本文關(guān)鍵詞：血管內(nèi)皮生長(zhǎng)因子對(duì)犬體外循環(huán)肺損傷的保護(hù)作用及機(jī)制研究　出處：《西南醫(yī)科大學(xué)》2016年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 體外循環(huán) 血管內(nèi)皮生長(zhǎng)因子(VEGF) 肺損傷 肺保護(hù)

【摘要】：背景及目的:隨著我國社會(huì)經(jīng)濟(jì)的變革和人們生活方式的變化及人口趨于老齡化,心血管病發(fā)病的危險(xiǎn)因素持續(xù)增長(zhǎng),其死亡率占總死亡原因的首位。體外循環(huán)(cardiopulmonary bypass,CPB)心臟直視手術(shù)是目前治療心臟器質(zhì)性病變的主要手段之一,盡管體外循環(huán)技術(shù)在設(shè)備、材料和心外科手術(shù)技術(shù)等方面已經(jīng)取得了巨大進(jìn)步,體外循環(huán)下心內(nèi)直視手術(shù)的并發(fā)癥和病死率逐步下降,但由于其本身的非生理性的血流動(dòng)力學(xué)特點(diǎn)以及低溫、低灌注、炎癥反應(yīng)等所造成各個(gè)器官和系統(tǒng)的損傷仍是體外循環(huán)術(shù)后常見的并發(fā)癥之一。凡是經(jīng)歷CPB的患者術(shù)后均有不同程度的肺功能減退,輕者僅有一過性癥狀,重者可出現(xiàn)呼吸窘迫甚至急性呼吸衰竭,造成不可挽救的后果。因此,如何避免體外循環(huán)中的肺損傷一直是人們關(guān)注的重點(diǎn)。血管內(nèi)皮損傷是各種缺血再灌注和炎性反應(yīng)導(dǎo)致器官損傷的重要途徑,作為血管修復(fù)因子的血管內(nèi)皮生長(zhǎng)因子(vascular endothelial growth factor,VEGF)目前被廣泛用于相關(guān)的研究。目前已有研究證明體外循環(huán)時(shí)使用血管內(nèi)皮生長(zhǎng)因子(VEGF)可以對(duì)缺血再灌注的心臟、腎臟有一定的保護(hù)作用,但VEGF對(duì)體外循環(huán)后肺損傷是否有保護(hù)作用研究較少。本研究設(shè)想利用外源性的VEGF干預(yù)來減輕CPB后肺損傷,故通過建立犬體外循環(huán)模型,觀察外源性VEGF對(duì)CPB后肺損傷的保護(hù)作用,旨在為CPB后肺保護(hù)提供新方法。方法:選擇12-15kg的雄性Beagle犬9只,術(shù)前12h禁食水,阿托品0.5mg術(shù)前30min肌肉注射,異戊巴比妥鈉3-5mg/kg、丙泊酚3mg/kg靜脈注射麻醉后迅速用6.5#導(dǎo)管行氣管插管,連接至呼吸機(jī)(吸入氧濃度100%,潮氣量15ml/kg,呼吸頻率17次/分)。股動(dòng)脈穿刺后連接心電監(jiān)護(hù)儀,用7F中心靜脈導(dǎo)管置入頸內(nèi)靜脈,用于監(jiān)測(cè)靜脈壓和泵入血管活性藥物。常規(guī)建立體外循環(huán)。體外循環(huán)轉(zhuǎn)流時(shí)間120min,復(fù)跳后輔助循環(huán)30min。保持轉(zhuǎn)機(jī)溫度32~34℃,維持平均體循環(huán)壓60-70mm Hg,體外循環(huán)流量80~120ml/(kg·min),通過自體輸血維持血細(xì)胞比容(Hematocrit,Hct)于24-28%之間。所有動(dòng)物隨機(jī)分成假手術(shù)組(sham組)、對(duì)照組(con組)和實(shí)驗(yàn)組(vegf組),每組各3只。sham組在手術(shù)前30min內(nèi)緩慢靜脈泵入生理鹽水0.5g/kg,再予以開胸及主動(dòng)脈、上下腔靜脈插管,不行體外循環(huán)轉(zhuǎn)流。con組在手術(shù)前30min內(nèi)緩慢靜脈泵入生理鹽水0.5g/kg,常規(guī)體外循環(huán)轉(zhuǎn)流120min,輔助循環(huán)30min。vegf組手術(shù)前30min內(nèi)緩慢靜脈泵注vegf 0.5g/kg,常規(guī)體外循環(huán)轉(zhuǎn)流120min,輔助循環(huán)30min。實(shí)驗(yàn)結(jié)束后取相同部位肺組織計(jì)算肺濕/干重(W/D)比值;并取一定量肺組織制成肺組織勻漿,離心后取上清液,分別測(cè)定MDA、SOD、IL-6及TNF-α含量。取一定量的肺組織固定、切片、HE染色后光鏡下觀察病理學(xué)結(jié)果。結(jié)果:1、W/D比值:體外循環(huán)后con組的W/D值(11.3±1.6)明顯高于sham組(6.3±0.8),P=0.003,差異具有統(tǒng)計(jì)學(xué)意義;con組的W/D值明顯高于vegf組(7.8±1.2),P=0.014,差異具有統(tǒng)計(jì)學(xué)意義;vegf組的W/D值稍高于con組,P=0.114,差異不具有統(tǒng)計(jì)學(xué)意義。2、MDA含量:體外循環(huán)后con組的MDA含量(268.121±4.424 ng/ml)較sham組(227.336±3.948 ng/ml)有明顯升高,P=0.001,差異具有統(tǒng)計(jì)學(xué)意義;vegf組的MDA含量(246.488±8.585ng/ml)明顯高于sham組,P=0.021,差異具有統(tǒng)計(jì)學(xué)意義;而con組的MDA含量明顯高于vegf組,P=0.009,差異具有統(tǒng)計(jì)學(xué)意義。3、SOD含量:sham組的SOD含量(1622.126±36.212 ng/ml)明顯高于con組(1364.391±92.761 ng/ml),P=0.006,差異具有統(tǒng)計(jì)學(xué)意義;vegf組的SOD含量(1541.142±25.539 ng/ml)明顯高于con組,P=0.018,差異具有統(tǒng)計(jì)學(xué)意義;sham組的SOD含量稍高于vegf組,P=0.218,差異不具有統(tǒng)計(jì)學(xué)意義。4、IL-6水平:體外循環(huán)后con組的IL-6水平(135.851±10.276 ng/ml)明顯高于sham組(106.129±1.986 ng/ml),P=0.005,差異具有統(tǒng)計(jì)學(xué)意義;con組的IL-6水平明顯高于vegf組(114.915±3.561 ng/ml),P=0.014,差異具有統(tǒng)計(jì)學(xué)意義;vegf組的IL-6水平稍高于sham組,P=0.224,差異不具有統(tǒng)計(jì)學(xué)意義。5、TNF-α含量:體外循環(huán)后con組的TNF-α含量(247.675±1.735 ng/ml)較sham組(206.798±2.414 ng/ml)有明顯升高,P=0.001,差異具有統(tǒng)計(jì)學(xué)意義;vegf組的TNF-α含量(222.618±9.000 ng/ml)較sham組有明顯升高,P=0.032,差異具有統(tǒng)計(jì)學(xué)意義;con組的TNF-α含量明顯高于vegf組,P=0.003,差異具有統(tǒng)計(jì)學(xué)意義。6、肺組織病理學(xué):con組肺組織水腫、充血,肺泡間隔增寬,大量炎性細(xì)胞和紅細(xì)胞浸潤明顯,vegf組肺組織輕度水腫,少量炎細(xì)胞浸潤,而sham組的肺組織病理學(xué)改變明顯輕于con組及vegf組。結(jié)論:1、本實(shí)驗(yàn)利用犬建立體外循環(huán)模型,操作簡(jiǎn)單,有效的模擬了人體體外循環(huán)后的病理生理狀況,實(shí)驗(yàn)重復(fù)性好,穩(wěn)定度高。2、血管內(nèi)皮生長(zhǎng)因子(VEGF)可以降低犬體外循環(huán)期間因肺缺血再灌注引起的肺微血管通透性增加,減少膜脂質(zhì)過氧化反應(yīng),增加機(jī)體清除自由基的能力。3、血管內(nèi)皮生長(zhǎng)因子對(duì)體外循環(huán)后肺損傷有一定的保護(hù)作用,可能系因其可修復(fù)血管內(nèi)皮損傷,減少肺部缺血缺氧狀況,減少氧自由基的破壞和抑制炎性細(xì)胞因子的聚集和激活,從而達(dá)到肺保護(hù)的目的。
[Abstract]:Background and objective: with the change of population and the change of our social economy and people's life style tends to be aging, the risk factors of cardiovascular disease continues to grow, the mortality rate of the total causes of death first. CPB (cardiopulmonary bypass, CPB) in open heart surgery is the major treatment of cardiac disorders at present although, extracorporeal circulation technology in equipment, materials and cardiac surgery technology and other aspects have made great progress, cardiopulmonary bypass heart surgery complications and mortality rate gradually declined, but because the hemodynamic characteristics of non physiological itself and the low temperature, low perfusion injury is a common complication of cardiopulmonary bypass in all the organs and systems caused by inflammation. All CPB patients experience postoperative pulmonary function showed different degrees of decline, only a few light There may be severe respiratory distress symptoms, acute respiratory failure and even cause irreparable consequences. Therefore, how to avoid the lung injury during cardiopulmonary bypass has been the focus of attention. Vascular endothelial injury of ischemia reperfusion and various inflammatory reaction leads to an important way of organ damage, as vascular repair factor, vascular endothelial growth factor (vascular endothelial growth factor, VEGF) is currently widely used in related research. At present it has been shown that the bypass using vascular endothelial growth factor (VEGF) on ischemia reperfusion injury of heart and kidney has certain protective effect, but VEGF on pulmonary injury after cardiopulmonary bypass have protective effect on this research is less. Envision the use of exogenous VEGF intervention to reduce lung injury after CPB, so through the establishment of cardiopulmonary bypass model, the effect of exogenous VEGF on lung injury after CPB And to provide new methods for lung protection after CPB. Methods: 12-15kg male Beagle dogs 9, preoperative fasting 12h, atropine 0.5mg 30min preoperative intramuscular injection of amobarbital sodium 3-5mg/kg, propofol 3mg/kg anesthesia rapidly after intravenous injection with 6.5# catheter connected to the tracheal intubation, ventilator (inhaled oxygen concentration 100% 15ml/kg, tidal volume, respiratory rate 17 / min). After puncture of femoral artery connecting ECG monitor, 7F central venous catheter into internal jugular vein for venous pressure monitoring, and infusion of vasoactive drugs. Routine extracorporeal circulation. The CPB time 120min, 30min. transfer assisted circulation temperature 32~34 Rebeating, maintain average the systemic circulatory pressure 60-70mm Hg, extracorporeal circulation flow 80~120ml/ (kg - min), maintaining hematocrit by autologous blood transfusion (Hematocrit, Hct) in 24-28%. All animal random divided into sham operation group (Group sham), The control group (CON group) and experimental group (VEGF group), each group had 3 rats in group.Sham before operation 30min slow intravenous infusion of normal saline 0.5g/kg, and then be open chest and aorta, inferior vena cava intubation, no cardiopulmonary bypass group.Con before the operation in 30min slow intravenous infusion of saline 0.5g/kg the conventional cardiopulmonary bypass, 120min, 30min.vegf group before surgery assisted circulation 30min slow intravenous infusion of VEGF 0.5g/kg, conventional cardiopulmonary bypass 120min, the end of 30min. assisted circulation after the experiment from the lung tissue the same parts of the lung wet / dry weight ratio (W/D); and taking a certain amount of lung tissue into lung homogenate and centrifugation after the supernatant were measured, MDA, SOD, IL-6 and TNF- alpha content. Take a certain amount of lung tissue fixation, slice, HE staining was observed under pathological results. Results: 1, the ratio of W/D: con after cardiopulmonary bypass group W/D (11.3 + 1.6) was significantly higher than that of sham group (6 .3 + 0.8, P=0.003), the difference was statistically significant; the W/D value of con group was significantly higher than that of VEGF group (7.8 + 1.2), P=0.014, the difference was statistically significant; the W/D value of VEGF group was slightly higher than that of group con, P=0.114, the difference was not statistically significant.2, MDA content: the content of MDA in group con after CPB (268.121 + 4.424 ng/ml) than in sham group (227.336 + 3.948 ng/ml) significantly increased, P=0.001, the difference was statistically significant; the content of MDA in group VEGF (246.488 + 8.585ng/ml) was significantly higher than that of group sham, P=0.021, the difference was statistically significant; while the content of MDA in con group was significantly higher than that of group VEGF, P=0.009, the difference was statistically the significance of.3, SOD content: the content of SOD in group sham (1622.126 + 36.212 ng/ml) was significantly higher than that of group con (1364.391 + 92.761 ng/ml), P=0.006, the difference was statistically significant; the content of SOD in group VEGF (1541.142 + 25.539 ng/ml) was significantly higher than that of group con, P=0.018, the difference has statistical meaning Meaning; SOD content of group sham was slightly higher than that of group VEGF, P=0.218, the difference was not statistically significant.4, IL-6 level: the level of IL-6 in group con after CPB (135.851 + 10.276 ng/ml) was significantly higher than that of group sham (106.129 + 1.986 ng/ml), P=0.005, the difference was statistically significant; the level of IL-6 in con group was significantly higher than that of VEGF group (114.915 + 3.561 ng/ml), P=0.014, the difference was statistically significant; the IL-6 level of VEGF group was slightly higher than that of group sham, P=0.224, the difference was not statistically significant.5, TNF- alpha content: after CPB in group con TNF- were (247.675 + 1.735 ng/ml) than in sham group (206.798 + 2.414 ng/ml) significantly increased P=0.001, the difference was statistically significant; the TNF- alpha in VEGF group (222.618 + 9 ng/ml) was significantly higher than that in group sham, P=0.032, the difference was statistically significant; the TNF- alpha con group were significantly higher than that in group VEGF, P=0.003, the difference was statistically significant.6, Lung Group Tissue pathology: con group lung tissue edema, congestion, alveolar septum, inflammatory cells and red blood cell infiltration, lung tissue in VEGF group was mild edema, infiltration of inflammatory cells, and pulmonary pathological changes in sham group was lower than that in the con group and VEGF group. Conclusion: 1. This experiment the establishment of extracorporeal circulation model, the dog has the advantages of simple operation, effective simulation of the pathophysiology of human body after cardiopulmonary bypass, good repeatability, high stability of.2, vascular endothelial growth factor (VEGF) can reduce the increase during cardiopulmonary bypass in dogs caused by pulmonary ischemia reperfusion injury of pulmonary microvascular permeability, reduce membrane lipid peroxidation. Increase the body's free radical scavenging ability of.3, vascular endothelial growth factor has a protective effect on lung injury after cardiopulmonary bypass, probably because of the repair of vascular endothelial injury, reduce lung ischemia and hypoxia condition, reduce oxygen free radical damage And inhibit the accumulation and activation of inflammatory cytokines, so as to achieve the purpose of lung protection.

【學(xué)位授予單位】：西南醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2016
【分類號(hào)】：R654.1;R563

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9 夏照帆;馬兵;衛(wèi)偉;賈一韜;;活化素受體樣激酶5活性抑制在炎性肺損傷發(fā)病機(jī)制中的意義[A];第五屆全國燒傷救治專題研討會(huì)燒傷后臟器損害的臨床救治論文匯編[C];2007年

10 夏金根;孫兵;張恒;王春亭;詹慶元;;自主呼吸對(duì)健康兔模型中呼吸機(jī)誘導(dǎo)肺損傷的影響[A];中華醫(yī)學(xué)會(huì)第五次全國重癥醫(yī)學(xué)大會(huì)論文匯編[C];2011年

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