【摘要】：背景體外循環(huán)(Cardiopulmonary bypass,CPB)技術(shù)是心臟手術(shù)得以順利開展的重要輔助措施之一。然而對患者來說,體外循環(huán)不同于機體自身的生理性循環(huán),體外循環(huán)這種非生理模式,會導(dǎo)致全身炎癥反應(yīng)綜合征(systemic inflammatory response syndrom,SIRS)的發(fā)生。失控的炎癥反應(yīng)可導(dǎo)致體外循環(huán)術(shù)后心肺、肝、腎、腦等重要臟器功能不全,顯著增加患者的致死率和致殘率。外科手術(shù)的創(chuàng)傷、血液直接暴露于異物表面、缺血-再灌注損傷(Ischemia-Reperfusion Injury, IRI)、腸道細(xì)菌移位所致內(nèi)毒素血癥、溫度變化等因素均可激活體內(nèi)中性粒細(xì)胞、單核細(xì)胞、內(nèi)皮細(xì)胞及血小板等多種細(xì)胞成分,激活血液中的補體系統(tǒng)、內(nèi)源性凝血和外源性凝血系統(tǒng)和纖溶系統(tǒng),引起多種與炎癥反應(yīng)有關(guān)的生物活性物質(zhì)的釋放,并形成難以控制的的炎癥瀑布效應(yīng),使得機體炎性反應(yīng)失控而形成全身炎癥反應(yīng)綜合征。近年大量研究資料表明,在體外循環(huán)心臟直視手術(shù)期間,對全身炎癥反應(yīng)起核心作用的炎性介質(zhì)主要有腫瘤壞死因子-α (Tumor Necrosis Factor,TNF-α)、白介素1(Interleukin-1,IL-1)、白介素-6(Interleukin-6,IL-6)、白介素-8(Interleukin-8,IL-8)、白介素-10(Interleukin-10,IL-10)等。其中,較為重要的是白介素系統(tǒng)。IL-1、IL-6和IL-8是促炎介質(zhì),IL-10是抗炎介質(zhì)。有報道,IL-6血漿水平在體外循環(huán)開始后即刻升高,2小時后出現(xiàn)第一次高峰,5-6小時降至術(shù)前水平,12-18小時出現(xiàn)第二次高峰,48小時后降至術(shù)前水平；IL-10血漿水平在升主動脈開放后逐漸升高,90分鐘后達到高峰,體外循環(huán)結(jié)束后4小時基本恢復(fù)至術(shù)前水平。適量的抗炎介質(zhì)有助于控制炎癥進展,恢復(fù)內(nèi)環(huán)境穩(wěn)定,但是機體過度的抗炎反應(yīng)也會產(chǎn)生免疫抑制,即代償性抗炎反應(yīng)綜合征(compensatory anti-inflammatory response syndrome,CARS)。SIRS的產(chǎn)生和發(fā)展是一個極其復(fù)雜的級聯(lián)過程,在體外循環(huán)所致SIRS的發(fā)生發(fā)展過程中,SIRS的嚴(yán)重程度主要是由下游促炎細(xì)胞因子(主要為IL-6、IL-8)和抗炎細(xì)胞因子(主要為IL-10)的平衡狀態(tài)決定。隨著醫(yī)學(xué)技術(shù)的進步,臨床上已有多種行而有效的方法用來減輕體外循環(huán)所致的炎癥反應(yīng),如應(yīng)用具有生物相容性的涂層材料、搏動灌注模式、使用白細(xì)胞濾器及超濾裝置、使用皮質(zhì)類固醇激素、烏司他丁、磷酸二酯酶抑制劑、單克隆抗體等。Omega-3多不飽和脂肪酸(ω-3Polyunsaturated Fatty Acids,ω-3PUFAs)主要包括a-亞麻酸(α-Linolenic Acid, ALA)、二十碳五烯酸(Eicosapentaenoic Acid,EPA)和二十二碳六烯酸(Docosahexaenoic Acid,DHA)。在自然界,Omega-3多不飽和脂肪酸主要來源于水生浮游植物合和深海魚類。陸地的動植物幾乎不含Omega-3多不飽和脂肪酸。研究證明Omega-33多不飽和脂肪酸可通過以下途徑調(diào)節(jié)機體炎癥與免疫反應(yīng)：(1)通過影響花生四烯酸(Arachidonic Acid,AA)的代謝而產(chǎn)生效應(yīng)。(2)通過改變細(xì)胞膜的流動性產(chǎn)生抗炎效應(yīng)。(3)作用于某些炎癥、免疫介質(zhì)產(chǎn)生效應(yīng)。(4)通過作用于細(xì)胞信號轉(zhuǎn)導(dǎo)和基因表達而產(chǎn)生抗炎調(diào)節(jié)免疫效應(yīng)等。近年來,Omega-3多不飽和脂肪酸的心臟保護作用引起了越來越多的重視。Mc Guinness等發(fā)現(xiàn),兔的心肌缺血再灌注模型中,ω-3多不飽和脂肪酸預(yù)處理可誘導(dǎo)心肌細(xì)胞HSP的大量表達,縮小心肌梗死面積。Charman等發(fā)現(xiàn)體外循環(huán)術(shù)前有計劃地給予病人服用魚油(主要成分為Omega-3多不飽和脂肪酸),可以減輕體外循環(huán)手術(shù)帶來的心肌損傷。亦有研究報道,Omega-3多不飽和脂肪酸可以減少心肌耗氧量,減少心肌缺血再灌注時氧化應(yīng)激及鉀離子的丟失,從而起到保護心肌作用。大規(guī)模的臨床試驗證明每日攝入500mg到1000mg的多不飽和脂肪酸可顯著的減少心血管事件的發(fā)生幾率。目前在臨床上,重點添加Omega-3多不飽和脂肪酸的的第一種治療型脂肪乳劑：Omega-3魚油脂肪乳劑問世并應(yīng)用于臨床,在膿毒癥、全身炎癥反應(yīng)綜合癥、嚴(yán)重創(chuàng)傷、頭顱、腹部等外科大手術(shù)后的重癥患者的治療上取得較好的療效。然而作為創(chuàng)傷大、炎癥因子釋放量大、風(fēng)險高的體外循環(huán)下心臟直視手術(shù)的抗炎治療方法中,補充Omega-3魚油脂肪乳在國內(nèi)外的研究報道尚不多見。目的觀察Omega-3魚油脂肪乳對體外循環(huán)心臟手術(shù)圍術(shù)期全身炎癥反應(yīng)的影響方法30例體外循環(huán)心臟手術(shù)患者隨機分為Omega-3魚油脂肪乳組(15例)和空白對照組(15例)。Omega-3魚油脂肪乳組于麻醉誘導(dǎo)后給予Omega-3魚油脂肪乳0.2g/kg；空白對照組于麻醉誘導(dǎo)后給予等量生理鹽水。記錄患者術(shù)前一般情況：年齡、性別、身高、體重和既往史,術(shù)中情況：手術(shù)時間、體外循環(huán)時間、升主動脈阻斷時間、術(shù)中出血量,術(shù)后情況：引流量、術(shù)后拔除氣管插管時間、抗生素使用時間、重癥監(jiān)護病房停留時間、術(shù)后住院時間、總輸血量；另外,分別于T1：麻醉誘導(dǎo)后,T2"升主動脈阻斷后30分鐘,T3：升主動脈阻斷后1小時,T4：升主動脈開放后30分鐘,T5-升主動脈開放后1小時,T6手術(shù)后6小時：T7：手術(shù)后12小時,T8：手術(shù)后24小時,T9：手術(shù)后48小時,T10-手術(shù)后72小時等10個時間點采集血液樣本檢測血漿白細(xì)胞介素-6、白細(xì)胞介素-10濃度水平。結(jié)果1.兩組患者在年齡(實驗組49.8±8.7歲,對照組49.4±11.9歲)、性別(實驗組男性46.7%,對照組男性40%)、身高(實驗組162.5±11.4cm,對照組159.6-+9.7cm)、體重(實驗組66.6±13.5kg,對照組61.1±11.6kg)、既往史等方面,均無統(tǒng)計學(xué)差異,P0.05。2.兩組患者在手術(shù)時間(實驗組249.2±44.8min,對照組241.1+37.4min)、體外循環(huán)時間(實驗組95.5±53.7min,對照組95.3-+31.4min)、升主動脈阻斷時間(實驗組69.8±44.Omin,對照組68.2±28.1min)、術(shù)中出血量(實驗組800±185.9m1,對照組741.4±288.3m1)均無統(tǒng)計學(xué)差異,P0.05。3.兩組患者在術(shù)后引流量(實驗組598.8±162.5m1,對照組687.3±276.7m1)、術(shù)后拔除氣管插管時間(實驗組12.8±5.3h,對照組12.1±5.1h)、抗生素使用時間(實驗組3.4±1.2d,對照組3.5±1.5d)、ICU停留時間(實驗組2.8±0.8d,對照組3.2±0.9d)、術(shù)后住院時間(實驗組14.7±1.5d,對照組18.6±7.9d)、總輸血量(實驗組741.6±698.6m1,對照組492.9±503.Oml),上述結(jié)果均無統(tǒng)計學(xué)差異,P0.05。4.實驗組患者血漿白介素-6(IL-6)水平分別是：T1(麻醉誘導(dǎo)后,6.81±0.20pg/ml)、T2(升主動脈阻斷后30分鐘,10.66±1.61pg/ml)、T3(升主動脈阻斷后1小時,29.16±4.73pg/m1)、T4(升主動脈開放后30分鐘,101.02±7.61pg/ml)、 T5(升主動脈開放后1小時,182.38±11.73pg/ml)、T6(手術(shù)后6小時,86.91±14.49pg/ml)、T7(手術(shù)后12小時,43.08±10.26pg/ml)、T8(手術(shù)后24小時,8.21±1.66pg/ml)、T9(手術(shù)后48小時,6.71±0.16pg/m1)、T10(手術(shù)后72小時,6.50±0.17pg/ml),其中T2至T8時間點IL-6血漿水平較術(shù)前比均有顯著統(tǒng)計學(xué)差異,P0.01；對照組患者血漿白介素-6(IL-6)水平分別是：T1(麻醉誘導(dǎo)后,6.71±0.16pg/ml)、T2(升主動脈阻斷后30分鐘,15.80±1.54pg/ml)、T3(升主動脈阻斷后1小時,53.43±5.15pg/ml)、T4(升主動脈開放后30分鐘,130.62±9.83pg/ml、T5(升主動脈開放后1小時,207.9±16.21pg/ml、T6(手術(shù)后6小時,132.91±15.21pg/ml)、T7(手術(shù)后12小時,98.58±10.17pg/ml)、T8(手術(shù)后24小時,29.57±9.42pg/ml)、T9(手術(shù)后48小時,11.14±3.2pg/ml)、T10(手術(shù)后72小時,6.71±0.16pg/m1),其中T2至T9時間點IL-6血漿水平較術(shù)前比均有顯著統(tǒng)計學(xué)差異,P0.01；實驗組血漿IL-6水平低于對照組,有顯著統(tǒng)計學(xué)差異,P0.01。5.實驗組患者血漿白介素-10(IL-10)水平分別是：T1(麻醉誘導(dǎo)后,21.88±4.14pg/ml)、T2(升主動脈阻斷后30分鐘,59.58±11.93pg/ml)、T3(升主動脈阻斷后1小時,262.34±20.99pg/ml)、T4(升主動脈開放后30分鐘,390.27±1.09pg/ml)、T5(升主動脈開放后1小時,299.32±41.63pg/ml)、T6(手術(shù)后6小時,115.66±21.06pg/ml)、T7(手術(shù)后12小時,63.64±13.29pg/ml)、T8(手術(shù)后24小時,52.11±9.67pg/ml)、T9(手術(shù)后48小時,30.03±7.05pg/ml)、T10(手術(shù)后72小時,19.29±5.36pg/ml),其中T2至T9時間點IL-10血漿水平較術(shù)前比均有顯著統(tǒng)計學(xué)差異,P0.01；對照組患者血漿白介素-10(IL-10)水平分別是：T1(麻醉誘導(dǎo)后,13.14±0.60pg/ml)、T2(升主動脈阻斷后30分鐘,49.93±6.44pg/ml)、T3(升主動脈阻斷后1小時,150.05±17.70pg/ml)、T4(升主動脈開放后30分鐘,303.53±34.72pg/ml)、T5(升主動脈開放后1小時,206.58±30.22pg/ml)、T6(手術(shù)后6小時,89.42±12.95pg/ml)、T7(手術(shù)后12小時,44.45±14.65pg/ml)、T8(手術(shù)后24小時,23.36±7.37pg/ml)、T9(手術(shù)后48小時,18.89±6.14pg/ml)、T10(手術(shù)后72小時,12.73±0.44pg/ml),其中T2至T9時間點IL-10血漿水平較術(shù)前比均有顯著統(tǒng)計學(xué)差異,P0.01,T10時間點IL-10血漿水平較術(shù)前比有統(tǒng)計學(xué)差異,P0.05；實驗組血漿IL-10水平高于對照組,有顯著統(tǒng)計學(xué)差異,P0.01。結(jié)論在體外循環(huán)心臟手術(shù)中,0mega-3魚油脂肪乳能夠有效的降低圍術(shù)期白細(xì)胞介素-6水平、提高白細(xì)胞介素-10水平；沒有明顯增加圍術(shù)期出血量；但對患者的ICU停留時間、住院時間等未見明顯影響。
[Abstract]:BACKGROUND Cardiopulmonary bypass (CPB) is one of the most important assistant measures for successful cardiac surgery. However, for patients, CPB is different from the physiological circulation of the body itself. This non-physiological mode of CPB can lead to systemic inflammatory response syndrome (SI). Out-of-control inflammation can lead to cardiopulmonary, liver, kidney, brain and other important organ dysfunction after cardiopulmonary bypass, significantly increasing mortality and disability. Surgical trauma, direct blood exposure to foreign body surfaces, ischemia-Reperfusion Injury (IRI), intestinal bacterial translocation caused by endotoxin blood Symptoms, temperature changes and other factors can activate the body's neutrophils, monocytes, endothelial cells and platelets and other cellular components, activating the complement system in the blood, endogenous and exogenous coagulation system and fibrinolysis system, causing a variety of inflammatory response-related release of bioactive substances, and the formation of uncontrollable inflammation In recent years, a large number of studies have shown that tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) play a central role in systemic inflammatory response during open heart surgery. Interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10) and so on. Among them, the more important is the interleukin system. IL-1, IL-6 and IL-8 are pro-inflammatory mediators, IL-10 is anti-inflammatory mediators. It has been reported that the plasma level of IL-6 increases immediately after the start of extracorporeal circulation, the first peak occurs 2 hours later, and 5-6 is small. IL-10 plasma levels gradually increased after aortic opening, reached a peak after 90 minutes, and basically returned to preoperative level after cardiopulmonary bypass 4 hours. Appropriate amount of anti-inflammatory mediators can help control inflammation and restore internal environment stability. Excessive anti-inflammatory response also produces immunosuppression, i.e. compensatory anti-inflammatory response syndrome (CARS). The production and development of SIRS is an extremely complex cascade process. The severity of SIRS is mainly caused by downstream pro-inflammatory cells during the development of SIRS induced by extracorporeal circulation. The balance of factors (mainly IL-6, IL-8) and anti-inflammatory cytokines (mainly IL-10) is determined. With the advancement of medical technology, there are many effective and practical methods to alleviate inflammation induced by cardiopulmonary bypass, such as the application of biocompatible coating materials, pulsatile perfusion patterns, the use of leukocyte filters and ultrafiltration packages. Omega-3 polyunsaturated fatty acids (_-3PUFAs) mainly include a-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (Docosa acid, EPA). In nature, Omega-3 polyunsaturated fatty acids are mainly derived from aquatic phytoplankton and deep-sea fishes. Almost no Omega-3 polyunsaturated fatty acids are found in terrestrial plants and animals. Studies have shown that Omega-33 polyunsaturated fatty acids can regulate inflammation and immune responses through the following pathways: (1) Arachidonic acid (Arachidonic A) Cid, AA metabolic effects. (2) through the change of cell membrane fluidity produced anti-inflammatory effects. (3) action on certain inflammation, immune mediators produced effects. (4) through the role of cell signal transduction and gene expression to produce anti-inflammatory regulatory immune effects. Mc Guinness et al. found that omega-3 polyunsaturated fatty acid preconditioning could induce the expression of HSP in myocardial cells and reduce the size of myocardial infarction. Charman et al. found that fish oil (mainly Omega-3 polyunsaturated fatty acid) could be given to patients before cardiopulmonary bypass in a planned manner. Studies have also reported that Omega-3 polyunsaturated fatty acids can reduce myocardial oxygen consumption, reduce oxidative stress and loss of potassium ions during myocardial ischemia-reperfusion, and thus protect the myocardium. Large-scale clinical trials have shown that daily intake of polyunsaturated fatty acids ranging from 500 mg to 1000 mg is significant. The first therapeutic fat emulsion, Omega-3 Fish Oil Fatty Emulsion, has been developed and used clinically in critically ill patients after major surgical operations such as sepsis, systemic inflammatory response syndrome, severe trauma, head and abdomen. However, as an anti-inflammatory therapy for open heart surgery under cardiopulmonary bypass, supplementation of Omega-3 fish fat emulsion is rare. Objective To observe the effect of Omega-3 fish fat emulsion on systemic inflammation during cardiopulmonary bypass. Methods Thirty patients undergoing cardiac surgery under cardiopulmonary bypass were randomly divided into Omega-3 fish oil fat emulsion group (15 cases) and control group (15 cases). Omega-3 fish oil fat emulsion group was given 0.2g/kg after anesthesia induction, and the blank control group was given the same amount of saline after anesthesia induction. Age, sex, height, weight and previous history, intraoperative conditions: operative time, cardiopulmonary bypass time, ascending aortic occlusion time, intraoperative bleeding volume, postoperative conditions: drainage, postoperative tracheal intubation time, antibiotic use time, ICU stay time, postoperative hospital stay, total blood transfusion; in addition, T1: anesthesia: anesthesia After induction, blood samples were collected at 30 minutes after T2 "ascending aorta occlusion, 1 hour after T3: ascending aorta occlusion, 30 minutes after T4: ascending aorta opening, 1 hour after T5 - ascending aorta opening, 6 hours after T6: T7: 12 hours after operation, 24 hours after T8: operation, 48 hours after T9: operation, 72 hours after T10 - operation, and 10 time points for blood testing. Plasma interleukin-6 and interleukin-10 levels. results 1. two groups of patients in the age (experimental group 49.8 + 8.7 years old, control group 49.4 + 11.9 years old), sex (experimental group male 46.7%, control group male 40%), height (experimental group 162.5 + 11.4 cm, control group 159.6 - + 9.7 cm), weight (experimental group 66.6 + 13.5 kg, control group 61.1 + 11.6 kg), past history and so on. There was no significant difference between the two groups (P 0.05.2). The operative time (249.2 + 44.8 min in experimental group, 241.1 + 37.4 min in control group), cardiopulmonary bypass time (95.5 + 53.7 min in experimental group, 95.3 - + 31.4 min in control group), ascending aorta occlusion time (69.8 + 44.Omin in experimental group, 68.2 + 28.1 min in control group), intraoperative bleeding volume (800 + 185.9 M1 in experimental group, 741.4 + 1.4 min in control group). There was no significant difference in 288.3 M1 between the two groups (P 0.05.3). The postoperative drainage volume (experimental group 598.8 [162.5 m1], control group 687.3 [276.7 m1]), time of tracheal intubation (experimental group 12.8 [5.3 h], control group 12.1 [5.1 h]), antibiotic use time (experimental group 3.4 [1.2 d], control group 3.5 [1.5 d]), ICU stay time (experimental group 2.8 [0.8], control group 3.2 [2] days]. There was no significant difference in the above results (P 0.05.4). The plasma levels of interleukin-6 (IL-6) in the experimental group were T1 (6.81+0.20pg/ml after anesthesia induction), T2 (30 minutes after ascending aorta occlusion, 10 minutes). 66 [1.61 pg / ml], T3 (1 hour after aortic occlusion, 29.16 [4.73 pg / m1], T4 (30 minutes after aortic occlusion, 101.02 [7.61 pg / ml], T5 (1 hour after aortic occlusion, 182.38 [11.73 pg / ml]), T6 (6 hours after aortic occlusion, 86.91 [14.49 pg / ml], T7 (12 hours after aortic occlusion, 43.08 [10.26 PG / ml]), T8 (24 hours after aortic occlusion, 18.21 [1.668] pg / ml], T9 (operation). The plasma levels of IL-6 at the time points of T2 to T8 were significantly different from those before operation (P 0.01); the plasma levels of IL-6 in the control group were: T1 (6.71.16 pg/ml after anesthesia induction), T2 (15.80.54 pg/ml 30 minutes after aortic occlusion), T3 (T3) and T1 (6.71.16 pg/ml after anesthesia induction). T4 (30 minutes after aortic occlusion, 130.62+9.83 pg/ml, T5 (1 hour after aortic occlusion, 207.9+16.21 pg/ml, T6 (6 hours after aortic occlusion, 132.91+15.21 pg/ml), T7 (12 hours after aortic occlusion, 98.58+10.17 pg/ml), T8 (24 hours, 29.57+9.42 pg/ml), T9 (11.14+3.2 pg/ml) and T9 (48 hours after aortic occlusion, respectively). The plasma levels of IL-6 in the experimental group were significantly lower than those in the control group (P 0.01.5). The plasma levels of IL-10 in the experimental group were significantly lower than those in the control group (P 0.01.5). T3, T4, T5, T6, T6, T6, 115.66 [21.06pg / ml] 6 hours after aortic occlusion, T7 (12 hours after aortic occlusion, 63.64 [13.29pg / ml], T4 (30 minutes after aortic occlusion, 390.27 [1.09pg / ml]), T5 (1 hour after aortic occlusion, 299.32 [41.63pg / ml], T6 (6 hours after aortic occlusion, 115.66 [21.06pg / ml]), T7 (12 hours after aortic occlusion, 63.64 [13.29pg / ml], T8 (surgery). The plasma levels of IL-10 at the time of T2 to T9 were significantly different from those before operation (P 0.01). The plasma levels of IL-10 in the control group were: T1 (13.14+0.60pg/ml after anesthesia induction), T2 (up) and T9 (up) respectively. Thirty minutes after aortic occlusion, 49.93 [6.44 pg / ml], T3 (1 hour after aortic occlusion, 150.05 [17.70 pg / ml], T4 (30 minutes after aortic occlusion, 303.53 [34.72 pg / ml]), T5 (1 hour after aortic occlusion, 206.58 [30.22 pg / ml]), T6 (6 hours after aortic occlusion, 89.42 [12.95 pg / ml], T7 (12 hours after aortic occlusion, 44.45 [14.65 pg / ml]), T8 (24 hours after aortic occlusion), T8 (small after aorti The plasma levels of IL-10 in the experimental group were higher than those in the control group (P 0.01, P 0.01, P 0.10 time point) and P 0.05. The plasma levels of IL-10 in the experimental group were higher than those in the control group (P 0.05). Conclusion 0 mega-3 fish oil emulsion can effectively reduce the level of interleukin-6 and increase the level of interleukin-10 during the perioperative period, and has no significant effect on the amount of perioperative bleeding, but has no significant effect on the ICU stay time and hospitalization time.
【學(xué)位授予單位】：南方醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R654.2

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