肌质网兰尼碱受体在心力衰竭中的作用

肌质网在心肌的舒缩功能中有重要作用 ,心力衰竭时其功能及组成蛋白发生变化 ,尤其是肌质网兰尼碱受体钙释放通道越来越受到重视。心力衰竭时兰尼碱受体通道过磷酸化使其与FKBP12 .6分子的结合能力下降 ,引起Ca2 + 信号传导的去耦联 ,兴奋 收缩耦联的丧失和舒张时肌质网的Ca2 + 释放等 ,可以导致心肌去极化和触发致死性的室性心律失常。β 肾上腺素能阻滞剂可以对兰尼碱受体钙释放通道进行调节     

肌质网兰尼碱受体在心力衰竭中的作用

肌质网在心肌的舒缩功能中有重要作用，心力衰竭时其功能及组成蛋白发生变化，尤其是肌质网兰尼碱受体钙释放通道越来越受到重视。心力衰竭时兰尼碱受体通道过磷酸化使其与FKBP12．6分子的结合能力下降，引起Ca^2 信号传导的去耦联，兴奋．收缩耦联的丧失和舒张时肌质网的Ca^2 释放等，可以导致心肌去极化和触发致死性的室性心律失常。β-肾上腺素能阻滞剂可以对兰尼碱受体钙释放通道进行调节。     

核因子-κB与脓毒症肝损伤

脓毒症是创伤、烧伤、休克、感染等临床急危重患儿的严重并发症之一.也是诱发脓毒性休克、多器官功能障碍综合征的重要原因.脓毒症是指由感染引起的全身炎症反应,其诊断标准同全身炎症反应综合征.目前认为其发生的根本原因在于机体细胞因子和炎性介质过度释放导致的炎症反应失控和免疫机能紊乱.     

L型Ca2+通道和心脏

电压依赖性L型Ca2+通道是心肌细胞正常兴奋和兴奋-收缩偶联中允许Ca2+内流的多亚单位跨膜蛋白.多种受体和信号通路参与钙电流(Ca2+current,Ica)的调节,主要通过蛋白激酶A和蛋白激酶C通路调节L型Ca2+通道.Ica的调节存在蛋白激酶A和蛋白激酶C通路的交叉作用.Ica的准确调节需要有正常的心功能,在心脏疾病中这些调节通路改变很重要.     

关于脓毒症3.0的争议

感染诱发的脓毒症是ICU最常见的疾病之一.为了统一认识,利于早期诊断和治疗,降低重症感染的病死率,1991年首次提出了脓毒症的概念.近20余年,伴随脓毒症病理生理研究的深入,其定义和诊断标准也不断更新和完善.2016年,欧洲危重病学会指定专家组重新修订了脓毒症的定义和诊断标准,即脓毒症3.0,主要强调感染导致宿主内环境稳态失衡、潜在致命性风险的器官功能障碍.每次更新都融入许多新的理论或观点,同时也充满了争议.本文主要介绍脓毒症的定义和诊断标准,以及脓毒症3.0存在的争议.     

脓毒症心功能障碍机制的研究进展

脓毒症心功能障碍是脓毒症多器官功能障碍的表现之一.脓毒症心功能障碍的临床和基础研究已超过50年,但其具体病理生理机制还不完全明确.现阶段的研究认为:线粒体功能障碍、循环中各种心肌抑制物、心肌细胞内钙稳态失调等共同作用促进了脓毒症时心功能障碍的发生.     

降钙素原在小儿脓毒症中的应用

脓毒症是目前小儿重症监护病房面临的棘手难题,特别是由其诱发的脓毒性休克和多器官功能障碍综合征,已成为危重患儿主要的死亡原因,病死率高达30％ ～ 70％.降钙素原无疑是目前最好的脓毒症诊断指标.该文就降钙素原在小儿脓毒症中的应用作一综述.     

线粒体融合-分裂在脓毒症发病机制中的作用

脓毒症是感染导致的全身炎症反应综合征,进一步发展可导致感染性休克和多器官功能障碍综合征.脓毒症具有高发病率及病死率,是危重症领域的研究热点.近年来,亚细胞相关研究提示线粒体损害在脓毒症患者(尤其是脓毒症休克患者)的病情发展中起着非常重要的作用.线粒体是细胞内高度动态变化的细胞器,在细胞内不断融合与分裂,形成动态平衡的网状结构.脓毒症时,线粒体融合与分裂失衡,导致细胞内分子、细胞以及器官均发生功能障碍.该文就线粒体融合-分裂改变在脓毒症发病机制中作用的研究进展作一综述.     

儿童脓毒症生物标记物的研究进展

脓毒症是机体对感染的反应失调而导致危及生命的器官功能障碍,是当今危重病医学所面临的焦点和难点问题.目前世界范围内儿童脓毒症的发生率仍居高不下,若治疗不及时可发展成脓毒性休克、多器官功能障碍综合征,严重威胁人类健康.因此脓毒症的早期识别、诊断、治疗对降低病死率有重要意义.而生物标记物在脓毒症的早期诊断、病情及预后判断,疗效评估中发挥重要作用.本文就近年来脓毒症的生物标记物进行总结.     

脓毒症3.0在儿童脓毒症诊断的运用——我们还有很多工作要做

脓毒症定义自1991年首次提出以来,定义主要内容由感染+全身炎症反应综合征演变为感染+器官功能障碍,而器官功能障碍通过序贯器官功能衰竭评估(sequential organ failure assessment,SOFA)评分的增加来表示.这一核心内容体现在2016年发布的脓毒症3.0中.在脓毒症3.0中SOFA评分在脓毒症的识别与诊断中具有突出地位,但该诊断标准主要是针对于成人,该诊断标准在儿童中如何应用,我们需要思考哪些问题,本文将对此进行探讨.     

儿童脓毒症与噬血细胞综合征的临床异同关系

儿童脓毒症是严重感染所致的宿主免疫反应失调,噬血细胞综合征(HLH)是自然杀伤细胞/细胞毒性T细胞过度激活导致的过度免疫活化综合征,两种疾病都可导致危及生命的多器官功能障碍,临床特征既有相似又存在差异,且脓毒症可能进展为HLH,HLH也可继发脓毒症。本文就脓毒症和HLH的临床异同关系进行综述,为临床医生提供更深入的认识。     

脓毒症与线粒体功能障碍

脓毒症为各种病原菌侵入机体后引起的全身炎症反应综合征。脓毒症、严重脓毒症、脓毒症休克、多脏器功能衰竭为疾病的进展过程。线粒体被称为“动力工厂”,为各脏器维持正常功能提供能量。脓毒症时免疫异常、多种炎症因子的激活及释放、细胞内信号传递异常及氧化应激等可引起线粒体功能障碍。最近研究提出,线粒体自噬在线粒体功能障碍中也起着一定作用。该文就脓毒症时引起机体线粒体损伤的机制进行综述。     

小儿脓毒症并腹内高压的危险因素分析

目的：探讨小儿脓毒症并腹内高压（IAH）的危险因素, 为早期诊断、及时干预治疗提供理论依据。方法：采用膀胱测压法对119例脓毒症患儿进行腹内压检测,根据腹内压检测结果将患儿分为腹内压正常组(对照组,n=80)与IAH组(n=39)。采用单因素和非条件logistic回归分析对两组患儿的临床资料进行分析,以调查脓毒症患儿并发IAH的危险因素。结果：单因素分析发现小儿危重病评分（PCIS）、降钙素原（PCT）、PaCO2、血清乳酸值及肠道/腹腔感染、腹水、胃肠功能障碍、机械通气、休克和多脏器功能不全（MODS）的发生比例在IAH和对照组间比较差异均具有统计学意义（P<0.05）。Logistic回归分析显示PCIS降低、MODS、休克、胃肠功能障碍和腹水是脓毒症合并IAH的主要危险因素。结论：PCIS降低、MODS、休克、胃肠功能障碍和腹水的脓毒症患儿, 有发生IAH的可能, 应重点监测,以早期诊断并予及时干预治疗。     

Pediatric sepsis and multiple organ dysfunction syndrome

Systemic inflammatory response syndrome may be viewed as the systemic expression of cytokine signals that normally function on an autocrine or paracrine level. Sepsis is defined as systemic inflammatory response syndrome caused by an infection. Multiple organ dysfunction syndrome may represent the end stage of severe systemic inflammatory response syndrome or sepsis. Many cells are involved, including endothelial cells and leukocytes and multiple proinflammatory and antiinflammatory mediators (cytokines, oxygen free radicals, coagulation factors, and so forth). Various pathophysiologic mechanisms have been postulated. The most popular theory is that the inflammatory process loses its autoregulatory capacity; however, microcirculatory dysregulation and apoptosis may also be important, and a new paradigm posits a complex nonlinear system. Many new treatments have been studied recently. The usefulness of immune modulating diets remains to be evaluated. Molecular immunomodulation is still of unclear value. The therapy of sepsis and multiple organ dysfunction syndrome remains mainly supportive.     

Increased cardiomyocyte intracellular calcium during endotoxin-induced cardiac dysfunction in guinea pigs

Septic shock is a complex pathophysiologic state characterized by circulatory insufficiency, multiple system organ dysfunction, and frequent mortality. Although profound cardiac dysfunction occurs during sepsis, the pathogenesis of this dysfunction remains poorly understood. To determine whether abnormalities in intramyocyte calcium accumulation might contribute to the development of cardiac dysfunction, we measured myocyte intracellular calcium during peak cardiac dysfunction after an endotoxin challenge. Intraperitoneal administration of Escherichia coli lipopolysaccharide 4 mg/kg to adult guinea pigs resulted in significantly impaired cardiac performance (Langendorff preparation) 18 h after challenge compared with control. This included diminished left ventricular pressure development (56 +/- 7 versus 95 +/- 4 mm Hg, p < 0.05), maximal rate of left ventricular pressure rise (998 +/- 171 versus 1784 +/- 94 mm Hg/s, p < 0.05) and left ventricular pressure fall (1014 +/- 189 versus 1621 +/- 138 mm Hg/s, p < 0.05). Assay of intracellular calcium in fura-2AM-loaded cardiac myocytes demonstrated increased intracellular calcium concentration in myocytes obtained from lipopolysaccharide-challenged animals compared with controls (234 +/- 18 versus 151 +/- 6 nM, p < 0.05). Inhibition of calcium-release channel (ryanodine receptor) opening by administration of dantrolene prevented the increase in intracytoplasmic calcium (159 +/- 8 versus 234 +/- 18 nM, p < 0.05) and partially ameliorated systolic and diastolic ventricular dysfunction. These data indicate that abnormalities of intracellular calcium contribute to the development of endotoxin-induced myocardial dysfunction.     

Sepsis, severe sepsis and septic shock in paediatric multiple organ dysfunction syndrome

OBJECTIVES: To determine the association between severity of sepsis with outcome and severity of illness in children with multiple organ dysfunction syndrome (MODS). MATERIALS: Four hundred and ninety-five consecutive paediatric intensive care unit (PICU) admissions were analysed. multiple organ dysfunction syndrome was defined as simultaneous dysfunction of >/= 2 organ system and sepsis by the American College of Chest Physicians and Society of Critical Care Medicine Consensus Conference definition. RESULTS: Eighty-four patients developed MODS. The incidence of sepsis, severe sepsis and septic shock in these patients was 10.7%, 23.8% and 17.9%, respectively. Worsening categories of sepsis were associated with: (1) a higher mean admission Paediatric Risk of Mortality (PRISM II): 36.6 +/- 25.9, 56.8 +/- 32.1 and 73.6 +/- 28.5%, respectively (P = 0. 005), (2) a larger number of organ dysfunctions: mean MODS index of 37%, 46% and 58%, respectively (P = 0.007), and (3) a higher mortality: 22.2%, 65% and 80%, respectively (P = 0.03). CONCLUSION: Presence of sepsis, severe sepsis and septic shock was associated with an increasing severity of illness, increased number of organ dysfunctions and a distinct risk of mortality among critically ill children.     

血小板在脓毒症中的研究进展

脓毒症为感染致全身免疫失调的炎症反应综合征,血小板在脓毒症发生发展中起着重要作用。血小板可通过黏附、聚集、活化、脱颗粒作用与病原微生物相反应,以达到保护机体的作用。同时,脓毒症时血小板还可与中性粒细胞等免疫细胞相互作用,参与微血栓、炎症的形成。因此,血小板有抗微生物效应及与其他先天免疫细胞协作,形成复杂的血管内免疫防御...     

儿童脓毒症新发功能障碍的特点

目的探讨儿科重症监护病房脓毒症患儿新发功能障碍的特点。方法回顾性分析2015~2016年入住儿科重症监护病房的脓毒症患儿的临床资料。比较重度脓毒症（34例）与非重度脓毒症（69例）患儿新发功能障碍发生率和入院、出院功能状态及其变化。结果重度脓毒症组新发功能障碍发生率显著高于非重度脓毒症组（38% vs 6%，P < 0.05）。非重度脓毒症组入院功能状态相对良好，出院总体功能状态较入院时改善。重度脓毒症组入院功能状态较差，出院时神志、感觉、沟通、呼吸功能状态处于轻、中度异常状态。结论非重度脓毒症患儿新发功能障碍率低，预后较好。重度脓毒症患儿新发功能障碍发生率高，预后较差。     

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??In the third international consensus definitions for sepsis and septic shock??sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. This new definition is similar to severe sepsis in the past. This article describes the epidemiological characteristics of this disease??including etiology??underlying diseases??organ dysfunctions??prevalence and prognosis.