ω-3鱼油脂肪乳对胃癌患者术后肝肾功能及预后的影响

目的 探讨ω-3鱼油脂肪乳对胃癌患者术后肝肾功能及预后的影响.方法 采用回顾性队列研究方法,收集南京市第一医院普外科2018年1月-2019年12月126例胃癌术后患者的资料,并将患者随机分为对照组(肠外营养中应用常规脂肪乳)和观察组(对照组基础上加用ω-3鱼油脂肪乳),每组63例.比较2组患者术前1d和术后7d的肝肾功能指标[谷氨酸-丙酮酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、总胆红素(TBIL)、肌酐(Cr)、血尿素氮(BUN)]、营养指标[总蛋白(TP)和白蛋白(ALB)]和血脂指标[甘油三酯(TG)和总胆固醇(TC)].比较2组住院时间、术后住院时间、术后并发症和术后通气时间.结果 观察组术后7d的ALT、TBIL和TG水平低于对照组,ALB高于对照组,差异有统计学意义(P＜0.05).2组患者住院时间、术后住院时间、通气时间和术后并发症比较,差异无统计学意义(P＞0.05).结论 ω-3鱼油脂肪乳可改善患者肝功能、脂肪代谢,减少ALB降低幅度,但在缩短住院时间、减少并发症和改善肾功能方面未观察到明显的优势.     

ω-3鱼油脂肪乳剂对严重腹腔感染患者免疫及肠屏障功能的影响

目的:探讨ω-3鱼油脂肪乳对严重腹腔感染患者免疫及肠屏障功能影响.方法:将确诊为严重腹腔感染的患者50例,随机分为ω-3鱼油脂肪乳治疗组(n=25)和常规治疗对照组(n=25).鱼油组在常规治疗的基础上加用ω-3鱼油脂肪乳100 mL/d 6~8 d.测定两组患者治疗前和治疗7 d后免疫球蛋白IgA、IgG、IgM,外周血T淋巴亚群CD3、CD4及反应蛋白(CRP)、血浆内毒素及血浆D-乳酸水平,同时观察两组患者全身炎症反应综合征(SIRS)评分、平均住院时间.结果:鱼油组SIRS评分、住院时间较对照组差异均有统计学意义(P<0.05).用药7 d后,对照组与鱼油组相比,IgA、IgG、IgM,外周血T淋巴亚群CD3、CD4,反应蛋白(CRP)、血浆内毒素及血浆D-乳酸水平比较差异均有统计学意义(P<0.05).结论:ω-3鱼油脂肪乳能减轻严重腹腔感染患者的炎症反应,改善免疫状态,保护肠屏障功能.     

全胃肠外营养联合ω-3鱼油脂肪乳对全身炎症反应综合征患者血清炎症介质释放的影响

目的 探讨ω-3鱼油脂肪乳对全身炎症反应综合征(SIRS)患者血清炎症介质释放的影响.方法 选择2006年6月-2007年6月入住本院重症加强治疗病房(ICU)的SIRS患者40例,随机分为常规全胃肠外营养(TPN)组(A组,20例)和ω-3鱼油脂肪乳 TPN组(B组,20例).两组患者均接受等氮、等热量的TPN,每日所需热量83.68 kJ/kg、氮入量0.2 g/kg.B组加用ω-3鱼油脂肪乳1～2 ml·kg-1·d-1,共7 d.治疗前及治疗1、3和7 d分别检测血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、IL-6的浓度.统计两组患者ICU住院时间、多器官功能障碍综合征(MODS)发生率及28 d病死率.结果 与常规TPN治疗比较,加用ω-3鱼油脂肪乳治疗后不同时间点血清TNF-α、IL-1、IL-6均明显降低(P<0.05或P<0.01);ICU住院时间明显缩短[(15.8±2.3)d比(11.5±2.4)d,P<0.05];MODS发生率显著下降(75%比50%,P<0.05);28 d病死率有所降低,但差异无统计学意义(25%比10%,P0.05).结论 ω-3鱼油脂肪乳可降低SIRS患者TNF-α、IL-1、IL-6的水平,从而起到阻断SIRS向MODS转化的作用,减少MODS的发生,缩短ICU住院时间,提高危重患者抢救成功率.     

ω-3鱼油脂肪乳剂减轻危重患者全身炎症反应的临床研究

目的 观察ω-3鱼油脂肪乳剂减轻危重患者全身炎症反应的临床疗效及其对患者体内细胞因子的影响.方法 选择重症监护病房(ICU)伴全身炎症反应综合征(SIRS)的危重患者76例,按随机数字表法分为对照组(37例)及试验组(39例).两组一般治疗措施相同,对照组加用普通20%中长链脂肪乳500 ml/d,试验组在对照组治疗基础上加用ω-3鱼油脂肪乳剂100 ml/d静脉滴注;两组均治疗7 d.两组治疗前后行急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分及C-反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)、白细胞介素(IL-1、IL-6、IL-8)、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)检测.结果 两组治疗前APACHEⅡ评分、CRP、细胞因子及肝功能指标比较差异均无统计学意义(均P>0.05).与治疗前比较,两组治疗后各指标均显著降低.与对照组比较,试验组治疗后APACHEⅡ评分(分:14.2±4.6比18.4±7.9)、CRP(mg/L:10.3±2.1比13.4±2.5)、TNF-α(ng/L:182.0±43.6比297.0±54.7)、IL-1(ng/L:54.0±17.4比89.0±16.8)、IL-6(ng/L:185.0±54.6比294.0±82.4)、IL-8(ng/L:59.9±7.3比72.3±8.1)、ALT(U/L:163.0±53.2比287.0±50.7)和AST(U/L:175.0±51.2比302.0±47.4)下降更为显著(均P<0.05). 结论ω-3鱼油脂肪乳剂能抑制危重患者的全身炎症反应,并能保护器官功能,改善患者预后.     

ω-3鱼油脂肪乳剂对内毒素致兔急性肺损伤保护作用机制的研究

目的 探讨ω-3鱼油脂肪乳剂对内毒素(ET)致兔急性肺损伤(ALI)的保护作用.方法 清洁级新西兰兔24只,随机分为对照组(A组)、ET致伤组(B组)、ω-3鱼油脂肪乳剂预处理组(C组).经静脉一次性注射ET复制兔ALI 模型,各组分别于0、0.5、1、2、4 h不同时间点测定呼吸频率、心率、血气分析;4 h点处死动物,测定肺组织TNF-α、髓过氧化酶(MPO)、白细胞介素10(IL-10)含量;取肺组织观察病理变化,并做病理评分、测湿/干质量比值(W/D)及肺含水量.结果与对照组相比,B组心率加快、呼吸急迫;动脉血氧下降,肺组织出现明显病理组织学损伤,W/D、肺含水量升高.TNF-α:B组明显升高,与A、C两组比较差异有统计学意义(P<0.05),C组与A组比较差异无统计学意义(P>0.05).IL-10:B、C两组较A组均升高(P<0.05),C组与B组比较差异无统计学意义.B、C两组MPO较A组均升高,三组差异有统计学意义.C组W/D、肺含水量、肺损伤病理组织评分均低于B组(P<0.05).结论 ω-3鱼油脂肪乳可以减少TNF-α生成,抑制PMN在肺内扣押,并有上调IL-10的趋势,对内毒素致兔ALI具有一定保护作用,但其影响IL-10的具体机制仍需进一步探讨.     

ω-3鱼油脂肪乳剂对严重创伤患者血白细胞介素-6及肿瘤坏死因子-α的影响

目的:探讨ω-3鱼油脂肪乳剂对严重创伤患者血白细胞介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)水平的影响.方法:将29例严重创伤患者随机分为治疗组和对照组,其中,治疗组14例,对照组15例.对照组采用常规治疗,治疗组在常规治疗的基础上加用ω-3鱼油脂肪乳剂.于入院第1、3、5天收集患者血清,放入-50℃冰箱保存,统一用ELISA法检测其中促炎细胞因子IL-6及TNF-α水平,并对两组的结果进行比较.结果:入院后两组患者血IL-6及TNF-α水平均明显升高,但治疗组IL-6、TNF-α升高程度明显低于对照组(P<0.05).结论:ω-3鱼油脂肪乳剂能抑制严重创伤患者血IL-6及TNF-α水平的上升.     

醛类应激介导ω-3鱼油脂肪乳剂预处理减轻大鼠脑局灶性缺血再灌注损伤的机制研究

目的探究ω-3鱼油脂肪乳剂预处理对大鼠脑局灶性缺血再灌注损伤的保护作用,分析其可能机制。方法将40RSD大鼠随机分成正常组（C组）、模型组（M组）、ω-3鱼油脂肪乳剂5d组（FOFE-5组）、ω-3鱼油脂肪乳剂10d组（FOFE-10组）、02—3鱼油脂肪乳剂15d组（FOFE～15组）,静脉尾注药物,并建立鼠脑局灶性缺血再灌注损伤模型,比较各组大鼠的神经行为评分、大脑梗死面积,脑组织中丙二醛（MDA）、乳酸脱氢酶（LHD）水平,核因子E2相关因子2（Nrf2）、血红素氧化酶Ho-1mRNA表达。结果c组大鼠的神经行为评分和大脑梗死面积均为0,FOFE-5、FOFE-10组以及FOFE-15组大鼠的神经行为评分和大脑梗死面积较M组显著降低;与M组比较,FOFE-5预处理使MDA、LHD水平显著降低;与c组比较,M组的大鼠脑组织中Nrt2和Ho-1mRNA相对表达量明显升高,FOFE-5预处理组的Nrf2和Ho—lmRNA相对表达量较M组明显升高,差异均具有显著性（P〈0．05）。结论ω-3鱼油脂肪乳剂预处理通过调节醛类应激介导的氧化应激以及Nrf2／HO-1信号通路对大鼠大脑局灶性缺血再灌注损伤起到了保护作用。     

ω-3鱼油脂肪乳对脑外伤后全身炎症反应综合征的影响

目的:探讨ω-3鱼油脂肪乳对脑外伤合并全身炎症反应综合征(SIRS)患者体内血C反应蛋白(CRP)及体液免疫的影响。方法:将2011年6月-2013年12月收治的脑外伤合并SIRS患者96例随机分为对照组和实验组各48例,分别给予常规静脉营养和联合ω-3鱼油脂肪乳治疗,比较两组静脉营养前1d,后第7 d的肿瘤坏死因子-α(TNF-α)、CRP、白介素-6(IL-6)的浓度。结果:治疗后两组血TNF-α、CRP、IL-6等水平均较治疗前明显降低(P0.05),但实验组第7 d时的观察指标均明显低于对照组(P0.05)。结论:ω-3鱼油脂肪乳可降低脑外伤合并SIRS患者体内TNF-α、CRP、IL-6浓度,具有抗炎和改善免疫功能的作用。     

ω-3鱼油脂肪乳注射液对重症急性胰腺炎患者临床治疗作用的观察

重症急性胰腺炎(severe acute pancreatitis,SAP)属于急性胰 腺炎的特殊类型,是一种病情险恶、并发症多、病死率较高的急腹症,是急性全身消耗性疾病,占整个急性胰腺炎的15%~30%.20世纪80年代,多数病例死于疾病早期,随着SAP外科 治疗的进展,治愈率有所提高,但总体病死率仍高达17%左右.     

肝移植后炎症因子谱改变及ω-3鱼油脂肪乳的影响

背景：ω-3鱼油脂肪乳可改变肝移植后机体的炎症状态。目的：观察ω-3鱼油脂肪乳对肝移植后炎症因子谱及预后的影响。方法：将36例同种异体原位肝移植患者前瞻性随机分为实验组和对照组。两组移植后给予等氮等热量的营养支持和相同的免疫抑制方案,实验组移植后第2天在中长链脂肪乳中添加ω-3鱼油脂肪乳,连用6d;对照组中长链脂肪乳中未添加。结果与结论：与对照组比较,实验组移植后第5,8天白细胞介素1β、白细胞介素2、白细胞介素6、肿瘤坏死因子α、前列腺素E2和白三烯B4等不同程度下调;白细胞介素4、白细胞介素10、转化生长因子β和白三烯B5等不同程度上调;移植后第8天白细胞介素6/白细胞介素10显著下降,白细胞介素10/肿瘤坏死因子α升高（P〈0.01）。两组围手术期死亡率和急性排斥反应发生率差异无显著性意义,但实验组重症监护时间和住院时间显著短于对照组（P〈0.05）。说明肝移植后添加ω-3鱼油脂肪乳可调整促炎/抗炎因子平衡,纠正过度炎症反应,改善预后。     

肝移植后炎症因子谱改变及ω-3鱼油脂肪乳的影响

背景:ω-3鱼油脂肪乳可改变肝移植后机体的炎症状态。目的:观察ω-3鱼油脂肪乳对肝移植后炎症因子谱及预后的影响。方法:将36例同种异体原位肝移植患者前瞻性随机分为实验组和对照组。两组移植后给予等氮等热量的营养支持和相同的免疫抑制方案,实验组移植后第2天在中长链脂肪乳中添加ω-3鱼油脂肪乳,连用6d;对照组中长链脂肪乳中未添加。结果与结论:与对照组比较,实验组移植后第5,8天白细胞介素1β、白细胞介素2、白细胞介素6、肿瘤坏死因子α、前列腺素E2和白三烯B4等不同程度下调;白细胞介素4、白细胞介素10、转化生长因子β和白三烯B5等不同程度上调;移植后第8天白细胞介素6/白细胞介素10显著下降,白细胞介素10/肿瘤坏死因子α升高(P<0.01)。两组围手术期死亡率和急性排斥反应发生率差异无显著性意义,但实验组重症监护时间和住院时间显著短于对照组(P<0.05)。说明肝移植后添加ω-3鱼油脂肪乳可调整促炎/抗炎因子平衡,纠正过度炎症反应,改善预后。     

富含鱼油脂肪乳的全胃肠外营养对全身炎症反应综合征患者炎症反应的影响

目的 探讨鱼油脂肪乳对全身炎症反应综合征(SIRS)患者炎症反应的影响.方法 选择2007年1月至2007年6月入住聊城市人民医院重症加强治疗病房(ICU)的SIRS患者40例,随机分为常规胃肠外营养(TEN)组(A组,20例)和鱼油脂肪乳+TPN治疗组(B组,20例).两组患者均接受等氮、等热量的TPN.患者所需热量按20 kcal/(kg·d),1 kcal=4.1868 kJ,氮入量0.2 g/(kg·d).B组加用鱼油脂肪乳(商品名:尤文,批号UK1580,中国无锡华瑞制药有限公司生产)1～2 tml(kg·d),共7d.治疗前及治疗后1 d、3 d和7 d分别检测血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、IL-6的浓度.统计两组患者住ICU时间,NODS发生例数及28 d死亡例数.所有数据采用SPSS 10.0进行统计学处理.结果 两组患者APACHF-Ⅱ评分差异无统计学意义,与常规TPN治疗组比较,加用鱼油脂畴乳治疗后不同时间点血清TNF-α、IL-1、IL-6差异均有统计学意义(P<0.05或P<0.01);住ICU天数明显缩短,差异有统计学意义[(11.5±2.4)d比(15.8±2.3)d,P<0.05],MODS发生例数及28d病死例数均明显少于对照组.结论 鱼油脂肪乳可降低SIRS患者TNF-α、IL-1、IL-6的水平,从而达到阻断SIRD向MODS转化的作用,减少MODS的发生,缩短住ICU时间,提高危重患者抢救成功率.     

Effects of sesame oil on oxidative stress after the onset of sepsis in rats

The aim of this study was to investigate effects of sesame oil on oxidative stress after the onset of sepsis in rats. Effects of sesame oil on lipid peroxidation, superoxide anion, superoxide dismutase, catalase, glutathione, and nitrite after the onset of endotoxin intoxication were determined. To further examine the protective effect of sesame oil on sepsis, a mortality study was also conduced in cecal ligation and puncture-induced sepsis in rats. Sesame oil was given orally 6 h after endotoxin administration and cecal ligation and puncture, and parameters were then measured in another 6 h. Data demonstrated that a single dose of sesame oil reduced lipid peroxidation 6 h after endotoxin intoxication. Superoxide anion counts were decreased, glutathione levels were increased, and activities of superoxide dismutase and catalase, as well as nitrite levels, were not altered in lipopolysaccharide plus sesame oil-treated groups compared with lipopolysaccharide-treated groups. Furthermore, sesame oil given 6 h after cecal ligation and puncture significantly increased survival rate. Thus, we suggested that sesame oil could be used as a potent antioxidant to reduce oxidative stress after the onset of sepsis in rats.     

Effective use of third generation fat emulsion in total parenteral nutrition program in patients with severe sepsis

The aim of the current research was to measure the clinical efficacy of 3rd generation fat emulsion in the program of complete parenteral nutrition of patients with severe sepsis. The work demonstrates the results of treatment of 25 patients with severe sepsis divided into 2 groups depending on the way of parenteral nutrition. In the 1st group (13 patients) the parenteral nutrition was carried out by 20% glucose, 15% solution of crystallic aminoacids and 20% of 2nd generation fat emulsion. In the 2nd group (12 patients) parenteral nutrition was carried out by 20% glucose, 15% solution of crystallic aminoacids and 20% of 3rd generation fat emulsion. The parenteral nutrition of Ist and 2nd group contributed to the correction of hypermetabolism syndrome and stabilization of the nutritive status parameters. It was observed that the parenteral nutrition used in the 2nd group showed statistically higher positive effect on the parameters of systemic inflammation and cellular part of immunity, rather than parenteral nutrition used in the 1st group. It is revealed that, the used methods of complete parenteral nutrition in patients with severe sepsis effectively eliminate the hypermetabolism syndrome. Parenteral nutrition of patients with severe sepsis by 3rd generation fat emulsion has a positive effect of parapeters of systemic inflammation.     

曲美他嗪对维持性血液透析患者氧化应激状态的影响

目的 探讨口服曲美他嗪对维持性血液透析(MHD)患者氧化应激状态的影响及其临床意义.方法 选择透析龄超过3个月的MHD患者86例,已排除急性感染及其他活动性疾病,随机分为患者治疗组46例,患者对照组40例.患者治疗组口服曲美他嗪20 mg,3次/d,治疗并观察随访24周;患者对照组不用曲美他嗪.分别检测治疗前后患者的血清谷胱甘肽过氧化物酶(GSHPx)、超氧化物歧化酶(SOD)、血清丙二醛(MDA)、血清晚期氧化蛋白产物(AOPP)等.另选健康对照者30名(健康对照组).分析曲美他嗪对MHD患者氧化应激状态的影响.结果 治疗前,2组MHD患者的GSHPx水平[(584.37±215.70)、(580.87±309.12)μmol/L]显著低于健康对照组[(769.06±302.46)μmol/L](P均<0.01),SOD水平[(347.87±82.09)、(348.16±75.33)kU/L]显著低于健康对照组[(428.34±15.23)kU/L],差异有统计学意义(P均<0.01),MDA水平[(4.94±1.32)、(4.97±1.61)nmol/L]显著高于健康对照组[(3.56±0.46)nmol/L],差异有统计学意义(P均<0.01),AOPP水平[(120.95±59.24)、(121.76±69.12)μg/L]显著高于健康对照组[(47.69±20.15)μg/L],差异有统计学意义(P均<0.05);治疗后,患者治疗组的GSHPx、SOD水平均较治疗前明显升高,差异有统计学意义(P<0.05,P<0.01),MDA水平较治疗前明显下降(P<0.01),AOPP水平也下降,但差异无统计学意义(P>0.05);患者对照组以上各项指标治疗前后均无明显变化(P均>0.05),但患者治疗组与对照组上述指标比较差异有统计学意义(P均<0.01).结论 MHD患者普遍存在氧化应激状态,使用口服曲美他嗪可明显改善患者的抗氧化能力,从而提高机体对氧化应激的防御功能.     

Circulating levels of peroxiredoxin 4 as a novel biomarker of oxidative stress in patients with sepsis

Oxidative stress, a situation with increased reactive oxygen species production and/or decreased antioxidant defense mechanisms, is evident in the pathogenesis of sepsis. Peroxiredoxin 4 (Prx4) is a hydrogen peroxide degrading peroxidase recently found circulating in blood of septic patients and potentially reflecting an antioxidant system in imbalance. We studied Prx4 serum levels of 79 consecutively enrolled medical intensive care unit patients. The diagnostic and prognostic performance of Prx4 was compared with other biomarkers, the APACHE II score and the SOFA score. Median Prx4 serum levels gradually increased with disease severity in patients classified on admission as having systemic immune response syndrome (2.32 arbitrary [arb.] U/L), sepsis (5.02 arb. U/L), severe sepsis (11.7 arb. U/L), or septic shock (11.4 arb. U/L). A positive correlation was found with the severity score Acute Physiological and Chronic Health Evaluation II (r = 0.27, P < 0.05) and the organ failure score Sequential Organ Failure Assessment (r = 0.55, P < 0.0001). Peroxiredoxin 4 correlated with the sepsis marker procalcitonin (r = 0.61, P < 0.0001), the inflammatory markers C-reactive protein (r = 0.65, P < 0.0001) and interleukin 6 (r = 0.62, P < 0.0001), and antioxidant blood compounds total bilirubin (r = 0.37, P < 0.001) and albumin (r = -0.54, P < 0.0001). Peroxiredoxin 4 distinguished noninfectious from infectious inflammatory response syndrome with an area under the receiver operating characteristic (ROC) curve of 0.82. [corrected] High Prx4 serum levels were associated with a poor prognosis of septic patients and revealed an area under the ROC curve of 0.76 in prediction of in-hospital mortality. In this study, elevated serum levels of the antioxidant Prx4 were associated with an increased disease severity and adverse outcome of critically ill patients with sepsis. Peroxiredoxin 4 may therefore be a helpful new biomarker for diagnosing, monitoring, and risk assessing these patients. The pathophysiological mechanisms behind the observed increase remain to be elucidated.     

Effects of intravenous fat emulsions on lung function in patients with acute respiratory distress syndrome or sepsis

OBJECTIVE: To investigate whether rapid or slowly infused intravenous fat emulsions affect the ratio of prostaglandin I2/thromboxane A2 in arterial blood, pulmonary hemodynamics, and gas exchange. DESIGN: Prospective, controlled, randomized, crossover study. SETTING: Operative intensive care unit of a university hospital. PATIENTS: Eighteen critically ill patients. Ten patients were stratified with severe sepsis, and eight patients had acute respiratory distress syndrome (ARDS). INTERVENTIONS: Patients were assigned randomly to receive intravenous fat emulsions (0.4 x resting energy expenditure) over 6 hrs (rapid fat infusion) or 24 hrs (slow fat infusion) along with a routine parenteral nutrition regimen, by using a crossover study design. MEASUREMENTS AND MAIN RESULTS: Systemic and pulmonary hemodynamics as well as gas exchange measurements were recorded via respective indwelling catheters. Arterial thromboxane B2 and 6-keto-prostaglandin-F1alpha plasma concentrations were obtained by radioimmunoassay, and 6-keto-prostaglandin-F1alpha/thromboxane B2 ratios (P/T ratios) were calculated. Data were collected immediately before and 6, 12, 18, and 24 hrs after onset of fat infusion. In the ARDS group, P/T ratio increased by rapid fat infusion. Concomitantly, pulmonary shunt fraction, alveolar-arterial oxygen tension difference [P(a-a)o2]/Pao2, and cardiac index increased as well, whereas pulmonary vascular resistance and Pao2/Fio2 declined. After slow fat infusion, a decreased P/T ratio was revealed. This was accompanied by decreased pulmonary shunt fraction, lowered P(a-a)o2/Pao2, and increased Pao2/Fio2. Correlations between plasma concentrations of 6-keto-prostaglandin-F1alpha or thromboxane B2 and measures of respiratory performance could be shown during rapid and slow fat infusion, respectively. In the sepsis group, the P/T ratio remained unchanged at either infusion rate, but pulmonary shunt fraction and P(a-a)o2/Pao2 decreased after rapid fat infusion, whereas Pao2/Fio2 increased. CONCLUSION: Pulmonary hemodynamics and gas exchange are related to changes of arterial prostanoid levels in ARDS patients, depending on the rate of fat infusion. In ARDS but not in sepsis patients clear of pulmonary organ failure, a changing balance of prostaglandin I2 and thromboxane A2 may modulate gas exchange, presumably via interference with hypoxic pulmonary vasoconstriction.