内毒素血症细胞因子一氧化氮在重度失血性休克发展中的作用

目的　探讨内毒素血症、细胞因子、ＮＯ在重度失血性休克发展过程中的作用和机制。方法　选用大白兔２６只，分为失血性休克组（１４ 只），对照组（１２ 只），休克组观察休克前后血浆内毒素、ＴＮＦα、ＩＬ－ ６、ＩＬ－８、ＮＯ的动态变化，对照组观察手术前后上述指标的变化，两组动物均观察２４ 小时、４８ 小时存活率。结果　大白兔发生失血性休克后血浆内毒素、ＴＮＦα、ＩＬ－６、ＩＬ－８ 、ＮＯ的水平与休克前及对照组比较有明显升高，死亡动物中血浆上述物质水平显著高于存活动物。结论　内毒素血症、细胞因子、ＮＯ等发挥重要的协同作用，促使失血性休克向不可逆方向进展。     

Defining the Microbiological Quality of Dialysis Fluid

With increasing awareness about the degree and the potential impact of microbiological contamination in dialysis fluids, there is a desire to improve their microbiological quality. To achieve this goal, the origin of the microbiological contamination has to be identified. The water, the bicarbonate concentrate, and the fluid distribution system can be major contributors. Regular disinfection of the entire fluid path is necessary to prevent the formation of biofilm. The bicarbonate concentrate should be handled with special attention because it constitutes an excellent growth medium for microflora that may not be detected with regular assays. With a well maintained reverse osmosis (RO) system, frequent disinfection of the entire flow path, and microbiological awareness, it is possible to produce dialysis fluid that meets the most stringent standard (<10² colony forming units (CFU)/ml and <0.25 IU/ml of endotoxin). Adding a step of ultrafiltration just before the dialyzer can make the dialysis fluid ultrapure (<10⁻¹ CFU/ml and <0.03 IU/ml). One additional step of controlled ultrafiltration provides sterile and pyrogen-free fluids (<10⁻⁶ CFU/ml and <0.03 IU/ml) that can be used for infusion.     

内毒素休克狗心脏腺苷酸环化酶的改变

本实验在高度纯化的心肌肌膜观察到,狗注射内毒素后4小时,心脏基础腺苷酸环化酶及NaF、Gpp(NH)p、isoproterenol刺激的腺苷酸环化酶活性均明显降低。并对其机制进行了讨论。     

异丙酚和异氟醚后处理对内毒素血症大鼠肺泡液体转运功能的影响

目的建立内毒素血症大鼠模型,应用异丙酚和异氟醚,以肺组织湿干重比、肺泡液体清除率、肺水通道1为指标,观察肺泡液体转运功能的变化。方法健康SD大鼠32只,随机分为4组。生理盐水组：尾静脉注射生理盐水;内毒素组、异丙酚组和异氟醚组均静注内毒素。1小时后,异丙酚组泵注异丙酚,异氟醚组持续异氟醚吸入。2小时后取标本,测定肺组织湿干重比、肺泡液体清除率;Westernblot法检测水通道1蛋白。结果各组肺组织湿/干比差异均无统计学意义。异氟醚组肺泡液体清除率（0.054±0.007）较异丙酚组（0.065±0.006）高;异氟醚组水通道1为（0.53±0.06）较异丙酚组（0.60±0.07）高,均有显著差异（P〈0.05）。结论与异丙酚相比,异氟醚后处理增加内毒素血症大鼠肺泡液体清除率和水通道1蛋白表达。     

The effect of norepinephrine on endotoxin-mediated macrophage activation

The effect of norepinephrine (NE) on the production of tumor necrosis factor (TNF) by rat spleen macrophages was determined. Following activation with lipopolysaccharide, analysis of both secreted and cell-associated samples showed that TNF activity was significantly suppressed in the presence of 10 microM NE. With the addition of the beta-receptor antagonist propranolol a partial reversal of the suppressive effect of NE was noted whereas the addition of the mixed alpha-receptor antagonist phentolamine induced a more pronounced suppressive effect in the supernatant fraction. Similar results were obtained with epinephrine and isoproterenol. Control experiments confirmed that this effect of NE was mediated at the level of macrophage activation. Analysis of lymphocyte activating factors demonstrated a similar pattern of response. Since factors released by macrophages participate in many aspects of the immune response, these results support a functional role for sympathetic innervation of the spleen in immune regulation.     

Airborne endotoxin associated with particles of different sizes and affected by water content in handled straw

High exposures to endotoxin are observed in environments where organic materials are handled and lower exposures are found in e.g. indoor air. Inhaled endotoxin contributes significantly to the induction of airway inflammation and dysfunction. The size of an inhaled particle influences the deposition in the airways and the following health symptoms. The objective is to characterise the distribution of endotoxin on airborne particles of different sizes in straw storage halls with high exposure and in other environments with lower exposure levels to endotoxin. Furthermore we have studied the influence of water content of handled straw on the size distribution of endotoxin containing particles. Total, inhalable, thoracic and respirable endotoxin and particles have each been quantified in aerosols from boiler rooms and straw storage halls at 24 power plants, including 21 biofuel plants. Inhalable, thoracic and respirable endotoxin have been quantified in aerosols from offices and outdoor air. The endotoxin concentration was higher in airborne thoracic dust than in airborne ‘total dust’. The median respirable fraction in the straw storage halls, boiler rooms at biofuel plants, boiler rooms at conventional plants, offices and outdoors was respectively 42%, 9%, 19%, 24% and 34%. Thoracic endotoxin per number of thoracic particles was higher than respirable endotoxin per number of respirable particles at the biofuel plants. In straw storage halls the fraction of endotoxin of respirable size was highest on the days with lowest water content in the received straw. Furthermore the exposures to all endotoxin fractions were highest on days with the lowest water content in the received straw. In conclusion the highest exposures and concentrations of endotoxin occur or tend to occur from thoracic dust. A high variation in endotoxin concentrations and in fractions of respirable or thoracic size is found in the different working areas. This is important in the risk assessment and makes attempts to influence the endotoxin exposure a possibility. Water content in straw affected the concentration, exposure level and size distribution of airborne endotoxin.     

鲎试验和家兔法测定干扰素和白蛋白中内毒素的比较

本文分别用鲎试验和家兔热原法对16批人白细胞干扰素及5批人血浆白蛋白中的内毒素进行了检测。两种方法检测人白细胞干扰素和人血浆白蛋白的符合率分别为81.75%和80%;阴性符合率为100%。     

内毒素刺激猪主动脉内皮细胞PGI_2生成

本文初步观察了 E Coli 内毒素对体外培养的猪主动脉内皮细胞 PGI_2生成的影响。结果发现内毒素显著刺激培养细胞 PGI_2的生成,并呈剂量(1—1000ng/ml)和时间(6—24小时)依赖性,但不同于其它刺激剂,内毒素的作用时间至少需要2小时以上。     

上海市血液净化中心透析用水及透析液细菌污染情况调查

目的　了解上海市透析用水、透析液的细菌污染状况。方法　采集上海市 10家医院反渗水及透析液标本 ,对反渗水及透析液标本进行细菌培养和菌落计数 ;用LAL试剂盒测定反渗水及透析液中的内毒素含量。结果　反渗水细菌培养有 3家医院阳性 ,细菌计数均 <2 0 0CFU/ml,内毒素为 (0 .5 19± 0 .6 87)EU/ml,其中 5家 >0 .2 5EU/ml;A浓缩透析液内毒素为 (0 .2 35± 0 .2 2 7)EU/ml;B浓缩透析液内毒素为 (0 .6 88± 0 .74 2 )EU/ml;透析液入口细菌培养 3家阳性 ,其中 1家 >2 0 0 0CFU/ml,内毒素为 (1.4 4 9± 3.4 73)EU/ml,其中 1家 >5EU/ml。结论　目前上海市部分血液净化单位仍存在反渗水及透析液的细菌污染 ,应定期检测运血导管、透析器、透析机和透析液的污染情况 ,并定期消毒。     

Effects of NO inhalation on pulmonary leukocyte sequestration and blood volume in porcine endotoxaemia

Objective: Sequestration and migration of activated neutrophils plays a major role in the pulmonary injury typical of septic shock and the adult respiratory distress syndrome. Inhaled NO may counteract alveolar-capillary damage attributed to activated neutrophils. The present study describes a method to directly demonstrate the effects of NO inhalation on endotoxin-induced sequestration of ^{99 m}Tc-labelled leukocytes [A_s(t)] in the lungs of pigs.¶Design: Prospective controlled study.¶Setting: Laboratory for experimental surgery at a university medical centre.¶Subjects: Anaesthetised and ventilated pigs.¶Interventions: To induce inflammatory shock 26 animals received a continuous endotoxin infusion. Thirteen animals inhaled NO from the start of the experiments, while 13 served as controls. In 13 animals from both groups, leukocytes were labelled in vitro and reinjected, while in the 13 others erythrocytes were labelled in vivo to provide corrections for changes in blood volume.¶Measurements and results: The pulmonary distribution of ^{99 m}Tc-labelled leukocytes or erythrocytes was studied dynamically for 180 min. After correction for changes in pulmonary and heart blood volume (PBV, HBV), leukocyte sequestration curves were generated. Endotoxin induced pulmonary vasoconstriction, reduced PBV, impaired oxygenation, and caused a maximum increase in A_s(t) of 30 % in the lungs. NO inhalation attenuated pulmonary vasoconstriction and the reduction in PBV. The maximum increase in A_s(t) was reduced to 15 % of baseline.¶Conclusions: Inhaled NO exerts its main vascular effects in the pulmonary microvasculature, the primary site of physiological neutrophil margination and pathological adhesion of activated leukocytes. Early use of NO inhalation may offer protection against the development of more lasting pulmonary failure in septic shock by reducing leukocyte sequestration in the lungs.