聚环氧乙烷对内毒素休克兔肾血流动力学的影响

摘要：目的应用超声监测内毒素休克新西兰兔肾血流,观察聚环氧乙烷(PEO)对内毒素休克兔肾血流的影响和肾脏的保护作
用。方法健康新西兰白兔20只,随机分成两组,生理盐水组(NS)和溶于生理盐水的减阻剂组(PEO),每组10只。每只兔静脉
注射内毒素0.6 mg/kg造内毒素休克兔模型。待血压下降≥30%时开始复苏,NS组使用生理盐水复苏,5 ml·h-1·kg-1),PEO组使
用等剂量含20 ng/g PEO的生理盐水复苏。分别于休克前、休克期、复苏1 h后经超声观察肾血流动力学指标并抽血查肾功能。
试验全程监测心率和动脉血压。结果两组兔各级肾动脉休克期流速明显低于休克前(P<0.05),动脉搏动指数(PI)和阻力指数
(RI)明显增高;复苏1 h后,NS组各级肾动脉血流流速下降,三级肾静脉流速减慢,PI、RI无明显降低;而PEO组肾段动脉及叶间
动脉流速较休克前明显增快(P<0.05),三级动脉PI、RI较之NS组相比明显下降(P<0.05)。肾功能指标：两组兔休克期BUN、Cr
均升高,复苏1 h后PEO组各项指标明显低于NS组(P<0.05)。结论小剂量聚环氧乙烷能够有效增加感染性休克肾脏的血流灌
注,对脓毒血症及感染性休克所致的早期肾脏损害有明显改善作用。
     

阿片受体拮抗剂狄普诺芬对内毒素休克狗血液动力学的影响

研究观察纳洛酮和狄普诺芬(M5050)对大肠杆菌内毒素休克狗血液动力学指标的影响。静脉注射纳洛酮(2mg/kg)和侧脑室注射M5050(40μg/狗),明显增加内毒素休克狗左心室内压、左心室内压最大上升速度、心脏每搏量及心输出量,平均动脉血压也显著回升。静脉注射M5050(2mg/kg)对内毒素休克狗血液动力学指标无明显作用。结果表明M5050改善内毒素休克狗的血液动力学的作用部位似在中枢神经系统,提示内毒素休克时中枢的内源性阿片样物质在休克发病学中的作用可能更为重要。     

精氨酸血管加压素对非控制性出血性休克大鼠彻底止血后的复苏效果

目的 观察精氨酸血管加压素(arginine vasopressin,AVP)对非控制性出血性休克大鼠彻底止血后复苏效果.方法 采用大鼠脾实质切除及脾动脉切断方法复制非控制性出血性休克模型,在止血前采用低压复苏(50 mmHg,1 h)后结扎血管彻底止血,观察乳酸林格氏液(Lactated Ringer's,LR)、AVP(0.4 U/kg和0.04 U/kg)对大鼠血流动力学指标、血气指标、存活时间和存活率的影响.LR组在彻底止血后输注2倍失血量LR;AVP 0.1 U/kg组和0.4 U/kg组在2倍量的LR中分别加入AVP0.4 U/kg和0.04 U/kg输注.结果 非控制性出血性休克大鼠在休克后以及低压复苏后血流动力学指标包括左心室收缩压(left intraventricular systolic pressure,LVSP)、左心室压力上升或下降的最大速率(the maximal change rate of left intraventricular pressure,±dp/dtmax)明显低于休克前(P<0.05),血气也发生了明显改变;2倍失血量的LR输注不能较好地恢复平均动脉血压(mean artery pressure,MAP)和血流动力学指标,AVP 0.4 U/kg和0.04 U/kg输注,明显增加MAP和改善休克大鼠血流动力学指标,延长休克动物存活时间并提高存活率,与LR组相比明显升高(P<0.05).结论 AVP对非控制性出血性休克大鼠彻底止血后有较好的复苏效果.     

聚环氧乙烷对内毒素休克兔肾血流动力学的影响

目的应用超声监测内毒素休克新西兰兔肾血流,观察聚环氧乙烷(PEO)对内毒素休克兔肾血流的影响和肾脏的保护作用。方法健康新西兰白兔20只,随机分成两组,生理盐水组(NS)和溶于生理盐水的减阻剂组(PEO),每组10只。每只兔静脉注射内毒素0.6 mg/kg造内毒素休克兔模型。待血压下降≥30%时开始复苏,NS组使用生理盐水复苏,5 ml.h-.1kg-1),PEO组使用等剂量含20 ng/g PEO的生理盐水复苏。分别于休克前、休克期、复苏1 h后经超声观察肾血流动力学指标并抽血查肾功能。试验全程监测心率和动脉血压。结果两组兔各级肾动脉休克期流速明显低于休克前(P<0.05),动脉搏动指数(PI)和阻力指数(RI)明显增高;复苏1 h后,NS组各级肾动脉血流流速下降,三级肾静脉流速减慢,PI、RI无明显降低;而PEO组肾段动脉及叶间动脉流速较休克前明显增快(P<0.05),三级动脉PI、RI较之NS组相比明显下降(P<0.05)。肾功能指标:两组兔休克期BUN、Cr均升高,复苏1 h后PEO组各项指标明显低于NS组(P<0.05)。结论小剂量聚环氧乙烷能够有效增加感染性休克肾脏的血流灌注,对脓毒血症及感染性休克所致的早期肾脏损害有明显改善作用。     

内毒素休克狗肺解聚功能受损机制探讨

麻醉狗注内毒素前左心血TXB_2/6-keto-PGF_(1α)及PAR均明显低于右心血;内毒素休克时,左、右心血TXB_2/6-keto—PGF_(1α)及PAR明显上升,且左、右心血之间的浓度梯度差消失;消炎痛明显减轻内毒素休克时的前述改变。注内毒素前及内毒素休克早期TXB_2/6-keto-PGF_(1α)与PAR之间呈显著正相关。结果提示:肺解聚功能与肺代谢TXA_2、PGI_2有关;内毒素休克早期,肺代谢TXA_2,PGI_2的失调是肺解聚功能受损原因之一。     

一氧化氮合酶抑制剂对大鼠创伤性休克的干预作用

目的评价选择性诱导型一氧化氮合酶(iNOS)抑制剂氨基胍(AG)和非选择性一氧化氮合酶抑制剂L-硝基精氨酸甲酯(L-NAME)对创伤性休克的治疗效果。方法用44只SD大鼠制作创伤性休克动物模型。双侧股骨干砸伤后并经股动脉放血至平均动脉压(MAP)35～45 mmHg(4.67~6.00 kPa),维持30 min,然后回输失血和等量的林格氏液。随机分为休克组(10只)、AG组(根据复苏时静脉注射AG含量为2、8、60 mg/kg·b.w.则分为AGⅠ、AGⅡ、AGⅢ组,各8只)、L-NAME组(10只,复苏时静脉注射L-NAME 8 mg/kg·b.w.),观察休克前后血浆NO浓度的动态变化及24 h大鼠存活率。并留取肺、肝、肾、小肠组织,观察病理改变。结果大鼠创伤性休克后,血浆NO水平明显高于休克前;AG各组动物复苏后血浆NO的水平明显降低,各脏器的病理损害亦显著减轻,存活率明显提高,并且AGⅢ组效果最好;L-NAME组动物复苏后血浆NO的水平也明显降低,各脏器的病理损害无明显变化,存活率无明显提高。结论NO在创伤性休克的病理发展过程中起着重要作用,应用AG有助于创伤性休克的改善;而L-NAME能降低NO的水平,但对休克的预后无明显改善。     

几种不同液体复苏失血性休克大鼠的适宜量研究

目的对几种不同液体复苏失血性休克大鼠适宜量进行探讨。方法SD大鼠分别做35%、45%放血失血性休克模型,以不同量的乳酸林格液(LR)、羟乙基淀粉(HES)、高渗氯化钠右旋糖酐(HSD)和LR HES进行复苏,观察其对失血性休克大鼠平均动脉血压(mean arterial blood pressure,MAP)、左心室收缩压(left intraventricular systolic pressure,LVSP)、左心室压力上升或下降的最大速率(the maximal change rate of left intraventricular pressure,±dp/dtmax)的影响,同时观察血气指标变化和存活率的变化。结果在35%失血性休克(中度休克)时,不同剂量的LR、HSD输注对休克大鼠血流动力学的影响无显著差异(P>0.05);30ml/kg HES输液后血流动力学指标明显优于20ml/kg HES(P<0.05);1倍失血量LR HES输注优于2倍和3倍失血量的LR HES(P<0.05)。在45%失血性休克(重度休克)时,3倍失血量LR输液后血流动力学指标明显比1倍和2倍失血量的LR效果好(P<0.05);6ml/kg的HSD输注后血流动力学效果比4、8ml/kg的HSD效果好(P<0.05)。同样,30ml/kg HES和2倍失血量的LR HES输液后改善血流动力学指标,血气指标和存活时间效果优于其他剂量组的HES和LR HES(P<0.05),除HSD各剂量组明显降低血pH值外,其他各液体对血气指标的影响均不大。结论LR除复苏重度休克以3倍失血量输注效果好外,其余液体以HES30ml/kg,HSD6ml/kg以及2倍失血量的LR HES复苏失血性休克效果较好,是较理想的失血性休克复苏容量。     

卡托普利对失血性休克兔肠黏膜血流灌注的影响

目的:研究卡托普利对失血性休克兔肠黏膜血流灌注的影响. 方法:新西兰白兔30只随机分为空白对照组、失血性休克组、药物治疗组,通过Tonometry张力计测定并计算休克前(S0)、休克起点(S1)及再灌注1 h (REP1 ),再灌注2 h(REP2)乙状结肠pHi及Pi-aCO2,同时在上述时间点测定肠系膜静脉血乳酸浓度(Lac)、血氧饱和度(SvO2)及二氧化碳分压(PCO2). 结果:休克组pHi(6.84±0.14)及肠系膜静脉血SvO2(44±7)%及PCO2(23.5±3.9) mmHg与对照组[分别为(7.31±0.06), (75±7)%, (40.4±0.8) mmHg]相比降低显著,肠系膜静脉乳酸值(3.62±0.32) mmol/L与对照组(1.49±0.72) mmol/L相比升高显著(P<0.01),尽管予以充分复苏,上述指标仍无明显改善;治疗组应用卡托普利后,肠黏膜的pHi(7.13±0.11)及肠系膜静脉血SvO2(66±6)%, PCO2(29.7±3.5)mmHg与休克组相比明显升高,肠系膜静脉血乳酸值(2.54±0.47) mmol/L明显下降(P<0.01). 结论:卡托普利能大大改善失血性休克兔肠黏膜的血流灌注.     

创伤性休克对大鼠胃肠激素水平的影响

目的探讨创伤性休克对大鼠胃粘膜中胃肠激素水平的影响。方法采用后肢创伤法建立创伤性休克大鼠模型,用放射免疫法(RIA)测定创伤前后及复苏后3、7、12h胃粘膜中胃泌素(GAS)、胃动素(MTL)、生长抑素(SS)水平。结果在休克末及复苏后3、7、12h,大鼠血浆GAS、MTL及SS水平发生明显变化。在创伤后及复苏后3、7、12h大鼠胃粘膜中GAS含量明显升高(268.36±118.37)ng/L,(306.17±150.56)ng/L、(405.04±164.48)ng/L、(395.26±158.38)ng/L(P<0.05,P<0.01,P<0.01,P<0.01);MTL含量下降(50.47±32.08)ng/L、(43.16±28.17)ng/L、(35.58±20.46)ng/L、(42.18±29.18)ng/L(P<0.05,P<0.05,P<0.01,P<0.05);SS水平增加(218.74±110.28)ng/L、(260.22±78.15)ng/L、(236.44±88.16)ng/L、(258.36±72.08)ng/L(P<0.05,P<0.01,P<0.05,P<0.01)。结论创伤性休克可导致大鼠胃粘膜中胃肠激素含量的变化。     

床旁超声检测下腔静脉直径快速评估老年创伤性休克患者血容量临床价值探讨

目的 探讨床旁超声检测下腔静脉直径(IVC)快速评估老年创伤性休克患者血容量的临床价值.方法 对43例老年创伤性休克患者(休克组)予6％羟乙基淀粉(HES 130/0.4)500ml,分别在输液前后用超声测量IVCmax、IVCmin,脉搏指示连续心输出量血流动力学监测(PiCCO)患者胸腔内血容量指数(ITBVI),比较输液前后IVC、ITBVI变化,并与50例健康体检的正常老年人(对照组)进行比较.结果 休克组输液前IVCrmax1.18±0.21)cm、lVCmix(0.63±0.18)cm、ITBVI(579.79±125.74)ml/m2明显小于输液后[(1 70±0.24)cm、(1.42±0.22)cm、(785.09±129.01)ml/m2](P＜0.01),);休克组输液前RVl(47.96±6.56)％明显大于输液后(15.52±4.53);休克组IVCmax、IVCmin与同期测得ITBVl呈正相关(rmax=0.780,rmin=0.753,均P＜0.01).结论 床旁超声测量老年创伤性休克患者IVC,可有效评估患者血容量,为临床诊治提供依据.     

EFFECTS OF ANISODAMINE ON CARDIOVASCULAR ACTIVITIES IN ENDOTOXIN-SHOCKED DOGS

Experiments were carried out in mongrel dogs anesthetized with pentobarbital. Escherichia coli endotoxin (5 mg/kg, iv) was given to produce circula- tory shock. In 6 dogs, 5 mg/kg of anisodamine was infused intravenously for 60 minutes causing an in- crease in heart rate, left ventricular systolic pressure, positive and negative maximum dp/dt and mean arterial pressure. Renal vascular resistance was decreased, while renal blood flow and urinary out flow increased. No such changes were observed in 6 control animals which were given saline infusion. The results obtained indicate that anisodamine given at early stage of endotoxin shock improves myocardial contractility.     

CI-IANGES IN THE PLASMA LEVELS OF PGE, PGF2a AND 6-Keto-PGFla IN CANINE ENDOTOXIC SHOCK

The plasma levels of PGE, PGF2a and 6-keto PGFla in the canine model of endotoxic shock were determined with radioimmunoassay. Following cndotoxin injection, the PGF2a levels were rapidly increased to peak at 5 minutes. There was a negative correlation between the PGE level and the change in total systemic peripheral resistance at early stage of shock. The administration of anisodamine 2 hours after endotoxin injection showed no effect on the changes of PGE and PGF2a levels in the shocked dogs. The plasma levels of PGE and PGF2a in the shocked children with fulminating epidemic menin gococcal meningitis were also markedly elevated dur- ing shock but fell within normal range at convales- sence. After the dogs were given endotoxin the plasma level of 6-keto-PGFla increased slowly during the first hour, reached a peak at 2 hours and re mained high for 12 hours. There was a negative correlation between the 6keto-PGFla level and the blood pressure. The plasma 6keto PGFla level was decreased and the blood pressure improved corres- pondingly with a negative linear correlation as a result of administration of anisodamine 5-10 minutes after endotoxin injection. These results suggested that PGE and PGI2, as one of the humoral factors, might participate at least partially in the endotoxin induced hypotension, and that the inhibition of PGI2 synthesis was considered contributable to certain degree to the antishock effect of anisodamine.     

纳洛酮对家兔失血性休克的影响

<正> 近几年有资料报告,在休克以及应激反应时脑内吗啡样物质释放增加。并且证明吗啡样物质对心血管活动有明显的抑制作用。有人认为,休克时脑内释放的吗啡样物质可能是形成低血压的因素之一。因此设想用专一性吗啡受体阻断剂纳洛酮升高血压可能为防止休克提供一条新途径。本工作采用小剂量纳洛酮作脑室或延髓池内注射,观察它对动物的血压、心率、失血量、输液量和交感神经传出电活动的影响,初步讨论纳洛酮在抗休克治疗中的可能作用及其与交感神经活动的关系。     

电针内关对内毒素休克大鼠血浆一氧化氮及肿瘤坏死因子α浓度的影响

目的 观察电针内关对内毒素休克大鼠血压和血浆一氧化氮(NO)、肿瘤坏死因子α(TNFα)浓度的影响。方法 静脉注射内毒素1．5mg/kg、腹腔注射D-氨基半乳糖100mg／kg造成内毒素休克大鼠模型，用电针内关和氨基胍作对照于预处理，右颈总动脉插管测量血压。取血浆检测NO、TNFα浓度。结果 电针内关可以使内毒素休克大鼠血压回升，降低血浆NO、TNFα浓度。结论 电针内关可以改善内毒素休克时的低血压．有抗休克作用，这种保护作用可能是通过调节血浆NO、TNFα浓度而产生的。     

TREATMENT OF EXPERIMENTAL RESPIRATORY DISTRESS SYNDROME WITH DEXAMETHASONE, SCOPOLAMINE AND ANISODAMINE IN DOGS

38 hybrid dogs were injected intravenously with oleic acid 0.03 mg/kg body weight to induce ex perimental respiratory distress syndrome. The an imals were divided into four groups, one was the control group and the other three groups were treated with dexamethasone, scopolamine hydrobromide and anisodamine. The animals were killed 24 hours after injection. The blood gas parameters of arterial and mixed venous blood were determined before, immediately and 0.5, 1, 2, 4, 6, 22, and 24 hours after oleic acid injection. The average pul- monary arterial pressure was measured hourly. Chest X-rays were taken before and 2, 4, 6, and 24 hours after injection. The histological specimens of the killed animals were examined by light and electron microscopy. It was found that dexame- thasone and anisodamine are effective in treating ex- perimental respiratory distress syndrome while scopo- 1amine is rather disappointing.     

L—四氢巴马汀L—千藤立定和四氢小蘖碱对犬心肌血流量和耗氧量的影响

L—四氢巴马汀(L—THP),L—千金藤立定(L—SPD)10mg/kg,iv,和四氢小蘖碱(THB)3mg/kg,iv,均能增加心肌血流量,分别为99,72,231％,降低冠脉阻力(各为48,63,68％),降低心肌耗氧量(分别为38,31,23％)。三药均可降低血压,持续1小时以上。心率略减慢,但不显著。     

刺激躯体神经对兔压力感受性反射的重调定

本工作用血压-肾交感放电反应曲线为指标,在家兔中观察了刺激躯体神经对压力感受性反射的影响。在浅麻醉状态下,刺激腓深神经对基础血压水平和肾交感放电并无明显影响,但可使血压-肾交感放电反应曲线的斜率明显增大;而在深麻醉状态下,同样参数的刺激并不引起压力感受性反射的明显改变。这一现象可能部分解释针刺对异常血压的调整作用。     

米托蒽醌的急性毒性研究

Acute toxicity of mitoxantrone (DHAQ) synthetized by Department of Organic Chemistry, School of Pharmacy, WCUMS was studied in mice and dogs. The toxic effects were compared with those of adriamycin (ADR). The LD50 were 6.6 +/- 1.3 and 7.1 +/- 1.6 mg/kg DHAQ, 7.9 +/- 2.1 and 10.7 +/- 2.2 mg/kg ADR (P = 0.95) respectively on observation with a single dose i.v. and i.p., for 21 days in Kunming mice. The toxicity appeared to be delayed with DHAQ and ADR. The earliest death occurred on 4th day after treatment in mice. In the third week still a few died. There were obvious decreases in WBC counts in the peripheral blood of mice receiving either 1-2.5 mg/kg DHAQ or 2.5-5 mg/kg ADR with a single dose i.p.. The WBC count could return to normality after 3 weeks with the withdrawal of the drugs. On electron microscopic examination of myocardial samples from mice 4 days after a single dose of 20 mg/kg DHAQ i.p., mitochondria swelling and vacuoles formation in some cells were shown. Besides the above-mentioned changes, some myocytes exhibited disorientation and loss of myofilaments in the mice which received equivalent dose of ADR. In dogs anaesthetized a temporary falling of blood pressure and slowing of heart rate were observed following 5-10 mg/kg DHAQ i.p.. When a dose of 50-100 mg/kg was given, the blood pressure dropped continuously until death.     

溴氰菊酯对家兔心血管机能的影响

观察溴氰菊酯对家兔心血管机能的影响。溴氰菊酯2.5mg/kg 静脉注射能引起麻醉家兔血压升高、心率减慢、心电图异常。这些变化在30分钟时表现最明显,以后逐渐恢复,提示溴氰菊酯对麻醉兔心血管系统的作用为短暂性的,能为机体内环境的调节机制所补偿。     

山莨菪碱对内毒素狗全血乳酸、肝糖原含量的影响

在观察山莨菪碱(654-2)对内毒素狗血流动力学指标影响的同时,观察了654-2对其动脉全血乳酸、血浆葡萄糖及肝细胞糖原含量的影响。实验结果;实验组(内毒素加654-2)动物高乳酸血症下降速度较对照组(内毒素加生理盐水)显著增快;注内毒素后第6h,肝糖原含量较对照组显著增高,而两组动物血流动力学指标变化无明显差异。提示654-2有改善内毒素狗肝脏对乳酸的糖异生作用,而这一作用似与血流动力学指标的改善关系不大。654-2对肝细胞的保护作用可能是其作用环节之一。