大鼠内毒素休克肝线粒体Ca^2＋,Mg^2＋含量变化与线粒体损伤

本文在大鼠内毒素休克模型上，观察了肝线粒体结构和功能与Ｃａ＾２＋，Ｍｇ＾２＋含量变化的关系。结果发现：休克动物肝组织和线粒体的Ｃａ＾２＋浓度升高，Ｍｇ＾２＋浓度下降与正常对照组相比有非常显著性差异；用图像分析仪定量分析显示线粒体结构明显受损，线粒体标志酶之一－琥珀酸脱氢酶（ＳＤＨ）活性明显下降，本文认为组织和线粒体内Ｍｇ＾２＋／Ｃａ＾２＋比值下降是休克细胞不可逆损伤重要因素之一。     

内毒素休克时大鼠肠系膜微血管对去甲肾上腺素反应性的变化

本文应用微循环显微也视录象技术,研究内毒素休克大鼠在休克不同时期肠系膜微血管对去甲肾上腺素(NA)反应性的变化。发现局部滴用由低至高浓度NA使微血管口径呈剂量依赖性缩小,对照组在相当于休克相应时间三次观察收缩反应曲线无明显差异(P>0.05),而休克早期微血管对NA的缩血管反应明显,晚期收缩反应减弱(均P<0.01);同时,休克早期浓度—反应曲线右移,EC_(50)减小,反应阈值降低;休克晚期浓度—反应曲线左移,EC_(50)增大,反应阈值增高;但对照组三次观察无明显变化。提示内毒素休克早期微血管对NA的反应性增高,晚期反应性降低,一、二级细动脉的变化尤为显著。可能是休克早期的代偿与晚期的失代偿机理之一。     

脑热清对内毒素性发热家兔下丘脑、脑脊液cAMP及腹中隔区AVP含量的影响

目的:探讨脑热清(NRQ)口服液的解热机制。方法:复制家兔内毒素(ET)性发热模型,观察NRQ对家兔体温的影响;用放射免疫法检测下丘脑和脑脊液(CSF)中cAMP及腹中隔区AVP含量的变化。结果:(1)NRQ+ET组的ΔT[(0.82±0.08)℃]、TRI₆(5.73±0.09)、下丘脑cAMP含量[(0.70±0.50)nmol/g]、CSF中cAMP含量[(56.86±1.34)nmol/L]及腹中隔区AVP含量[(11.91±3.47)ng/g],分别低于ET组的ΔT[(1.80±0.16)℃]、TRI₆(11.31±0.20)、下丘脑cAMP含量[(1.35±0.21)nmol/g]、CSF中cAMP含量[(66.69±1.82)nmol/L]、腹中隔区AVP含量[(30.80±9.59)ng/g],两者相比有显著差异(P<0.01)。(2)4组的体温变化分别与下丘脑和CSF中cAMP以及腹中隔区AVP的变化呈正相关(下丘脑:r=0.899,P<0.05;CSF:r=0.991,P<0.01;AVP:r=0.972,P<0.01)。结论:NRQ的解热机制可能是通过抑制下丘脑cAMP的生成与释放,同时通过促进腹中隔AVP释放两种途径发挥作用。     

小鼠内毒素休克某些血液变化和细胞超微结构损伤的发生

小鼠内毒素休克有血液的乳酸、ＮＰＮ、ＡＫＰ、ＬＤＨ水平升高和ｐＨ值降低并可用６５４－２或ＡＬ所预防，只是预防ＮＰＮ升高的效应须在早期的肾血管挛缩消失后才能显示出来；心、肝、肠和肺的ＭＤＡ含量升高并可被６５４－２预防，除肺外还可被ＡＬ预防；将高肺ＭＤＡ只能用６５４－２预防结合注射内毒素后１０ｍｉｎ有ＷＢＣ入肺扣押来看，损伤肺的自由萁坷能主要来自被激活的中性粒细胞；血中ＡＫＰ和ＬＤＨ升高分别反映溶酶体     

脾切除对大鼠血浆及肝肺组织中内毒素廓清的影响

目的 观察脾切除对血浆中内毒素清除的影响及内毒素在主要脏器的分布特征,探索脾切除后上反应与组织损害的发生机制。方法 雄性Ｗｉｓｔａｒ大鼠１１２只,随机分为有脾组（ｎ＝５６,行大网膜切除术,保留脾脏）、脾切除组（ｎ＝５６,行脾切除术）。术后１周静脉注射内毒素０．１ｍｇ／ｋｇ,分别于注射前、注射后１０ｍｉｎ、０．５、１．５、４、１２、２４ｈ活杀动物,测定血浆和肝、肺组织内毒素水平,同时检测肝、肺脏器功     

三羟异黄酮保护内毒素诱导急性肺损伤实验研究

目的探讨三羟异黄酮对内毒素(LPS)诱导急性肺损伤(ALI)的保护作用及作用机制。方法将32只大鼠随机分为4组(每组8只):生理盐水组(S组)、三羟异黄酮组(G组)、LPS组(L组)和三羟异黄酮预处理组(G L组)。LPS刺激后,观察6 h。以肺湿干重比(W/D)和支气管肺泡灌洗液(BALF)蛋白含量作为肺损伤的指标。通过检测髓过氧化物酶(MPO)活性及BALF中细胞学分析来评估中性粒细胞的聚集和活性。采用RT-PCR,检测ICAM-1mRNA在肺组织表达的变化。肺组织经HE染色后,观察组织病理学上的改变。结果L组大鼠BALF总蛋白和W/D都较对照组明显升高(P<0.01);同S组比较,在G L组LPS导致了BALF、肺组织匀浆MPO活性及BALF中PMN数目显著增加(P<0.01);L组大鼠肺组织中ICAM-1mRNA表达水平显著高于S组(P<0.01)。预先给予三羟异黄酮可以非常显著抑制LPS引起这些指标的改变(P<0.05或0.01)。三羟异黄酮预处理也改善了LPS所致肺组织形态学上严重的损伤。上述所有参数在G组与S组间差异无统计学意义。结论三羟异黄酮预处理能够减轻LPS诱导的大鼠急性肺损伤。这种效果可能与其下调ICAM-1的表达而抑制PMN在肺组织的聚集、激活有关。     

注射用对氨基水杨酸钠细菌内毒素检验探讨

用<中国药典>2000年版附录细菌内毒素检验法对PAS进行细菌内毒素检测并建立实验方法.实验结果表明用TAL试剂对PAS最大无干扰浓度为5mg/ml,无干扰作用,提示用细菌内毒素检查法检查PAS中的内毒素是可行的.     

Does supplemental photodynamic therapy optimize the disinfection of bacteria and endotoxins in one-visit and two-visit root canal therapy? A randomized clinical trial

AimTo evaluate the effectiveness of supplemental photodynamic therapy (PDT) in optimizing the removal of bacteria and endotoxins from primarily infected root canals after one-visit and two-visit treatments.MethodologyTwenty-four primarily infected root canals with apical periodontitis were selected and randomly divided into one-visit (n = 12) and two-visit treatment groups (n = 12). Chemo-mechanical preparation (CMP) was performed by using the single-file reciprocating technique + 2.5% NaOCL and a final rinse with 17% EDTA. The photosensitizer agent (methylene blue 0.1 mg/mL) was applied to root canals for 60 s before application of laser with a potency of 60 mW and energy density of 129 J/cm² for 120 s after CMP in the one-visit treatment and after 14-day inter-appointment medication with Ca(OH)₂ + Saline solution (SSL) in the two-visit treatment. Samples were collected before and after root canal procedures. Endotoxins were quantified by chromogenic limulus amebocyte lysate assay. Culture techniques were used to determine bacterial colony-forming unit counts.ResultsBacteria and endotoxins were detected in 100% of the initial samples, with median values of 1.97 × 10⁵ CFU/mL and 24.983 EU/mL, respectively. The CMP using single-file reciprocating technique was effective in the reduction of bacteria and endotoxins (All, p < 0.05). The supplemental PDT was effective in reducing bacterial load in the one-visit (p < 0.05) but not in the two-visit treatment after use of Ca(OH)₂ medication for 14 days (p > 0.05). In the two-visit group, after 14 days of inter-appointment medication with Ca(OH)₂, a significant reduction in the median levels of endotoxins was found in comparison to CMP alone (from 1.041 to 0.094 EU/mL) (p < 0.05). Despite the type of treatment, the supplemental PDT was not effective against endotoxins (p > 0.05).ConclusionsThe photodynamic therapy optimized the disinfection of bacteria from root canals in one-visit but not for two visit treatment modality with the accomplishment of calcium hydroxide medication. Despite the type of treatment, the supplemental PDT was not effective against endotoxins.     

Bacterial translocation induces proinflammatory responses and is associated with early death in experimental severe injury

Objective

An experimental model of severe injury with great lethality was studied to define the impact of bacterial translocation on survival and on inflammatory response.

Methods

Forty-one rabbits were divided into two groups: A, femur myotomy; and B, myotomy and fracture of the femoral bone. Vital signs and survival were recorded. Serum circulating endotoxins (lipopolysaccharides; LPS) were determined and tissue cultures were performed at necropsy. A subgroup of animals was sacrificed at 48 h post injury; LPS was determined in abdominal aorta and portal vein, apoptosis of spleen cells was assessed by flow cytometry, and ex vivo production of tumor necrosis factor alpha by splenocytes was measured.

Results

Tissue bacterial burden was increased in animals that died early (i.e., within 48 h after injury) versus rabbits that died later. Portal vein LPS at 48 h was increased in group B compared with group A, whereas circulating LPS did not differ. No difference in apoptosis of either lymphocytes or macrophages of the spleen was found in group B compared with group A. Following stimulation with LPS or phytohemagglutinin, tumor necrosis factor α production by splenocytes of group B was greater than that of group A.

Conclusions

Bacterial translocation primes enhanced proinflammatory responses and it is associated with early death in severe trauma.     

TNF-α、LPS、IL-6、PAF与重症胸腹损伤凝血功能障碍的相关性研究

目的 探讨肿瘤坏死因子-α(TNF-α)、内毒素(LPS)、白细胞介素-6(IL-6)和血小板活化因子(PAF)与重症胸腹创伤后凝血功能障碍的相关性与机制.方法 收集2009年1月-2012年6月在解放军第二五三医院急诊科就诊,创伤指数(TI)≥17分,排除合并颅脑损伤及在急诊死亡的胸腹创伤患者82例,在救治同时抽血检查血小板计数(PLT)、部分活化凝血酶原时间(APPT)、凝血酶原时间(PT)、TNF-α、LPS、IL-6、PAF,对检验结果行相关性分析.结果 凝血功能检验结果:PLT:(83.44±38.52)×109/L),APTT:(68.24 ±24.12)S,PT:(28.42±10.83)S;损伤因子检测结果:TNF-α:(36.41±18.09) ng/mL,LPS:(343.66±106.02) IU/L,IL-6:(393.83±143.86) ng/mL,PAF:(15765.31±4431.65) ng/L.PLT与TNF-α、LPS、IL-6、PAF之间相关系数(r)均小于-0.8811,呈显著负相关.APTT、PT与TNF-α、LPS、IL-6、PAF之间r均大于0.9142,呈显著正相关.结论 TNF-α、LPS、IL-6、PAF可能参与了重症胸腹创伤凝血功能障碍的发生过程,对TNF-α、LPS、IL-6、PAF早期干预,或可改善胸腹创伤患者的凝血功能障碍.