發(fā)布時(shí)間：2018-04-03 15:41

  本文選題：氫氣　切入點(diǎn)：亞低溫　出處：《第三軍醫(yī)大學(xué)》2016年碩士論文

【摘要】：心臟驟停復(fù)蘇后患者死亡的主要原因是復(fù)蘇后心、腦損傷。近年來(lái),院外心臟驟停數(shù)據(jù)報(bào)道中,不可除顫節(jié)律患者所占的比例越來(lái)越大,并且預(yù)后較差。治療性亞低溫作為目前研究唯一有效的治療措施被寫(xiě)進(jìn)復(fù)蘇指南,但因其帶來(lái)的副作用及對(duì)不可除顫患者保護(hù)效果不顯著引起爭(zhēng)議。在心室顫動(dòng)心臟驟停動(dòng)物模型中,氫氣被證明具有腦保護(hù)作用并且可以顯著改善復(fù)蘇后存活,然而,氫氣對(duì)于心、腦的保護(hù)作用在不可除顫節(jié)律模型中未被研究。本研究運(yùn)用動(dòng)物實(shí)驗(yàn)以及組織病理生物學(xué)、生化學(xué)的分析方法,證明氫氣對(duì)無(wú)脈電活動(dòng)大鼠復(fù)蘇后的心、腦損傷有改善作用,主要研究?jī)?nèi)容和實(shí)驗(yàn)結(jié)果如下:一、建立窒息法致心臟驟停大鼠復(fù)蘇后心肌損傷及神經(jīng)功能損傷的疾病模型,探討吸入2%氫氣對(duì)心肺復(fù)蘇大鼠心、腦損傷及存活率的改善作用,并與傳統(tǒng)亞低溫治療方式進(jìn)行比較。方法:健康SD大鼠72只,維持窒息心臟驟停未處理五分鐘,隨后給予心肺復(fù)蘇及機(jī)械通氣,動(dòng)物自主循環(huán)恢復(fù)后隨機(jī)分為三組:常溫機(jī)械通氣2%氮?dú)?98%氧氣(對(duì)照組);亞低溫(33℃)機(jī)械通氣2%氮?dú)?98%氧氣(低溫組);常溫機(jī)械通氣2%氫氣+98%氧氣(氫氣組)�；旌蠚怏w機(jī)械吸入1小時(shí),降溫方法為恢復(fù)自主循環(huán)后體表物理降溫,十分鐘左右將核心溫度將至亞低溫范圍(32℃-34攝氏度),且維持33℃亞低溫兩小時(shí),之后兩小時(shí)復(fù)溫至基礎(chǔ)體溫,復(fù)蘇后連續(xù)監(jiān)測(cè)4小時(shí)且持續(xù)觀察96小時(shí)。對(duì)各組大鼠進(jìn)行生存率評(píng)價(jià)和形態(tài)學(xué)觀察,每24小時(shí)進(jìn)行神經(jīng)功能缺陷評(píng)分,分析各組大鼠在不同時(shí)間點(diǎn)的超聲數(shù)據(jù),用ELISA方法測(cè)定各組大鼠不同時(shí)間點(diǎn)的心肌損傷指標(biāo)c TnT及腦功能損傷指標(biāo)s-100B。結(jié)果:各組動(dòng)物在基礎(chǔ)狀態(tài)均無(wú)差異,所有動(dòng)物均復(fù)蘇成功,低溫組復(fù)蘇早期血清中cTn T與s-100b的含量均顯著低于對(duì)照組(p0.05),氫氣組復(fù)蘇后左心室射血分?jǐn)?shù)顯著提高(p0.05),其神經(jīng)功能缺損評(píng)分顯著改善(p0.05);96小時(shí)生存率分別為:氫氣組75.0%(p=0.004 vs.對(duì)照組;p=0.039 vs.低溫組),低溫組45.8%(p=0.376 vs.對(duì)照組),對(duì)照組33.3%。方法:健康大鼠36只隨機(jī)分為三組:(1)假手術(shù)組:僅麻醉,氣管插管及動(dòng)靜脈插管手術(shù);(2)對(duì)照組:復(fù)蘇后機(jī)械通入1小時(shí)2%氮?dú)?98%氧氣,觀測(cè)終點(diǎn)為4小時(shí);(3)實(shí)驗(yàn)組:復(fù)蘇后機(jī)械通入1小時(shí)2%氫氣+98%氧氣,觀測(cè)終點(diǎn)為4小時(shí)。觀察終點(diǎn)處死取材,做血液生化與病理生化檢測(cè)。結(jié)果:與對(duì)照組相比,實(shí)驗(yàn)組復(fù)蘇后四小時(shí)血清炎癥因子IL-6,IL-8,IgG及凋亡因子TFAR19均顯著減少,差異有統(tǒng)計(jì)學(xué)意義(p0.05)。本研究證明,在窒息致大鼠心臟驟停模型中,吸入小劑量氫氣比低溫更能有效的減輕心腦功能損傷及改善復(fù)蘇后存活,初步探討氫氣的保護(hù)作用與其抗炎癥抗凋亡反應(yīng)有關(guān)。二、初步探討吸入氫氣對(duì)復(fù)蘇后心、腦保護(hù)作用機(jī)制。
[Abstract]:The main cause of death after cardiac arrest resuscitation is cardiac and brain injury after resuscitation.In recent years, the proportion of patients with undefibrillation rhythm is increasing, and the prognosis is poor.Therapeutic mild hypothermia, as the only effective treatment in current studies, has been included in the resuscitation guidelines, but its side effects and protective effects on patients with undefibrillation are not controversial.In ventricular fibrillation and cardiac arrest animal models, hydrogen has been shown to have a brain protective effect and can significantly improve survival after resuscitation. However, the protective effect of hydrogen on heart and brain is not studied in the undefibrillation rhythm model.In this study, animal experiments, histopathological and biochemical methods were used to prove that hydrogen can improve cardiac and brain injury after resuscitation in rats with no pulse electrical activity. The main contents and experimental results are as follows: 1.To establish the model of myocardial injury and nerve function injury after resuscitation in rats with cardiac arrest induced by asphyxia, to investigate the effects of inhaling 2% hydrogen on the improvement of heart and brain injury and survival rate in rats with cardiopulmonary resuscitation, and to compare it with the traditional mild hypothermia therapy.Methods: 72 healthy SD rats were given cardiopulmonary resuscitation and mechanical ventilation.After mechanical inhalation of mixed gases for 1 hour, the cooling method is physical cooling of body surface after recovery of spontaneous circulation, the core temperature will reach 32 鈩，

本文編號(hào)：1705844