急性有机磷中毒患者内毒素和肿瘤坏死因子与多器官功能障碍综合征的相关研究

目的：探讨血浆内毒素（LPS）及肿瘤坏死因子（TNF）在中重度急性有机磷中毒（AOPP）后多器官功能障碍综合征（MODS）发生发展中的作用机制及其临床意义。方法：应用动态浊度法及放射免疫法动态监测46例中重度AOPP患者血浆LPS和TNF和水平,比较MODS组与非MODS组及正常对照组LPS及TNF的变化。结果：46例患者血浆LPS及TNF水平均明显升高,较正常对照组差异有非常显著性（P均＞0．01）,且血浆高水平持续较长时间,MODS组升高的峰值较非MODS组更显著（P＜0．05和P＜0．01）。结论中重度AOPP的早期即可导致内毒血症的发生,内毒素可能是导致炎性介质产生和释放的重要机制,是有机磷中毒机制的重要组之一,血浆LPS与TNF的高水平可能参与了中重度AOPP后MODS的发病的过程。     

急性有机磷中毒患者内毒素和肿瘤坏死因子与多器官功能障碍综合征的相关研究

目的 探讨血浆内毒素(LPS)及肿瘤坏死因子(TNF)在中重度急性有机磷中毒(AOPP)后多器官功能障碍综合征(MODS)发生发展中的作用机制及其临床意义.方法 应用动态浊度法及放射免疫法动态监测46例中重度AOPP患者血浆LPS和TNF和水平,比较MODS组与非MODS组及正常对照组LPS及TNF的变化.结果 46例患者血浆LPS及TNF水平均明显升高,较正常对照组差异有非常显著性(p均<0.01),且血浆高水平持续较长时间,MODS组升高的峰值较非MODS组更显著(p<0.05和p<0.01).结论 中重度AOPP的早期即可导致内毒素血症的发生,内毒素可能是导致炎性介质产生和释放的重要机制,是有机磷中毒机制的重要组成之一.血浆LPS与TNF的高水平可能参与了中重度AOPP后MODS的发病的过程.     

血必净注射液对急性梗阻性黄疸大鼠心肌损伤的保护作用

目的：观察血必净注射液对急性梗阻性黄疸大鼠心肌损伤的保护作用。方法：采用结扎SD大鼠胆总管的方法制作急性梗阻性黄疽动物模型。将54只SD大鼠随机均分为胆总管结扎（BDL）组、胆总管结扎血必净治疗组（XBJ）、假手术组（SO）3组。XBJ组在胆总管结扎后48h开始尾静脉注射血必净注射液,BDL组和SO组同样方法注射等量生理盐水。分别于给药后第3、7、14天各取6只大鼠采样,观察血清胆红素（TBIL）、肌酸激酶同工酶（CK—MB）、内毒素（ET）含量,心肌组织丙二醛（MDA）和超氧化物歧化酶（SOD）含量,以及光镜下观察心肌病理变化。结果：急性胆道梗阻后,血清TBIL、CK—MB、ET水平及心肌组织MDA含量随梗阻时间延长逐渐增高,心肌组织SOD含量减少。XBJ组与同时相BDL组比较,血清TBIL、CK—MB、ET水平及心肌组织MDA含量减少,心肌组织SOD含量增高。光镜下可见随胆道梗阻时间延长,心肌损伤加重,XBJ组与同时相BDL组比较,心肌损伤减轻。结论：血必净注射液对急性胆道梗阻所致心肌损伤有保护作用,作用机制可能与其抗内毒素血症、TNF—α作用及对抗氧自由基有关。     

维生素E对家兔多器官功能障碍血管内皮细胞的保护作用

利用家免多器官功能障碍综合征（MODS）模型观察维生素E（VitE）对血管内皮细胞的保护作用。采用内皮细胞形态观察并同步检测血液MDA、SOD、CAT、TXB2、6－K－PGFIα以及应用VitE后对其影响。结果示MODS组动物血中MDA和TXB2含量随MODS的发生发展显著升高（P＜0．01），而SOD、CAT及6－K－PGFIα含量降低（P＜0．01）。利用扫描和透射电镜观察MODS血管内皮细胞发生显著损伤，失去正常形态；而补充VitE组前述各项指标均得到不同程度的改善．观察结果提示，MODS动物体内脂质过氧化损伤明显增强，而抗氧化能力明尼降低。这种变化可能在MODS发病中具有重要的病理生理意义。早期应用VitE对MODS的防治是有益的。     

血必净治疗社区获得性肺炎的研究进展

内毒素是革兰氏阴性杆菌细胞壁中的一种成分,叫做脂多糖,脂多糖对宿主有毒性作用。内毒素在社区获得性肺炎患者中的作用不容忽视,尤其是伴有高热、白细胞升高、全身炎症反应综合症的老年和危重症患者。近年来研究证实血必净可拮抗内毒素,降低内毒素引发的血清TNF-α水平,在社区获得性肺炎的治疗中疗效可靠。本文就血必净治疗社区获得性肺炎作用机制及临床应用效果作一综述。     

血必净注射液对重症蝮蛇咬伤患者免疫功能的影响

目的 研究血必净注射液对重症蝮蛇咬伤患者对机体免疫调节功能的影响。方法 对2014年7月~2017年10月本院急诊科收治的重症蝮蛇咬伤患者46例,常规治疗组按照经典的毒蛇治疗法,观察组使用血必净注射液治疗;健康对照组选择为同期体检正常人。分析各组在治疗前、治疗第1天、第3天及第7天,检测其血清促炎介质IL-6和抗炎介质IL-10水平,代表性评估患者的免疫功能。结果 治疗前和治疗第1天,2个治疗组IL-6无明显区别,但均高于对照组,两治疗组于治疗第3天、第7天IL-6水平均降低,差异有统计学意义（P＜0.05）,但观察组较常规治疗组下降（P＜0,05）;各组IL-10水平在治疗前与治疗第1天,差异无统计学意义（P＞0.05）,但第3天、第7天,治疗组则高于健康对照组（P＜0.05）,两治疗组间,差异无统计学意义（P＞0.05）。结论 重症蝮蛇咬伤患者的免疫功能可出现紊乱,表现为早期促炎介质占优势,后期抗炎介质升高明显,血必净注射液可下调促炎介质（IL-6）水平,在一定程度上调节机体免疫功能。     

多器官功能障碍综合征发病机制的某些研究进展

多器官功能障碍综合征(multiple organ dysfunction syndrome，MODS)是指机体在各种感染、炎症、创伤、休克及大手术等原发病发生24h后，同时或序贯性地发生两个或两个以上器官或系统功能不全的一种临床综合征，继续发展可导致多器官衰竭(MOF)。90年代以来，随着细胞生物学和分子生物学技术的发展和进步，人们对MODS     

重症急性胰腺炎与多器官功能障碍综合征

微循环障碍是重症急性胰腺炎 (SAP)和多器官功能障碍综合征 (MODS)的启动因子和持续损害因子 ,失控的炎症反应最终导致多器官损伤。核转录因子 κB(NF κB)调控着许多重要的炎症介质 ,从而在SAP的炎症反应中起着重要作用。     

血必净联合生长抑素对重症急性胰腺炎患者炎症因子及预后的改善作用

目的:探究血必净联合生长抑素对重症急性胰腺炎(severe acute pancreatitis,SAP)患者炎症因子及预后的改善作用.方法:选取2018年1月至2021年3月安徽省第二人民医院收治的108例SAP患者为研究对象,随机分为对照组和观察组,每组54例.对照组予以生长抑素治疗,观察组予以血必净联合生长抑素治...     

感染相关的多器官功能障碍发病机制的研究进展

会阴部(肛周)坏死性筋膜炎,又名Fournier综合征,是肛肠外科急重症之一,病情凶险,发展迅速,病死率较高,其主要死因是严重感染导致的多器官功能障碍(衰竭),本文就多器官功能障碍的发病机制,结合近年来国内外的相关研究,做一回顾性总结与分析。主要包括几个方面院与全身炎性反应综合征的关系,多种细胞因子与炎性介质的作用,各种发病假说,如院肠道动力学说,缺血再灌注和自由基学说,细胞凋亡,基因多态性学说,以及最近提出的PICS(Persistent inflammation,Immunosuppres ion,and Catabolism Syndrome持续性炎症-抗炎反应代谢综合征),免疫机制的负向调控等等。     

单核细胞HLA-DR表达与多脏器功能障碍综合征

目的：观察多脏器功能障碍综合征患者单核细胞表面ＨＬＡ－ＤＲ抗原表达。方法：采用直接免疫荧光法流式细胞术对重症感染、严重损伤患者单核细胞表面ＨＬＡ－ＤＲ抗原的表达进行连续监测。结果：发生ＭＯＤＳ的患者入院后ＨＬＡ－ＤＲ的表达水平比未发生ＭＯＤＳ者显著降低，而且其动态变化与预后有明显的相关性。结论：可以通过检测患者单核细胞表面ＨＬＡ－ＤＲ抗原的表达，对早期ＭＯＤＳ进行诊断，为指导ＭＯＤＳ的临床救治提供良好的帮助。     

产科多器官功能障碍综合征临床分析

目的探讨产科多器功能障碍综合征（MODS）的诱因、临床诊断及处理。方法对16例MODS的临床资料进行回顾性分析。结果导致MODS的主要因素为妊娠期高血压疾病及产后出血,器官功能障碍以肾功能衰竭为最多见。结论及时处理MODS的诱发因素,积极治疗妊娠期高血压疾病及产后出血,早期诊断及治疗肾功能衰竭及凝血功能障碍,是减少产科MODS患者死亡的关键。     

持续血液净化在热射病合并多器官功能障碍综合征治疗中应用

目的探讨持续血液净化（CBP）对热射病（HS）合并多器官功能障碍综合征（MODS）治疗效果。方法选择2005年5月～2009年8月HS合并MODS患者11例,其中男性10例,女性1例,年龄17～25岁。每次治疗24～48h,置换液以前稀释方式输入,流量为2～4L/h,血流量150～250mL/min,采用普通肝素抗凝,而对于部分严重出血倾向患者,在给予补充血小板、凝血酶原复合物、纤维蛋白原等凝血底物的同时给予小剂量肝素抗凝。结果11例患者中9例痊愈出院,2例死亡;CBP治疗中患者血流动力学保持相对稳定,平均动脉压、心率和氧合指数均有所改善,多巴胺剂量逐渐减少（P〈0.05）,急性生理学及慢性健康状况（APACHEⅡ）评分降低（P〈0.05）;血中肌酐、尿素氮、肌红蛋白、肌酸激酶下降明显（P〈0.05）,但胆红素无明显变化（P〉0.05）;治疗中未发现明显副作用。结论CBP对HS合并MODS患者有改善预后的作用,患者耐受性好,是抢救HS合并MODS患者有效手段之一。     

Increased expression of matrix metalloproteinases in the murine zymosan-induced multiple organ dysfunction syndrome

Matrix metalloproteinases (MMPs) have been implicated as mediators of tissue damage in several inflammatory diseases. Since the multiple organ dysfunction syndrome (MODS) is thought to result from systemic inflammation, overactivation of MMPs could contribute to the organ damage observed. The expression and activity of several MMPs were studied in a murine model for MODS. Sixty mice were given an aseptic intraperitoneal injection of lipopolysaccharide, followed, after 6 days, by zymosan. At days 2, 5, 8, 12, and 16 after the injection of zymosan, the liver, lungs, spleen, and kidneys were collected from groups of mice for either RNA extraction, gelatinase zymography and collagenase (MMP-1 and -13) assays (six mice per time point), or immunohistochemistry (three mice per time point). A group of nine mice did not receive zymosan and acted as controls. The expression of MMP-2 mRNA in zymosan-treated mice was strongly up-regulated in liver tissue only. For MMP-9, this was the case in all organs examined. Quantitative gelatin zymography demonstrated the near complete absence of any gelatinase activity in tissues from control mice. However, in the liver, lungs, and especially the spleen of zymosan-treated animals, significantly increased activity of proform and active MMP-2 and -9 was observed with time. Overall, MMP-1 and -13 activities were very low in all samples from the liver and lungs. In the spleen, however, high levels of MMP-1 and -13 were observed in zymosan-treated animals. Immunohistochemical staining for MMP-2 was detected in the liver and spleen, but not in lung and kidney tissue of zymosan-treated animals. Staining for MMP-9 could be detected in liver, lung, and spleen tissues of zymosan-treated mice. For both MMPs, staining appeared to be limited to phagocytes. In conclusion, the data suggest a role for MMPs, especially MMP-9, in the pathogenesis of MODS.     

Multiple organ dysfunction syndrome,an unusual complication of heroin intoxication: a case report and review of literature

Multiple organ dysfunction syndrome (MODS) has rarely been described in patients with heroin intoxication. Here, we report a rare case of MODS involving six organs, due to heroin intoxication. The patient was a 32-year-old Chinese man with severe heroin intoxication complicated by acute pulmonary edema and respiratory insufficiency, shock, myocardial damage and cardiac insufficiency, rhabdomyolysis and acute renal insufficiency, acute liver injury and hepatic insufficiency, toxic leukoencephalopathy, and hypoglycemia. He managed to survive and was discharged after 10 weeks of intensive care. The possible pathogenesis and therapeutic measures of MODS induced by heroin intoxication and some suggestions for preventing and treating severe complications of heroin intoxication, based on clinical evidence and the pertinent literature, are discussed in this report.     

Histopathological and cytological examination of autopsy cases with multiple organ dysfunction syndromes

To evaluate the role of small scavenger receptor A (SRA)‐positive (SRA⁺) cells and large SRA⁺ cells in the peripheral blood (PB) in the pathophysiological mechanisms underlying multiple organ dysfunction syndromes (MODS), 24 autopsy cases with MODS were examined. In addition to histopathological and immunohistochemical examination, cytokine levels of cardiac blood, the SRA index (number of small SRA⁺ cells in 10 high power fields, upper limit <30), and appearance of large SRA⁺ cells in PB were examined. The SRA index exceeded 30 in all cases. Large SRA⁺ cells and tumor necrosis factor (TNF)‐α⁺ cells were detected in PB in all cases. Macrophage colony stimulating factor (M‐CSF), interleukin (IL)‐6 and IL‐8 levels exceeded the normal level in all cases, and 18 and 15 cases had TNF‐α and IL‐1β levels above the normal threshold, respectively. Lung injury and necrosis of cardiac myocyte were observed in all cases. Neutrophils and platelets accumulated in the capillaries of injured organs and endothelial cells were extensively injured. From these results, large SRA⁺ cells differentiated from monocytes in PB were considered to play an important role in the development of MODS, and necrosis of cardiac myocytes together with lung injury might be the leading cause of death in MODS patients.     

Continuous veno-venous hemodiafiltration alleviates multiple organ dysfunction syndrome in dogs

Context: Multiple organ dysfunction syndrome (MODS) is a major cause of death in critically patients. It has been hypothesized that inactivation or removal of pro-inflammatory molecules may prevent or reverse MODS.

Objective: The purpose of this paper was to investigate the efficacy of continuous veno-venous hemodiafiltration (CVVHDF) as treatment for MODS in an established animal model.

Materials and methods: Male Beagle dogs (n = 18) were used to establish the model and were randomly assigned to a CVVHDF, sham, or control group. The serum levels of ALT, AST, Cr, BUN, PaO₂, and PaCO₂ were measured as functional makers of major organs. Apoptosis, DLA-DR expression, and cytokine levels of peripheral monocytes were determined.

Results: The MODS model was successfully established. After CVVHDF treatment, the WBC and neutrophil counts were lower and the monocyte count and percentage were greater, but these were unchanged in the sham and control groups. Apoptosis of CD14+ monocytes was significantly lower in the CVVHDF group than in the sham and control groups. The fraction of DLA-DR⁺ monocytes and IL-1β secretion was significantly greater in the sham and control groups than in the CVVHDF group. Moreover, IL-4 secretion increased significantly in the CVVHDF group but not in the control group.

Discussion and Conclusion: Our study of an experimental model of MODS indicated that MODS leads to significant disruption of physiological and immune functions. CVVHDF treatment alleviated some of these symptoms due to the improvement of monocyte function, reduction of monocyte apoptosis, and increase of anti-inflammatory cytokines.     

CCR7在多器官功能障碍综合征小鼠脾脏树突状细胞迁移变化中的作用

目的:探讨CCR7在多器官功能障碍综合征(MODS)脾脏中的表达变化及其对树突状细胞(DC)迁移的影响.方法:用酵母多糖腹腔注射复制小鼠MODS模型,分为正常对照组和实验3～6小时组、24～48小时组、5～7天组及10～12天组.运用免疫组化方法检测CD11c和CD205标记阳性DC在各组小鼠脾脏中分布的变化,用流式细胞术检测CD86/CD11c和CCR7/CD11c标记阳性细胞在脾脏中含量的变化.结果:正常小鼠脾脏DC含量较少,主要分布在脾脏边缘区;在3～6小时组CCR7表达率较正常对照组显著增加,DC含量显著增加、活性增高,并向白髓T细胞区大量迁移;24～48小时组T细胞区中DC含量开始减少,而CCR7表达率升高达到峰值;5～7天组DC与CCR7含量接近正常对照组,边缘区和T细胞区均可见DC分布;10～12天组DC含量再次升高,但多呈不成熟状态,且以边缘区分布为主,CCR7表达率下降.结论:在MODS病程中脾脏DC的含量和分布变化与CCR7的表达率密切相关,CCR7可以作为评估脾脏DC迁移能力及功能活性的重要指标.     

Distant organ dysfunction in acute kidney injury

Acute kidney injury (AKI) is a common complication in critically ill patients and it is associated with increased morbidity and mortality. Epidemiological and clinical data show that AKI is linked to a wide range of distant organ injuries, with the lungs, heart, liver, and intestines representing the most clinically relevant affected organs. This distant organ injury during AKI predisposes patients to progression to multiple organ dysfunction syndrome and ultimately, death. The strongest direct evidence of distant organ injury occurring in AKI has been obtained from animal models. The identified mechanisms include systemic inflammatory changes, oxidative stress, increases in leucocyte trafficking and the activation of proapoptotic pathways. Understanding the pathways driving AKI‐induced distal organ injury are critical for the development and refinement of therapies for the prevention and attenuation of AKI‐related morbidity and mortality. The purpose of this review is to summarize both clinical and preclinical studies of AKI and its role in distant organ injury.     

The role of the microcirculation in multiple organ dysfunction syndrome (MODS): a review and perspective

Major advances in intensive care medicine during the past two decades have altered the spectrum of disease encountered by intensive care physicians, anaesthesiologists, traumatologists and pathologists. One of the most important manifestations of severe trauma or infections is the multiple organ dysfunction syndrome (MODS), a life-threatening condition that often ends in multiple organ failure (MOF) and death. Evidence gathered from clinical and morphological observations in humans, taken together with experimental animal studies and a vast accumulation of in vitro data, clearly indicate that the microcirculation lies at the centre of this complex process, which results in peripheral vascular insufficiency, inadequate oxygen delivery to vital organs, and hence, severe organ dysfunction. The multifunctional nature of the endothelium makes it a prime candidate for study of the pathomechanisms of MODS. This paper reviews the evidence for the hypothesis that the microcirculation, and in particular its endothelial component, has a central role in the pathogenesis of MODS. The evidence is reviewed principally from the standpoints of classical morbid anatomy and cell pathobiology.Dedicated to Professor Dr. Christian Mittermayer on the occasion of his 60th birthday