合液+回输失血(HSH组);(2)乳酸林格液复苏+回输失血(LR组);(3)假休克组,只进行血管置管;观察休克前后血浆NO浓度的动态变化,并留取小肠组织观察病理改变.结果:HSH组大鼠复苏后血浆NO无明显下降,复苏前(30.03μmol/L±4.77μmol/L)和复苏后(27.33μmol/L±8.76μmol/L)比较,无显著差异(P>0.05),小肠的病理损伤也显著减轻.LR组血浆NO浓度明显降低,复苏前(28.37μmol/L±6.24μmol/L)和复苏后(17.48μmol/L±5.24μmol/L)比较,有显著差异(P<0.05),小肠的病理损伤无明显改善.结论:应用HSH有助于改善失血休克引起的肠道损伤;其机制可能与HSH减少内皮细胞功能损害有关.     

RL联合PTX对重度失血性休克大鼠肺缺血再灌注损伤的影响

目的探讨乳酸钠林格液（RL）联合己酮可可碱（PTX）复苏对重度失血性休克大鼠肺缺血再灌注损伤的保护作用及机制。方法将48只健康雄性SD大鼠随机分为对照组、模型组、RL组及RL＋PTX组各12只,后三组均采用改良Wigger′s法制备重度失血性休克模型,模型制备成功后RL组予3倍失血量的RL复苏;RL＋FTX组复苏方案同RL组,但复苏液中加入PTX;对照组仅行麻醉。分别于休克前、复苏前及复苏后1、2,4h检测四组呼吸指数（RI）;复苏后4h检测肺通透指数、肺湿干质量比（W／D）,观察肺组织病理学变化并进行肺损伤评分,测定肺组织中基质金属蛋白酶-2（MMP-2）和IL-8水平。结果与对照组比较,其余三组啼损伤评分、肺W／D、肺通透指数均显著升高,尤以RL组和RL＋FIX组为著（P均〈0．05）;与RL组比较,RL／PTX组RI、肺通透指数、肺W／D显著降低,肺组织病理学变化显著减轻,肺损伤评分显著减少,肺组织MMP-2、IL-8水平显著降低（P均〈O．05）。结论 RL联合FTX复苏可显著减轻重度失血性休克大鼠肺缺血再灌注损伤,可能机制为抑制肺组织内IL-8和MMP-2生成而减轻炎性反应。     

不同晶体溶液在自体血液回收中的应用比较

目的:观察失血性休克患者自体血液回收中输注不同晶体溶液的临床应用效果。方法:以106例失血性休克急诊手术患者为研究对象。按入院顺序将106例患者分为醋酸组和乳酸组,奇数入醋酸组,偶数入乳酸组,每组53例,在自体血液回收时醋酸组应用醋酸林格氏液,对照组应用乳酸林格氏液。监测所有患者术前、自体血回输后2、24h的平均动脉压(MAP)、心率(HR)和毛细血管充盈时间(CFT),以及静脉血红细胞(RBC)、血红蛋白浓度(HGB)。观察2组患者术前失血量、术后回收血量及术中输血反应情况,比较2组患者术前和术后24h血乳酸水平、血小板计数(PLT)及肝功能(GTP)情况。结果:1106例急诊手术患者术中自体血均经血液回收机回收,回输后MAP比术前明显增高,HR比术前明显降低,CFT比术前明显缩短,而RBC、HGB与术前相比均有明显提高,差异均有统计学意义(P0.01或0.05)。2 2组患者术前失血量、术后回收血量及术中输血反应发生率比较,差异无统计学意义(P0.05)。2组术前血乳酸水平、PLT及GPT差异无统计学意义(P0.05)。醋酸组血乳酸水平、GPT术后24h与术前相比差异无统计学意义(P0.05),但乳酸组术后24h比术前明显升高(P0.01);醋酸组术后24h血小板计数明显升高(P0.01),与乳酸组比较差异有统计学意义(P0.01)。结论:自体血回收中应用醋酸林格氏液可改善血液质量,防止血乳酸水平明显升高,同时对血小板和GTP也具有一定的保护作用。     

平衡盐液在休克手术病人中的应用

乳酸钠林格氏液(简称平衡盐液)有抗休克及补充血容量的作用,并有减少输血并发症及弥补血源不足的特点。我院用平衡盐液治疗休克手术病人34例,其中失血性休克12例,创伤并失血性休克20例,中毒性休克2例。术前测不到血压者6例,收缩压低于     

腰麻联合硬膜外麻醉下应用贺斯预防低血压的临床研究

目的 :比较 6 0 ml/ L 贺斯 （HES）和乳酸林格氏液对预防腰麻联合硬膜外麻醉 （CESA）下低血压的作用。方法 :CESA择期行妇科手术患者 2 2例 ,随机分为两组 ,静脉输注 6 0 ml/ L 贺斯或乳酸林格氏液 5 0 0 ml,观察收缩压（SBP）、舒张压 （DBP）、心率 （HR）和脉搏血氧饱和度 （SPO2 ）的变化。结果 :两组患者上述指标基本稳定 ,与基础值相比 ,差异不显著 （P>0 .0 5 ）。结论 :输注 6 0 ml/ L 贺斯或乳酸林格氏液均能有效地防止 CESA后血压降低 ,两者作用无明显差异     

不同液体复苏策略对失血性休克大鼠血浆代谢指标的影响

目的探讨不同液体复苏策略对失血性休克(HS)大鼠血浆代谢指标的影响。方法将50只260~280 g雄性SD大鼠随机分为假手术组(C组)、无液体复苏组(NF组)、乳酸林格液组(LRS组)、羟乙基淀粉组(HES组)和LRS+HES组,待休克稳定1 h后进行相应液体复苏,2 h后抽血,检测各组血浆中的乳酸、丙酮酸、葡萄糖和丙酮水平,同时采用比色法检测各组血浆天门冬氨酸氨基转移酶(AST)、肌酸激酶(CK)、碱性磷酸酶(ALB)和丙氨酸氨基转移酶(ALT)活性。结果与C组相比,NF组的乳酸、葡萄糖水平均降低,丙酮酸、丙酮水平均升高(均P0.05);除LRS+HES组的乳酸外,LRS组、HES组和LRS+HES组的其他各指标与C组均有统计学差异(均P0.05);除LRS组的乳酸外,LRS组、HES组和LRS+HES组的其他各指标均优于NF组(均P0.05);其中,LRS+HES组的4项指标均优于LRS组和HES组(P0.05)。各组间ALT、AST、CK和ALB活性均无统计学意义(均P0.05)。结论 HS大鼠血浆代谢指标紊乱,给予及时限制性液体复苏可缓解HS的代谢紊乱,以LRS联合HES的效果最好。     

西沙必利对大鼠失血性休克复苏后胃损害的作用

目的：观察西沙利对大鼠失血性休克复苏后胃损害的作用。方法：108例只Wistar大鼠随机分为假休克（SS）组、失血性休克复苏（HS）组和失血性休克复苏后西沙必利治疗（HSC）组，同位素标记生物微球法测量胃血流量，同时测定胃粘膜内pH(pHi)、胃排空、胃MDA含量和Na^ -K^ -ATPase活性，以及门静脉血乳酸水平。结果：HSC组与HS相比，大鼠胃内色素相对残留低率显降低，胃血流量显下降，胃pHi有显回升，4h胃粘膜MDA含量降低、Na^ -K^ -ATPase活性增加，门静脉血乳酸水平显下降。结论：失血性休克复苏后西沙必利促胃动力治疗，通过增加胃血流量，有助于改善复苏后持续存在的胃缺血缺氧状况。     

失血性休克大鼠内皮细胞蛋白C受体表达的研究

30只健康SD大鼠随机分为正常对照组、假休克组、失血性休克组,采用ELISA、RT-PCR、Western blot技术分别对3组血浆中可溶性内皮细胞蛋白C受体(sEPCR)水平和小肠组织EPCR mRNA及蛋白的表达进行检测.发现失血性休克组sEPGR平均水平较正常对照组、假休克组增高;失血性休克组EPCR mRNA平均水平较正常对照组、假休克组明显增高,失血性休克组:EPCR蛋白水平较正常对照组、假休克组明显下降.认为失血性休克大鼠外周血循环系统sEPCR升高可能是早期诊断该病的一个可靠指标,其水平高低可能反映疾病的预后.     

链激酶对大鼠肝脏缺血再灌注损伤的保护作用

目的:研究链激酶对大鼠肝脏缺血再灌注损伤的保护作用.方法:36只Wistar大鼠随机分成3组,每组12只.对照组大鼠肝脏经门脉10 mL乳酸林格液灌洗后,低温4℃UW液中保存24h.实验组大鼠肝脏经含链激酶7500 IU乳酸林格灌洗后,分别低温或低温静脉持续氧气灌注保存24 h后.离体常温再灌注45 min,观察灌洗液谷氨酰胺丙氨酸转氨酶(alanine aminotransferase.ALT)、谷氨酸乳酸脱氢酶(glutamate-lactate dehydrogenase,GLDH)和嘌呤核苷磷酸化酶(purine nucleoside phosphorylase,PNP)活性及肝脏胆汁分泌量、肝组织5'核苷酸酶活性的变化.结果:实验组再灌注过程中灌洗液ALT、GLDH和PNP活性均明显降低于对照组(P＜0.05或P＜0.01);胆汁分泌量增加[3.7±0.7μL/(g·45 min),9.1±0.μL/(g·45 min)vs1.1±0.9μL/(g·45 min),P＜0.05,P＜0.01);5'核苷酸酶活性染色明显增强.结论:链激酶改善低温保存肝脏的微循环,减轻缺血再灌注损伤.     

PICCO监测在失血性休克合并肺水肿患者治疗中的应用价值

目的 探讨脉搏指示连续心排量(PICCO)监测失血性休克合并肺水肿患者的临床价值.方法 回顾多发伤导致失血性休克合并肺水肿的患者42例,分别采用PICCO(PICCO组)和中心静脉压(CVP)监测(CVP组)指导治疗各21例,比较两组治疗48 h后的机械通气时间、氧合指数(PaO2/FiO2)、乳酸值、平均动脉压(MAP)以及APACHEⅡ评分.结果 入院时两组年龄、PaO2/FiO2、乳酸、MAP、APACHEⅡ评分比较,P均＞0.05;治疗48 h后,与CVP组比较,PICCO组机械通气时间缩短、PaO2/FiO2升高、乳酸降低、MAP下降、APACHEⅡ评分减少(P均＜0.01).结论 PICCO监测失血性休克合并肺水肿患者可稳定患者的生命体征,缩短机械通气时间.     

Protection mechanism of deacetylase inhibitor on spleen of rats with severe hemorrhagic shock

Objective: To explore the protection and molecular mechanism of histone deacetylase inhibitors(HDACIs) on the spleen of rats with hemorrhagic shock. Methods: A total of 60 SPF male SD rats were selected for the modeling of severe hemorrhagic shock using the method of arterial and venous cannulation with the time-divided bleeding. The measurement of mean arterial blood pressure and blood lactic acid was used to verify the modeling. The modeled rats were randomly divided into shock group, shock+suberoylanilide hydroxamic acid(SAHA) group, shock+autogenous transfusion group, and shock+SAHA+autogenous transfusion group. Three hours after the treatment, the spleen of rats was collected and TUNEL method was employed to detect the apoptosis of spleen cells in each group. Afterwards, real-time PCR and western blot were employed to detect the expression of BCL-2, BAX, and caspass3 in the spleen of rats in each group. Results: A total of 55 rats had successful modeling of severe hemorrhagic shock, with success rate of 92%. Cell apoptosis in the severe hemorrhagic model group was the most serious. After the intervention of HDACIs and the autogenous transfusion, the tissue injury was a bit recovered. Cell apoptosis was least in the shock+SAHA+autogenous transfusion group(P0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BCL-2 was significantly increased(P0.05), with highest relative expression of BCL-2 in shock+SAHA+autogenous transfusion group(P0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BAX was significantly decreased(P0.05), with lowest relative expression of BAX in the intervention group of single HDACIs. The change in the expression of caspass3 was similar to BAX, namely the relative expression of caspass3 was significantly decreased after the intervention of HDACIs and the autogenous transfusion(P0.05). Conclusions: HDACIs and autogenous transfusion can all protect the spleen injury because of the severe hemorrhagic shock. Its molecular mechanism may be related to the regulation on the expression of BCL-2/BAX and caspass3, which may affect the apoptosis process of cells.     

Granulocytes and no-reflow phenomenon in irreversible hemorrhagic shock

Recent evidence shows that circulating granulocytes play an important role in capillary stasis and tissue injury. We investigated two aspects of the problem in a Wiggers hemorrhagic shock model of the rat: the survival rate and the microvascular no-reflow phenomenon. A conventional group of rats with normal blood cells and a neutropenic group of rats pretreated with intraperitoneal antigranulocyte antibody were used to evaluate the effects of granulocytes. Two hemorrhagic shock protocols (HSP) were carried out. In HSP-1, the rats were subjected to 40 mm Hg mean arterial pressure for 3 hours. The conventional group (n = 11) showed a 36% survival rate compared with 100% in the neutropenic group (n = 6). In HSP-2, the hypotension was more severe, 30 mm Hg mean arterial pressure for 7 hours. There were no survivors in the conventional group (n = 8), compared with a 100% survival rate in the neutropenic group (n = 6). The extent, location, and mechanism of the no-reflow phenomenon was investigated by examining histological sections from several organs after infusion of a contrast medium to mark vessels with flow in a control group without shock and in the HSP-2 model 2 hours after blood replacement. The arterioles and venules uniformly contained contrast medium in all three groups; only capillaries showed no-reflow. A significantly higher percentage of no-reflow was observed in the capillaries of the conventional shock group than in the neutropenic shock group. We concluded that the obstruction of capillaries was largely due to trapped granulocytes, suggesting that these leukocytes play a key role in the capillary no-reflow phenomenon and survival from hemorrhagic shock.     

Protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury after hemorrhagic shock in rats

AIM: To study the protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury and its mechanism after hemorrhagic shock in rats. METHODS: A total of 32 SD rats were randomly divided into four groups (n = 8, each group): normal group, model group, low dosage group (treated with 10 g/kg Astragalus membranaceus) and high dosage group (treated with 20 g/kg Astragalus membranaceus). The model of hemorrhagic shock for 60 min and reperfusion for 90 min was established. Therapeutic solution (3 mL) was administrated before reperfusion. At the end of the study, the observed intestinal pathology was analyzed. The blood concentrations of lactic acid (LD), nitric oxide (NO), endothelin-1 (ET-1), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) in intestinal mucosa were determined. RESULTS: The intestinal mucosa pathology showed severe damage in model group and low dosage group, slight damage in high dosage group and no obvious damage in normal group. The Chiu's score in low dose group and high dose group was significantly lower than that in model group. The content of MDA in model group was higher than that in low and high dose groups, while that in high dose group was almost the same as in normal group. The activity of SOD and GSH-PX was the lowest in model group and significantly higher in high dose group than in normal and low dose groups. The concentrations of LD and ET-1 in model group were the highest. The concentrations of NO in model group and low dose group were significantly lower than those in high dose group and normal group. CONCLUSION: High dose Astragalus membranaeus has much better protective effect on hemorrhagic shock-reperfusion injury of intestinal mucosa than low dose Astragalus membranaceus. The mechanism may be that Astragalus membranaceus can improve antioxidative effect and regulate NO/ET level during hemorrhagic reperfusion.     

Effect of abdominal trauma on hemorrhagic shock-induced acute lung injury in rats

AIM: To evaluate the effects of abdominal trauma on hemorrhagic shock-induced acute lung injury in rats. METHODS: Five groups were allocated (n = 8) in the study. GroupⅠwas taken as the control group, groupⅡas the hemorrhagic shock group, groupⅢas hemorrhagic shock laparotomy, groupⅣas hemorrhagic shock splenectomy and groupⅤas splenec-tomy omentectomy hemorrhagic shock group. Hemorrhagic shock was induced by drawing blood and reducing mean arterial pressure (MAP) to 40 mmHg within 10 min. After a hypotensive period of 1 h, animals were resuscitated. Bronchoalveolar lavage (BAL) was performed to recover cells from the alveolar space with 40 ml of BAL fluid after resuscitation malondialdehyde (MDA) and L-γ-glutarnyl-L-cysteinyl-glycine (GSH) levels were measured in serum, eryth-rocytes and lung tissue. RESULTS: Serum, erythrocyte, lung tissue MDA and GSH levels were significantly increased in hemorrhagic shock groupsⅡ-Ⅴ(P < 0.05). Lymphocyte, neutrophil and alveolar macrophage counts in BAL fluid indicated a significant difference between control and shock groups (P < 0.05). CONCLUSION: The degree of trauma increases hemorrhagic shock-induced acute lung injury.     

益母草注射液对失血性休克大鼠多组织器官NO的影响

目的 观察益母草注射液(LHI)对失血性休克大鼠肝、肾、心肌、肺等组织器官一氧化氮(NO)含量及其合酶(NOS)活性的影响.方法 LHI组、休克组大鼠(均n=6)经颈总动脉放血至40 mmHg,复制失血性休克模型.维持低血压60 min后,LHI组缓慢输注LHI(5 g/ml,5 g/kg),再输入放出的全血及等量生...     

失血性休克大鼠L-选择素转录、翻译水平表达的研究

目的 探讨失血性休克大鼠L－选择素转录及翻译水平表达对创伤及休克病理生理过程的影响。方法 大鼠剪尾取血作为正常对照,颈部去皮颈动脉结扎剪断插管作为实验对照,建立失血性休克动物模型;遂将其分为正常对照组、实验对照组（创伤组）和实验休克组（失血性休克组）,每组均为8只。用单克隆抗体标记,流式细胞仪检测大鼠失血休克急性期中性粒细胞表面L－选择素的动态表达,以及用半定量逆转录聚合酶链反应（RT－PCR）检测大鼠白细胞胞质L－选择素mRNA半定量变化。结果 正常对照组大鼠中性粒细胞表面不同时间点L－选择素表达量（平均荧光道数）之间的差异无显著性（P＞0.05)。与正常对照组相比,实验对照组细胞表面及胞质mRNA表达均上调,细胞表面3h达峰值,4、5h持续高水平;mRNA进行性升高,于5h达峰值。与正常对照组比,实验休克组两者亦均上调;但与创伤组比,3h后则呈下调趋势。结论 创伤后中性粒细胞L－选择素表达上调,增强白细胞－内皮细胞黏附反应,有助于局部创伤愈合,修复并抵抗感染。休克组L－选择素表达下调,可减少白细胞－内皮细胞过度黏附及嵌塞毛细血管,有助于机体疏通微循环,改善灌流量。     

Cytokine blockade attenuates sympathoexcitation in heart failure: cross-talk between nNOS, AT-1R and cytokines in the hypothalamic paraventricular nucleus

OBJECTIVE: To investigate evidence for the interplay between cytokines, angiotensin II and nNOS in the paraventricular nucleus (PVN), for regulating sympathetic outflow in a rat model of CHF. METHODS AND RESULTS: Heart failure was induced in Sprague-Dawley rats by coronary artery ligation. One group of rats was treated with pentoxifylline (PTX, 30 mg/kg IP), a cytokine blocker, or vehicle, for 5 weeks. Another group of rats was pre-treated with PTX before coronary ligation to study prior cytokine blocking effect on survival. Both groups were combined in the analysis. Echocardiography demonstrated an increase in LV end-diastolic pressure and Tei index after 5 weeks in CHF rats. ELISA revealed a significant increase in plasma TNF-alpha and IL-1beta in CHF rats. Inducible NOS (iNOS) and angiotensin receptor-type 1 (AT-1R) mRNA expressions were increased, while neuronal NOS (nNOS) was decreased in the PVN of CHF rats; these changes were reversed by PTX. PTX treatment also decreased plasma norepinephrine and epinephrine levels and improved baroreflex control of renal sympathoexcitation in CHF rats. Immunohistochemistry revealed elevated 3-nitrotyrosine formation in the heart and the PVN of CHF rats, but not in PTX treated rats. CONCLUSION: PTX decreased both peripheral and central cytokine expression, alleviated nitric oxide dysregulation, and inhibited the formation of peroxynitrite in the PVN resulting in decreased sympathoexcitation in CHF rats.     

Effects of in vivo pentoxifylline treatment on survival and ex vivo vascular contractility in a rat lipopolysaccharide shock model.

Depending on the dose and dosing, pentoxifylline (PTX) treatment can improve or worsen survival from lipopolysaccharide (LPS) shock in rats. Intraperitoneal (i.p.) PTX, 20 mg/kg, administered once 15 min after intravenous (i.v.) LPS (17 mg/kg), significantly improved survival in unanesthetized LPS-shocked rats. Multiple 20 mg/kg PTX injections (five total, spaced at 45 min intervals starting 15 min after LPS) significantly worsened survival. A lower dose, 12 mg/kg, given as a single or multiple injections, did not alter survival. We tested the ex vivo contractile response to norepinephrine (NE) of aortic rings isolated 3.75 hr after i.v. injection of PBS or LPS. Both untreated LPS-shocked and multiple 12 mg/kg PTX treated normal rats (i.v. PBS) had significantly diminished maximum contractility. The ex vivo vascular hypocontractility found in untreated LPS-shocked rats was not aggravated nor ameliorated by multiple 12 mg/kg PTX injections. The ex vivo effects on contractility of multiple 20 mg/kg PTX treatment of LPS shock could not be studied because survival times were shorter than 3.5 hr. In using PTX to treat LPS shock, potentially harmful vasodilation must be considered.