本文關(guān)鍵詞：深低溫停循環(huán)后再灌注肺損傷的臨床和基礎(chǔ)研究　出處：《福建醫(yī)科大學(xué)》2016年博士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： Stanford A型主動脈夾層 急性呼吸窘迫綜合征 深低溫停循環(huán) 輸血相關(guān)性肺損傷 腫瘤壞死因子-α 缺血再灌注損傷 動物模型 深低溫停循環(huán) 大鼠 缺血再灌注損傷 急性呼吸窘迫綜合征 深低溫停循環(huán) 腫瘤壞死因子-α

【摘要】：目的評估急性呼吸窘迫綜合征(acute respiratory distress syndrome,ARDS)對Stanford A型主動脈夾層(aorta dissection,AD)手術(shù)患者預(yù)后的影響,尋找Stanford A型AD術(shù)后發(fā)生ARDS的危險因素,為相關(guān)疾病的臨床防治提供參考依據(jù)。材料與方法選取329例于2013年1月至2015年7月在我科接受常規(guī)開胸手術(shù)的Stanford A型AD患者作為研究對象,以回顧性巢式病例對照作為研究手段,對其中的126例患者(非ARDS組和ARDS組各63例)一般情況、病因、術(shù)前并發(fā)癥、術(shù)式、術(shù)中情況、圍術(shù)期輸血情況、血清TNF-α水平變化進行統(tǒng)計學(xué)分析。在初步篩選Stanford A型AD術(shù)后發(fā)生ARDS的可疑危險因素后,通過多元logistics回歸分析找出獨立危險因素。通過比較患者死亡率差別、術(shù)后并發(fā)癥和預(yù)后、住院總費用、繪制生存曲線等方法評估ARDS對Stanford A型AD手術(shù)患者預(yù)后的影響。結(jié)果Stanford A型AD術(shù)后ARDS總的發(fā)生率20.7%。兩組間年齡、性別等一般臨床資料無顯著性差別;主動脈弓部處理方式、手術(shù)操作涉及的范圍亦無顯著性差異。ARDS組患者的CPB時間和DHCA時間顯著長于非ARDS組,而主動脈阻斷時間兩組間無顯著性差異。相比非ARDS組,ARDS組患者圍術(shù)期輸注了更多的紅細胞、血小板及新鮮冰凍血漿。肺部感染發(fā)生率、MODS發(fā)生率及死亡率顯著增加,入住ICU時間、呼吸機輔助時間顯著延長,及住院總費用顯著增加。兩組圍術(shù)期的OI值和ApacheⅡ分值變化有顯著性差異,ARDS組術(shù)后OI值總體水平低于非ARDS組,ApacheⅡ分值總體水平高于非ARDS組。ARDS組患者的血清TNF-α作用強度水平及變化趨勢顯著高于非ARDS組。多元logistic回歸分析提示DHCA時間、血清TNF-α作用強度和圍術(shù)期輸血量(不論輸注類型)是Stanford A型AD術(shù)后ARDS的獨立危險因素。生存曲線分析顯示ARDS組患者術(shù)后的總體存活率明顯低于非ARDS組。結(jié)論Stanford A型AD術(shù)后ARDS嚴重影響Stanford A型AD患者的預(yù)后,其發(fā)生與DHCA時間、圍術(shù)期輸血及血清TNF-α水平密切相關(guān)。通過改進手術(shù)技術(shù),減少DHCA時間和圍術(shù)期輸血,降低術(shù)后血清TNF水平可能成為改善Stanford A型AD術(shù)后肺功能的有效手段。目的尋找建立深低溫停循環(huán)(deep hypothermic circulatoryarrest,DHCA)下大鼠肺缺血再灌注損傷(ischemia-reperfusion injury,IRI)在體模型的有效方法,為動物體內(nèi)干預(yù)試驗提供實驗基礎(chǔ)。材料與方法以體重相近的健康成年雄性SD大鼠為實驗對象,分成缺血再灌注組(I/R組,n=15)和假手術(shù)組(S組,n=15),以氣管插管全麻和直視開胸手術(shù)作為操作方法,以恒溫水浴箱為控溫設(shè)備,制作深低溫停循環(huán)下的大鼠左下肺葉缺血再灌注的在體模型。通過觀察和比較兩組間的血氣分析結(jié)果、氣道阻力、濕/干重比率、BALF細胞數(shù)和成分、組織切片下的病理學(xué)改變,來評估I/R后ARDS。結(jié)果本實驗共消耗大鼠32只,成功建立大鼠在體I/R肺模型15例,匹配假手術(shù)組15例,1例死與低氧血癥,來自實驗組;1例術(shù)后未觀察到典型的ARDS表現(xiàn),建模失敗。I/R建模成功率88.2%(15/17),術(shù)后12h存活率100%。麻醉及術(shù)前準備耗時25.5±6.4min,手術(shù)過程耗時41.2±9.2min,復(fù)蘇過程耗時23.6±3.2min,總手術(shù)時間耗時96.5±12.3min。結(jié)論該模型停循環(huán)范圍局限于左下肺葉,對大鼠的呼吸功能損傷較小,死亡率低,手術(shù)操作簡便,單人肉眼即可完成。模型可復(fù)制性好,成功率高,易于批量建模,為進行后續(xù)的大規(guī)模干預(yù)實驗研究提供了堅實的基礎(chǔ)。麻醉藥量控制、氣管插管、頸動脈插管和停循環(huán)時間的把握是建模成功的關(guān)鍵。目的以大鼠深低溫停循環(huán)下肺缺血再灌注損傷模型為基礎(chǔ),探討TNF-α對Stanford A型AD術(shù)后ARDS的影響及機制,為Stanford A型AD術(shù)后ARDS尋找新的臨床治療靶點。材料與方法以72只雄性SD大鼠為研究對象,均分為假手術(shù)組(S組)、對照組(C組)和實驗組(Ab組),每組再按肺組織標本留取時間均分為術(shù)后4h亞組、術(shù)后12h亞組和術(shù)后24h亞組。實驗?zāi)M主動脈夾層手術(shù)中的深低溫停循環(huán)過程,造成肺組織缺血再灌注損傷,實驗組術(shù)前常規(guī)應(yīng)用抗TNF-α單克隆抗體拮抗TNF-α的作用。術(shù)后通過肉眼和HE染色鏡檢觀察肺組織大體和微觀結(jié)構(gòu)改變;血氣分析測定動脈血Pa O2和Pa CO2評估大鼠圍術(shù)期肺氧合功能和肺泡通氣功能;稱重法檢測肺組織干濕重比率評估肺水腫程度;呼吸機參數(shù)讀取氣道峰壓評估圍術(shù)期氣道阻力變化;TUNEL法檢測肺組織細胞凋亡指數(shù);ELISA法檢測術(shù)后血清TNF-α、IL-6/10水平和肺組織MPO、MDA、SOD含量;RT-PCR法檢測肺組織術(shù)后caspase3/8和NF-κB表達水平;生存曲線分析評估大鼠存活率差異。結(jié)果C組大鼠肺組織水腫、氣道分泌物增加,鏡檢見肺間質(zhì)水腫、肺泡結(jié)構(gòu)破壞、炎癥細胞和紅細胞浸潤。S組未發(fā)現(xiàn)上述病理改變,Ab組病變程度居中;與S組相比,C組和Ab組術(shù)后動脈血Pa O2明顯降低,Pa CO2明顯升高;術(shù)后肺組織干濕重比率、氣道阻力、肺組織凋亡指數(shù)、肺組織TNF-α表達強度、血清TNF-α、IL-6水平、肺組織MPO、MDA含量、肺組織TNF-α、caspase3/8和NF-κB表達水平均明顯增加,C組增加程度顯著高于Ab組;與S組相比,C組和Ab組術(shù)后血清IL-10水平明顯增高,Ab組增高更明顯;三組大鼠術(shù)后肺組織SOD含量變化無顯著性差異。共計85只SD大鼠進行了上述實驗,死亡13只(除外麻醉意外和大出血所致的死亡),其中S組2只,C組7只,Ab組4只,總死亡率15.3%,三組大鼠術(shù)后24h內(nèi)的存活率有顯著性差異。結(jié)論TNF-α可通過誘導(dǎo)肺水腫損害肺泡氧合和通氣功能、募集和激活中性粒細胞、促進炎癥反應(yīng)和氧化應(yīng)激、誘導(dǎo)肺泡上皮細胞凋亡等機制促進深低溫體循環(huán)術(shù)后肺損傷的發(fā)生。通過術(shù)前預(yù)防性的使用TNF-α拮抗劑可在一定程度上減輕上述機制造成的肺損傷。TNF-α有可能成為防治Stanford A型AD術(shù)后ARDS的新靶點。
[Abstract]:Objective to evaluate the acute respiratory distress syndrome (acute respiratory distress syndrome, ARDS) of Stanford type A aortic dissection (aorta dissection AD) affect the prognosis of patients, the risk factors for ARDS Stanford A after AD, to provide reference for clinical prevention and treatment of related diseases. Materials and methods: 329 cases in January 2013 to July 2015 in our department to accept the Stanford A type AD patients with conventional thoracic surgery as the research object, in a retrospective nested case-control study as a means of one of the 126 patients (non ARDS group and ARDS group with 63 cases in each group) general condition, etiology, preoperative complications, operation, intraoperative, peri perioperative blood transfusion, changes of serum levels of TNF- were analyzed. The suspicious risk factors of ARDS in the preliminary screening of Stanford A type AD postoperatively, by multivariate logistics regression analysis to identify independent risk factors By comparing the difference. The mortality of patients, postoperative complications and prognosis, the total hospitalization expenses, draw survival curves were used to analyze effects of ARDS on the prognosis of patients with Stanford type A AD surgery. Results the incidence rate of ARDS 20.7%. between the two groups of age total Stanford type A after AD, there is no significant difference between gender and other general clinical data; aortic arch approach, scope of operation involved and there were no significant difference in.ARDS group were CPB time and DHCA time was significantly longer than non ARDS group, and aortic clamping time had no significant difference between two groups. Compared with non ARDS group, infusion of more red blood cells of ARDS patients during the perioperative period, platelet and fresh frozen plasma. The incidence of pulmonary infection, the incidence of MODS and mortality increased significantly in the ICU time, ventilation time was significantly prolonged, and the total cost of hospitalization was significantly increased. The changes of Apache and II scores of two groups of perioperative OI value There was significant difference in OI value, the overall level of ARDS group were lower than non ARDS group, Apache II score overall level higher than the non ARDS group.ARDS serum TNF- alpha intensity levels and trends were significantly higher than non ARDS group. Multivariate logistic regression analysis showed that the DHCA time, serum TNF- intensity and perioperative blood transfusion the amount (whether infusion type) is the independent risk factors of ARDS Stanford A AD after operation. The survival curve analysis showed that the patients of the ARDS group after the overall survival rate was significantly lower than that in non ARDS group. Severe ARDS influence the prognosis of patients with Stanford type A AD type A AD conclusion Stanford after operation, the occurrence and duration of DHCA, Wai blood transfusion and serum levels of TNF- patients are closely related. Through the improvement of surgical technique, reduce the DHCA time and perioperative blood transfusion, reduce the postoperative serum TNF level may be an effective means of improving pulmonary function of Stanford A after AD. To build Vertical deep hypothermic circulatory arrest (deep hypothermic, circulatoryarrest, DHCA) lung ischemia reperfusion injury in rats (ischemia-reperfusion injury, IRI) in the method body model, to provide the experimental basis for animal test in vivo intervention. Materials and methods with similar weight healthy adult male SD rats were divided into ischemia reperfusion group (group I/R, n=15) and sham operation group (group S, n=15), with tracheal intubation anesthesia and open thoracotomy as the operation method, with constant temperature water bath box for temperature control equipment, production of deep hypothermic circulatory arrest in rats with left lower lobe ischemia / reperfusion in vivo. Through the observation and comparison of two blood gas between group analysis, airway resistance, wet / dry weight ratio, the number and composition of BALF cells, the pathological changes of the tissue sections, to assess the I/R ARDS. after the results of this experiment consumed a total of 32 rats were successfully established in vivo in rat lung model 15 I/R Cases, the sham operation group 15 cases, 1 cases died of hypoxemia, from the experimental group; 1 cases were not observed in the typical ARDS findings,.I/R modeling modeling failed success rate of 88.2% (15/17), the postoperative survival rate of 12h 100%. anesthesia and preoperative preparation time was 25.5 + 6.4min, 41.2 + operation time 9.2min, the recovery process takes 23.6 + 3.2min, the total operation time consuming 96.5 + 12.3min. conclusion the model of circulatory arrest is confined to the left lower lobe, respiratory function injury in rats is small, the mortality rate is low, the operation is simple, single eye can be completed. Model can be replicated, high success rate, easy batch modeling, provide a solid foundation for the study of large-scale intervention in subsequent experiments. The amount of anesthetic drug control, tracheal intubation, carotid artery intubation and circulatory arrest time is the key to successful modeling. With the purpose of deep hypothermic injury of rat model of lung ischemia-reperfusion cycles Based on the mechanism of ARDS on TNF- alpha and Stanford type A after AD, to find a new target for clinical treatment of Stanford type A AD ARDS after the operation. Materials and methods: 72 male SD rats as the research object, divided into sham operation group (S group) and control group (C group) and experimental group (Ab group), each group according to the lung tissue specimens divided into postoperative 4H subgroups, postoperative 12h subgroup and 24h subgroup. After experimental simulation of deep hypothermic circulatory arrest in aortic dissection, causing pulmonary ischemia reperfusion injury in experimental group, the preoperative routine the application of anti TNF- alpha monoclonal antibody against TNF- alpha. After operation by changing the gross and microscopic observation of HE staining of lung tissue specimens and microstructure; blood gas analysis of arterial blood Pa O2 and Pa CO2 in rats were evaluated perioperative pulmonary oxygenation and pulmonary ventilation function; weighing method for detection of lung tissue wet / dry weight ratio the evaluation process of pulmonary edema The degree of ventilator parameters; read peak airway pressure to evaluate peri operative changes of airway resistance; apoptosis of the lung cells was detected by TUNEL ELISA method after surgery; detection of serum TNF- level and lung tissue IL-6/10, MPO, MDA, SOD content; RT-PCR lung tissues were detected after caspase3/8 and NF- K B expression; survival curve analysis and evaluation of the survival rate of rats. The differences in lung tissue of rats in C group were edema, airway secretions increase, the histological examination showed pulmonary interstitial edema, alveolar structural damage, inflammatory cells and red blood cell infiltration.S group found no pathologic changes in the Ab group, the severity of the middle; compared with S group, C group and Ab group. After arterial blood Pa O2 were decreased, Pa CO2 increased significantly; postoperative lung wet / dry weight ratio, airway resistance, apoptosis index of lung tissue, lung tissue expression of TNF- alpha, alpha IL-6 levels, serum TNF-, lung MPO, MDA content in lung tissue of TNF- alpha, caspase3/8 and NF- K B expression The C group was significantly increased, increased significantly higher than group Ab; compared with S group, serum IL-10 levels were significantly increased in C group and Ab group after operation, Ab group was more obvious; there was no significant difference in SOD content in lung tissue of rats in three groups after operation. A total of 85 SD rats of the experiment. Only 13 deaths (except the anesthetic accident and death caused by bleeding), 2 rats in S group, 7 rats in group C, 4 rats in group Ab, the total mortality rate was 15.3%, three groups of rats at the survival rate of 24h had significant difference. Conclusion TNF- can be induced by alpha damage of oxygenation and pulmonary edema ventilation function, recruitment and activation of neutrophils, promote inflammation and oxidative stress induced apoptosis of alveolar epithelial cells and other mechanisms to promote the circulation of deep hypothermia after lung injury. The preoperative prophylactic use of TNF- antagonists in some extent caused by reducing the mechanism of lung injury is likely to become the alpha.TNF- A new target for the prevention and treatment of ARDS after Stanford A AD.

【學(xué)位授予單位】：福建醫(yī)科大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R654.2

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