交感神经对大鼠失血性休克过程中淋巴微循环的调控

为了探讨交感神经对失血性休克过程中淋巴微循环变化的影响,应用显微电视录像技术,观察了切断内脏大神经的大鼠在失血性休克及输血、补液过程中肠中系膜微淋巴管（ＭＬ）收缩性的变化。结果表明,去神经后ＭＬ自主收缩频率及总收缩活性旨数（ＩｎｄｅｘⅡ）、淋巴管力学指数（Ｌ．Ｋ－Ｉｎｄｅｘ）显著降低,失血性休克时神经完整组及去神经组ＭＬ的自主收缩性均降低,神经完整组在回输血液及输液期,ＭＬ自主收缩性显著高于休克前     

肠淋巴液对大鼠血压的影响

本文用引流及输入肠淋巴液的方法,研究了肠淋巴液对大鼠血压的影响。结果如下：１．经肠淋巴管插管引流肠淋巴液的大鼠,自引流后１５０ｍｉｎ起,血压显著低于假手术期。２．在丢失肠淋巴液同时,补充等量白蛋白或脂肪乳,仍不能防止血压下降,但肠淋巴管－颈静脉搭桥大鼠,在４ｈ观察过程中,血压不出现显著降低。３．重症失血性休克大鼠输入小量肠淋巴液后,血压显著回升,其血压水平及存活时间显著优于对照组。     

肾上腺髓质素对大鼠肠系膜微血管和微淋巴管的作用

应用活体显微电视录象技术,观察上腺髓质素对大鼠肠系膜微血管微淋巴管的作用及其对去甲肾上腺素,内皮素作用的是结果表明,ＡＤＭ直接扩张肠系膜各级微血管和向一淋巴管,拮抗ＮＥ和ＥＴ引起的微血效及微循环血流液态的异常改变。ＡＤＭ的上述作用可被一氧化氮生成抑制剂Ｎ＾９－ｎｉｔｒｏ－Ｌ－ａｒｇｉｎｉｎｅ（Ｌ－ＮＮＡ）显著抑制。     

一氧化氮对失血性休克大鼠离体淋巴管收缩性双相变化的调节作用

本文旨在离体观察失血性休克后不同时间淋巴管的收缩性变化及一氧化氮(nitric oxide,NO)的作用。分离失血性休克进程中不同时间点(0,0.5,1,2,3h)的大鼠胸导管条,采用微血管压力-直径测定技术,离体观察淋巴管在不同跨壁压(1,3,5,7,9cmH2O)下的收缩频率(contraction frequency,CF)、收缩末期口径(end diastolic diameter,EDD)、舒张末期口径(end systolicdiameter,ESD)、被动管径(passive diameter,PD)的变化,计算淋巴管的收缩幅度(contraction amplitude,CA)、紧张性指数(tonicindex,TI)和泵流分数(fractional pump flow,FPF)。结果显示,在多个跨壁压下,休克0h、休克0.5h淋巴管的CF、TI、FPF显著高于对照组,随着休克的发展,休克2h和休克3h淋巴管在多个跨壁压下的CF、TI、FPF显著低于对照组。用NO相关的工具药单独或联合孵育休克0.5h和休克2h的淋巴管,然后在3cmH2O跨壁压条件下测定淋巴管的收缩性。NO供体L-Arg使休克...     

淋巴液对失血性休克大鼠心肌收缩功能的影响

淋巴液对失血性休克大鼠心肌收缩功能的影响＊邱丽颖王德宝吕莉张静１（张家口医学院生理教研室,１病理生理教研室,张家口０７５０２９）淋巴系是组织液回流的主要途径,但我们发现淋巴液对失血性休克大鼠有明显的升压作用。为了围绕心脏功能探讨其抗休克机制及淋巴系的...     

自发性高血压大鼠肠系膜微静脉白细胞-内皮细胞相互作用和微淋巴管收缩特性的研究

目的:探讨自发性高血压大鼠(Spontaneously Hypertensive Rat,SHR)肠系膜微静脉白细胞-内皮细胞相互作用和微淋巴管收缩的特性。方法:取8周龄Wistar大鼠、8周龄SHR(SHR8W)和13周龄SHR(SHR13W),麻醉、固定并暴露肠系膜后,微循环显微镜下观察肠系膜微循环并录像;回放录像,计算微静脉白细胞滚动数和滚动的白细胞-内皮细胞接触时间(Rolling leukocyte-endothelial contact time,RLECT),用Vas Track自动测量系统对微淋巴管口径进行动态测量,并计算微淋巴管收缩特性指标。结果:SHR13W的白细胞滚动数显著低于Wistar;SHR8W和SHR13W的RLECT均显著低于Wistar,且SHR13W的RLECT显著低于SHR8W;进一步按照管径分级后,三组间白细胞滚动数在10~20μm管径级别下未见差异;各个管径级别下,SHR8W和SHR13W的RLECT均未见差异。SHR13W的淋巴管收缩分数显著低于Wistar和SHR8W;SHR8W及SHR13W的总收缩活性指数均显著低于Wistar;SHR13W的淋巴管动力指数显著低于Wistar。结论:SHR肠系膜微静脉白细胞滚动数及RLECT减少,其中白细胞滚动数在不同管径级别微静脉中的分布不均匀,而RLECT随SHR周龄降低,意味着SHR淋巴管收缩功能降低。     

淋浆对内毒素休克大鼠微循环障碍的干预作用

目的：探讨淋浆对内毒素休克的干预作用及其机制。方法：Wistar雄性大鼠60只,随机分为对照组、模型组和淋浆组,以颈静脉注射LPS（15 mg/kg）复制内毒素休克模型,造模15 min后,淋浆组自颈静脉注射正常淋浆（占全血量1/15）,观察对平均动脉血压（MAP）、回肠下段肠系膜微循环、细静脉壁白细胞粘附数、血浆P-选择素和细胞间粘附分子（ICAM-1）含量的影响。结果：正常淋浆可防止内毒素休克的MAP进行性下降,解除肠系膜微血管的病理性缩窄,减少白细胞在细静脉壁的粘附,改善微循环的流态,降低血浆P-选择素和ICAM-1的水平。结论：小量正常淋浆对LPS攻击导致内毒素休克的微循环障碍和低血压均有良好的干预作用,其机制与减少细胞粘附分子生成有关。     

失血性休克大鼠离体淋巴管对P物质的反应性

目的:应用离体淋巴管灌流技术,观察失血性休克(HS)发展进程中淋巴管对P物质(SP)的反应性。方法:Wistar雄性大鼠随机分为对照组(仅麻醉与手术)和HS组(通过股静脉放血至平均动脉血压为40 mmHg,复制HS模型,分为休克0h、0.5 h、1 h、2h、3 h五个亚组)。各组在相应时间点分离胸导管,制备淋巴管,3 cmH2O跨壁压下行离体灌流,分别给予从低到高浓度的SP,测量淋巴管收缩末期口径、舒张末期口径、收缩频率(CF)和被动管径,计算收缩幅度(CA)、泵流分数(FPF)和紧张指数(TI),以给予SP前后淋巴管的CF、TI、CA、FPF的差值△CF、△TI、△CA、△FPF作为评价淋巴管对SP反应性的指标。结果:Shock 0 h与shock 0.5 h大鼠淋巴管对多个或一个SP浓度的△CF、△TI、△CA、△FPF显著高于对照组,shock 2 h淋巴管对SP的△CF(3×10-7mol/L)、△TI(1×10-7mol/L)以及shock 3 h淋巴管对SP的△CF(1×10-7mol/L、3×10-7mol/L)、△TI(1×10-7mol/L)、△CA(1×10-7mol/L)均显著低于对照组。结论:休克淋巴管对SP反应性呈双相变化,即早期升高,晚期降低。     

肠淋巴途径对休克大鼠心肌自由基、炎性介质的影响

目的：观察结扎肠系膜淋巴管对重症失血性休克大鼠不同时期心肌自由基、炎症介质的影响。方法：雄性Wistar大鼠78只,分为假手术组、休克组、结扎组。休克组与结扎组复制重症失血性休克模型,结扎组于休克复苏后行肠系膜淋巴管结扎术。于休克后90min、输液复苏后0h、1h、3h、6h、12h、24h等时间点处死大鼠,制备心肌组织匀浆,检测MDA、SOD、TNFα、IL-6、NO、NOS以及MPO水平,RT—PCR方法测定心肌组织iNOS mRNA表达。结果：休克组大鼠输液复苏后多个时间点心肌匀浆MDA、TNFα、IL-6、MPO、NO、NOS和iNOS mRNA表达均有不同程度的升高,3h-12h持续在较高水平,均显著高于假手术组,心肌匀浆SOD活性显著低于假手术组：结扎组多个时间点心肌匀浆MDA、TNFα、IL-6、MPO、NO、NOS以及iNOS mRNA显著低于休克组相应时间点,SOD活性高于休克组相应时间点。结论：肠系膜淋巴管结扎阻断肠淋巴液回流,可减少心肌PMN扣押、降低TNFα、IL-6的释放、抑制NO生成及iNOS mRNA表达、减少自由基释放与SOD消耗。     

正常淋巴液与血液的流变性及成分比较

目的：观察大鼠正常肠淋巴液与血液流变性及成分的差别。方法：从45只雄性Wistar大鼠肠系膜淋巴管引流正常肠淋巴液,并记录其流量;同时留取正常颈总动脉血液。检测表观粘度、淋浆及血浆粘度,常规白细胞计数及分类;检测血浆及淋浆的各项生化指标以及蛋白电泳。结果：正常大鼠的肠淋巴流量为（0．68±0．37）ml／h;正常肠淋巴液中的白细胞总数与血液近似,但淋巴细胞数高于血液（P〈0．01）;淋巴液表观粘度、相对粘度及淋浆粘度均显著低于血液或血浆（P〈0．01）;淋浆中的Ca^2＋、BUN、Cre、CHO、HDL、AMY、AFu、C3、IgG、IgM、AIb、TP以及α1-G、β2-G及γ-G所占百分比均显著低于血浆,TG、TBA、CKMB、ADA、CO2-CP以及Alb、β1—G所占百分比均显著高于血浆（P〈0．05—0．01）。结论：肠淋巴途径在物质代谢过程中发挥着重要作用,淋巴液的低粘特征可能是小量淋巴液抗休克的作用机制之一。     

Involvement of protein kinase C in enhancement of vascular calcium sensitivity by blocking mesenteric lymph return in hemorrhagic shock rats

The aim of the present study was to investigate whether protein kinase C (PKC) was involved in the effect of mesenteric lymph duct ligation or mesenteric lymph drainage on vascular calcium sensitivity in hemorrhagic shock rats. Male Wistar rats were randomly divided into Sham, Shock (hemorrhagic shock), Shock+Ligation (mesenteric lymph duct ligation plus shock) and Shock+Drainage (mesenteric lymph drainage plus shock) groups. After being in shock (hypotension 40 mmHg) for 3 h, the tissue of superior mesenteric artery (SMA) was taken out for detecting the PKC expression and phospho-PKC (p-PKC) activity, and the vascular rings of SMA were prepared and used to measure the response to gradient calcium concentration for assaying the calcium sensitivity, the parameters of which including tension, maximum tension (E(max)) and negative logarithm of EC(50), called the pD(2). Other vascular rings from Shock+Ligation and Shock+Drainage groups were incubated with PKC regulator PMA or Staurosporine before the measurement of calcium sensitivity. The results showed that, PKC expression, p-PKC activity and calcium sensitivity of SMA in Shock group was significantly lower than that of Sham group, whereas the above-mentioned indexes were significantly elevated in Shock+Ligation and Shock+Drainage groups compared with those in Shock group. PKC agonist PMA enhanced the contractile activity of vascular rings to gradient calcium ions, and increased E(max) of SMA in Shock+Ligation and Shock+Drainage groups. On the contrary, PKC inhibitor Staurosporine significantly decreased the response to gradient calcium ions and E(max) of SMA in Shock+Ligation and Shock+Drainage groups. These results suggest that PKC plays a role in the improvement of vascular calcium sensitivity by blockade of mesenteric lymph return in hemorrhagic shock rats.     

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     

肠淋巴液引流对失血性休克大鼠红细胞流变性的影响

目的:观察肠淋巴液引流对失血性休克大鼠红细胞流变性指标以及血液黏度的作用。方法:Wistar雄性大鼠均分为假休克组、休克组(复制失血性休克模型)、引流组(复制失血性休克模型,自低血压1 h引流休克肠淋巴液)。在低血压3 h或相应时间,经腹主动脉取血,检测红细胞参数、红细胞电泳、红细胞沉降率(ESR)以及血液黏度,计算红细胞聚集指数、红细胞变形指数。结果:与假休克组比较,休克组红细胞数量、红细胞比积(HCT)、血红蛋白(Hb)、平均红细胞血红蛋白浓度(MCHC)、红细胞电泳率与迁移率、红细胞变形指数、全血黏度、全血低切与高切相对黏度和还原黏度显著降低,休克组平均红细胞体积、红细胞电泳时间、ESR、血沉方程K值与校正K值、红细胞聚集性指数、血浆黏度显著升高;引流组MCHC、红细胞电泳率与迁移率、全血黏度、全血低切与高切还原黏度均显著降低,引流组红细胞体积分布宽度(RDW-SD)显著增加。同时,引流组HCT、RDW-SD、红细胞变形指数、全血黏度、全血低切与高切相对黏度显著高于休克组;ESR、血沉方程K值与校正K值、红细胞聚集性指数、血浆黏度显著低于休克组。结论:休克肠淋巴液引流可改善失血性休克大鼠红细胞流变行为,从而改善血液流变性。     

Inhibition of active lymph pump by simulated microgravity in rats

During spaceflight the normal head-to-foot hydrostatic pressure gradients are eliminated and body fluids shift toward the head, resulting in a diminished fluid volume in the legs and an increased fluid volume in the head, neck, and upper extremities. Lymphatic function is important in the maintenance of normal tissue fluid volume, but it is not clear how microgravity influences lymphatic pumping. We performed a detailed evaluation of the influence of simulated microgravity on lymphatic diameter, wall thickness, elastance, tone, and other measures of phasic contractility in isolated lymphatics. Head-down tail suspension (HDT) rats were used to simulate the effects of microgravity. Animals were exposed to HDT for 2 wk, after which data were collected and compared with the control non-HDT group. Lymphatics from four regional lymphatic beds (thoracic duct, cervical, mesenteric, and femoral lymphatics) were isolated, cannulated, and pressurized. Input and output pressures were adjusted to apply a range of transmural pressures and flows to the lymphatics. Simulated microgravity caused a potent inhibition of pressure/stretch-stimulated pumping in all four groups of lymphatics. The greatest inhibition was found in cervical lymphatics. These findings presumably are correlated to the cephalic fluid shifts that occur in HDT rats as well as those observed during spaceflight. Flow-dependent pump inhibition was increased after HDT, especially in the thoracic duct. Mesenteric lymphatics were less strongly influenced by HDT, which may support the idea that lymph hydrodynamic conditions in the mesenteric lymphatic during HDT are not dramatically altered.     

Adrenergic innervation of lymph nodes and the thoracic duct

By means of incubation of slices in 2% solution of glyoxylic acid distribution of adrenergic fibers in the rabbit lymph nodes and in the thoracic lymphatic duct has been studied. Adrenergic fibers get into parenchyma of the lymph nodes via two ways. The first--the perivascular, when the nervous fibers make a plexus and get into the node along the blood vessels, the second--diffuse nervous fibers get together with trabecules in between the lymphoid nodules. The distribution density of the adrenergic fibers is not the same in different groups of the lymph nodes. In the lumbar nodes it is the highest. In the lymph nodes of the cervical part the density of the sympathetic fibers is, as a rule, lower than in the lumbar, but higher than in the axillary nodes. The lowest density of th adrenergic fibers is in the mesenteric, superficial inguinal lymph nodes and in the lymph nodes, situating near the thoracic part of the aorta. In the lymphatic duct wall small amount of adrenergic fibers are revealed, they form a plexus, predominantly in the cranial part.     

Role of the lymphatic system in the transport of biologically active substances in shock of various etiologies

The content of histamine, serotonin, adrenaline and noradrenaline in the thoracic and lymphatic duct lymph and blood as well as absolute quantity of lymph transported biogenic amines and mediators into the general circulation were studied on 68 dogs during anaphylactic and endotoxin shock (ASh and ESh, respectively). Both ASh and ESh were accompanied by considerable changes in the hemodynamics, lymph circulation, content of biologically active substances in lymph and blood and in their lymph transport to the blood stream. The most profound and early changes in the content of biologically active substances during ASh and ESh were found in the lymph, which shows an important role of the lymphatic system in their resorption and transport from organs and tissues into the general circulation.     

A novel monoclonal antibody specific for lymphatic endothelium

The difficulty of identifying and differentiating lymphatic and blood microvessels in tissue sections can be overcome by a monoclonal antibody specific for lymphatic endothelium. Unfortunately, the only known antibody also reacts with the endothelium of some blood vessels. The technique of double immunization (passive, with an antiserum to blood endothelium, and active, with a suspension of lymphatic endothelial cells) was, therefore, used to increase the chances of recognizing specific lymphatic antigens by the mouse immune system. The monoclonal antibody obtained, LyMAb, a G₁ immunoglobulin, reacted strongly with the endothelium of bovine thoracic duct, mesenteric collecting vessels and lymphatic vessels of gall-bladder and lymph nodes and moderately with those of the intestinal wall. Blood vessels (intercostal arteries, azygos vein and blood microvessels of all organs tested) were consistently negative. The antibody was species-specific and did not react with formalin-fixed, paraffin-embedded sections. Cross-reactivity was limited to some connective tissue fibres and scattered cells in the lymph node parenchyma, intestinal villi and hepatic lobules.     

硝苯地平与硫酸镁治疗妊娠高血压综合征的临床疗效及对患者血清肌 酐、HSP70 及尿微量白蛋白水平的影响

目的:探讨硝苯地平联合硫酸镁对妊娠高血压综合征患者血清肌酐、HSP70及尿微量白蛋白水平的影响。方法:选取近5年在我院接受治疗的妊娠高血压综合征患者60例,随机分为实验组和对照组,每组30例。对照组患者采用硫酸镁治疗,实验组患者采取硝苯地平联合硫酸镁治疗。观察并比较治疗前后两组患者血清肌酐(Scr)、血尿素氮(BUN)、血尿酸(UA)热休克蛋白70(HSP70)及24 h尿微量白蛋白水平以及收缩压及舒张压的变化。结果:与治疗前相比,两组患者Scr、BUN、UA、HSP70及24 h尿微量白蛋白水平和收缩压及舒张压均显著降低(P0.05);与对照组相比,实验组患者上述指标均明显降低(P0.05)。结论:硝苯地平联合硫酸镁能够降低妊娠高血压综合征患者血压,保护患者肾功能。     

Mechanical characteristics of the canine thoracic duct: what are the driving forces of the lymph flow?

This study is designed to better understand the mode of lymph transport, particularly through the extrinsic pumping by external compression of the lymph vessel. The pressure-diameter relationship of lymphatic segments isolated from the canine thoracic duct was examined using a laser optical micrometer measurement system. Results revealed that the thoracic duct displayed a high extensibility or compliance in the physiological pressure range, yet became progressively less so with increasing internal pressure. The calculated incremental circumferential modulus of the thoracic duct under physiological pressure (range of 2 to 6 cm H2O) showed values ranging from 1.2 x 10(4) to 3.61 x 10(5) dyn/cm2. At a pressure of 35 cm H2O, the modulus reached a limiting value of approximately 6.0 x 10(6) dyn/cm2. In the physiological pressure range, the relative wall thickness (h/R0) of the canine thoracic duct was approximately 3.5%, which was much lower than that reported for canine arterial segments and similar in value to that of the canine jugular vein. In conclusion, the pressure-diameter curve of the canine thoracic duct was shown to resemble that of venous vessels. However, the circumferential elastic modulus of the thoracic duct wall was lower than the moduli of veins, proving that lymphatics are more compliant than veins. This suggests lymph flow in the thoracic duct may be better promoted by external compression of the lymphatic vessel.