本文選題：七氟醚 + 缺血-再灌注損傷　； 參考：《中國協(xié)和醫(yī)科大學(xué)》2010年博士論文

【摘要】： 目的： 1、觀察七氟醚缺血后處理對健康成年大鼠離體心臟缺血-再灌注損傷的保護(hù)作用,研究活性氧(ROS)、細(xì)胞外信號調(diào)節(jié)激酶(ERK1/2)及線粒體通透性轉(zhuǎn)換孔(mPTP)可能的作用； 2、觀察七氟醚缺血后處理對慢性心梗大鼠離體心臟缺血-再灌注損傷的保護(hù)作用,研究蛋白激酶B (PKB/Akt)、細(xì)胞外信號調(diào)節(jié)激酶(ERK 1/2)及線粒體通透性轉(zhuǎn)換孔(mPTP)在其中的可能作用； 3、比較七氟醚缺血預(yù)處理、七氟醚缺血后處理及七氟醚缺血預(yù)處理聯(lián)合七氟醚缺血后處理3種方式對健康成年大鼠離體心臟缺血-再灌注損傷保護(hù)效果及相關(guān)機(jī)制； 4、系統(tǒng)評價和薈萃分析七氟醚、異丙酚用于行冠脈搭橋手術(shù)時對患者的心肌保護(hù)效果。 方法： 1、大鼠心臟離體,以K-H緩沖液灌注,全心缺血30 min后復(fù)灌60 min建立缺血-再灌注損傷模型。七氟醚缺血后處理的心臟于缺血后復(fù)灌最初15 min以3%七氟醚飽和的K-H緩沖液灌注。分別單獨(dú)給予或與七氟醚同時給予ROS清除劑NAC (4mM)或ERK 1/2阻斷劑PD98059 (20μM),用以評價ROS及ERK 1/2在七氟醚缺血后處理中的作用。比較各組間血流動力學(xué)、心肌梗死面積、冠脈流出液中乳酸脫氫酶(LDH)及肌酸肌酶-MB (CK-MB)水平。同時,測定各組缺血30 min復(fù)灌60 min后心肌丙二醛(MDA)含量以反映氧化應(yīng)激損傷程度。Western blotting測定ERK 1／2的磷酸化情況。測定心肌煙酰胺腺嘌呤二核苷酸(NAD+)含量以反映mPTP的開放情況。 2、大鼠在體結(jié)扎冠狀動脈左前降支(LAD)建立梗死模型,6周后開胸取心,以K-H緩沖液離體灌注,全心缺血30 min后復(fù)灌60 min建立缺血-再灌注損傷模型。七氟醚缺血后處理組的心臟在缺血后復(fù)灌最初15 min以3%七氟醚飽和的K-H緩沖液灌注。為評價PKB/Akt及ERK 1／2在七氟醚缺血后處理中的作用,分別單獨(dú)給予或與七氟醚同時給予兩激酶的特異性抑制劑LY294002 (15μM)及PD98059 (20μM)。比較各組間血流動力學(xué)、心肌梗死面積、冠脈流出液中LDH及CK-MB水平。以Western blotting測定復(fù)灌15 min時PKB/Akt及ERK 1/2的磷酸化情況。測定心肌中NAD+含量以反映mPTP的開放情況。 3、健康成年大鼠離體心臟經(jīng)緩沖液平衡期灌注10 min后,隨機(jī)分為4組：對照(CTRL)組：繼續(xù)灌注25 min后,行30 min全心缺血,后復(fù)灌120 min,實(shí)驗(yàn)過程中未給予其它藥物干預(yù)；七氟醚缺血預(yù)處理(SpreC)組：缺血前,給予3%七氟醚15 min后洗出10 min行預(yù)處理；七氟醚缺血后處理(SpostC)組：缺血后復(fù)灌最初15 min給予3%七氟醚行后處理；七氟醚缺血預(yù)處理聯(lián)合七氟醚缺血后處理(SpreC+SpostC)組：聯(lián)合使用SpreC和SpostC組的實(shí)驗(yàn)方案。比較組間相同時點(diǎn)及組內(nèi)不同時點(diǎn)間的血流動力學(xué)指標(biāo)。實(shí)驗(yàn)結(jié)束后,用TTC染色法比較組間心肌梗死面積。測定平衡期及復(fù)灌120 min時冠脈流出液中的LDH和CK-MB作為心肌損傷指標(biāo)。蛋白印跡法(WB)觀察PKB/Akt和ERK 1/2在實(shí)驗(yàn)中不同時點(diǎn)的動態(tài)變化趨勢。通過測定復(fù)灌15 min心肌NAD+含量以反映mPTP的開放程度。此外,復(fù)灌120 min時左室心肌取材行全基因芯片表達(dá)譜分析。 4、計(jì)算機(jī)檢索Pubmed、EMBASE等國外文獻(xiàn)數(shù)據(jù)庫及中國生物醫(yī)學(xué)文獻(xiàn)數(shù)據(jù)庫、中國期刊網(wǎng)等中文數(shù)據(jù)庫,并配合手工檢索所有文獻(xiàn)全文,由兩位作者分別進(jìn)行有關(guān)資料的提取,主要包括患者一般情況、手術(shù)情況及體外循環(huán)后心排指數(shù)(CI)、術(shù)后肌鈣蛋白Ⅰ水平(cTnI)、術(shù)后機(jī)械通氣時間、正性肌力藥物支持等指標(biāo)參數(shù)、ICU和住院時間、死亡率、心肌梗死、心肌缺血和心房纖顫發(fā)生率等終點(diǎn)事件,隨后用RevMan 5.0進(jìn)行薈萃分析。 結(jié)果： 1、與ISCH組相比,復(fù)灌之初給予3%七氟醚可顯著改善心功能(增加左室發(fā)展壓力、左室最大收縮／舒張速率、冠脈流量、心率,并降低左室舒張末期壓力)、降低心肌梗死面積及減少LDH及CK-MB釋放(P0.05)。七氟醚的心肌保護(hù)作用同樣表現(xiàn)在降低缺血-再灌注損傷后心肌的MDA含量(P0.05)。然而,給予NAC或PD98059不僅可消除上述保護(hù)作用,而且可以抑制七氟醚增強(qiáng)ERK 1/2磷酸化及抑制mPTP開放的保護(hù)作用(P0.05)。 2、與缺血-再灌注損傷組相比,復(fù)灌之初給予3%七氟醚可顯著改善心功能(增加左室發(fā)展壓力、左室最大收縮／舒張速率、冠脈流量、心率、并降低左室舒張末期壓力)、降低心肌梗死面積及減少LDH及CK-MB釋放(P0.05)。然而,給予LY或PD分別抑制PKB/Akt或ERK 1/2磷酸化后可消除上述保護(hù)作用(P0.05),而且導(dǎo)致心肌NAD+含量降低(P0.05)。 3、與CTRL組相比,七氟醚處理(SpreC、SpostC及SpreC+SpostC)的3組心臟缺血-再灌注損傷后心功能改善(表現(xiàn)為LVDP、+dp/dt、-dp/dt、CF和HR的升高及LVEDP的降低)、梗死面積降低、LDH和CK-MB釋放減少(P0.05)。就上述指標(biāo)在3個七氟醚處理組間行組內(nèi)比較可見：SpreC+SpostC的保護(hù)效果最佳(P0.05),而SpreC和SpostC間比較差異無統(tǒng)計(jì)學(xué)意義(P0.05)。WB分析顯示,CTRL組心臟缺血-再灌注后PKB/Akt和ERK-1/2的磷酸化程度較平衡期增強(qiáng)(P0.05)；SpreC和SpreC+SpostC組心臟均出現(xiàn)雙時相的PKB/Akt和ERK-1/2的磷酸化增強(qiáng)(分別出現(xiàn)在預(yù)處理和后處理后)；與此不同的是SpostC組僅出現(xiàn)單時相的PKB/Akt和ERK-1/2磷酸化增強(qiáng)(后處理后)。組間比較：SpreC+SpostC組中先后施行的SpreC和SpostC對PKB/Akt及ERK-1/2的磷酸化增強(qiáng)作用在復(fù)灌15 min和120 min出現(xiàn)累加。CTRL組復(fù)灌15 min時心肌NAD+含量最低(P0.05),SpreC+SpostC組最高(P0.05),提示SpreC和SpostC抑制mPTP開放的作用也可累加。以Agilent大鼠全基因表譜芯片對3種七氟醚缺血處理方式后的心肌和未經(jīng)處理的缺血-再灌注損傷心肌進(jìn)行基因差異表達(dá)分析,僅有少數(shù)基因同時受SpreC、SpostC和SpreC+SpostC同向調(diào)節(jié)。 4、薈萃分析共納入13項(xiàng)前瞻性隨機(jī)對照研究(RCT),包括696例患者,其中七氟醚組402人,異丙酚組294人。結(jié)果顯示：兩組患者術(shù)后機(jī)械通氣時間、正性肌力藥物支持、死亡率、心梗和房顫發(fā)生率等方面的差異均無統(tǒng)計(jì)學(xué)意義(P0.05)。與異丙酚組相比,七氟醚組患者體外循環(huán)后CI增高(P=0.003),術(shù)后cTnI降低(P0.00001),術(shù)后心肌缺血發(fā)生率降低(P=0.02),ICU和住院時間縮短(P=0.24和P=0.21)。 結(jié)論： 1、3%七氟醚缺血后處理通過ROS-ERK 1/2-mPTP信號通路可為健康大鼠離體心臟的缺血-再灌注損傷提供保護(hù)。 2、3%七氟醚缺血后處理通過激活PI3K-PKB/Akt及MEK 1/2-ERK 1/2途徑,并抑制mPTP開放,從而為慢性梗死大鼠離體心臟的缺血-再灌注損傷提供保護(hù)。 3、3%的SpreC和SpostC對離體心臟的心肌缺血-再灌注損傷的保護(hù)效果相當(dāng),主要表現(xiàn)在改善心功能、降低梗死面積、減少心肌損傷、促進(jìn)保護(hù)性激酶活化及抑制mPTP開放。聯(lián)合應(yīng)用SpreC和SpostC則能夠提供額外的心肌保護(hù)效果。三種七氟醚缺血處理后心肌基因表達(dá)譜的差異懸殊。 4、現(xiàn)有證據(jù)表明,對行冠脈搭橋手術(shù)的患者而言,七氟醚較異丙酚顯示了更好的心肌保護(hù)效果。
[Abstract]:Objective:
1, to observe the protective effect of sevoflurane ischemic postconditioning on ischemic reperfusion injury in healthy adult rats, and to study the possible role of reactive oxygen species (ROS), extracellular signal regulated kinase (ERK1/2) and mitochondrial permeability transition pore (mPTP).
2, to observe the protective effect of sevoflurane ischemic postconditioning on myocardial ischemia reperfusion injury in rats with chronic myocardial infarction, and to study the possible role of protein kinase B (PKB/Akt), extracellular signal regulated kinase (ERK 1/2) and mitochondrial permeability transition pore (mPTP).
3, compared with sevoflurane ischemic preconditioning, sevoflurane ischemic postconditioning and sevoflurane ischemic preconditioning combined with sevoflurane ischemic postconditioning, the protective effect and mechanism of 3 ways of ischemic reperfusion injury in healthy adult rat heart were compared.
4, systematic review and meta analysis of sevoflurane and propofol for myocardial protection in patients undergoing coronary artery bypass grafting.
Method:
1, rat heart was perfused in vitro, perfusion of K-H buffer, and reperfusion injury model of reperfusion 60 min after 30 min of heart ischemia. After ischemia, the heart of sevoflurane ischemic reperfusion was initially 15 min with 3% sevoflurane saturated K-H buffer. They were given individually or in conjunction with sevoflurane, NAC (4mM) or ERK 1/2 blocking with sevoflurane. PD98059 (20 mu M) was used to evaluate the role of ROS and ERK 1/2 in the post-treatment of sevoflurane ischemia. The hemodynamics, myocardial infarction area, lactate dehydrogenase (LDH) and creatine muscle enzyme -MB (CK-MB) in the coronary effluent were compared between each group. Meanwhile, the content of MDA (MDA) in the 30 min reperfusion 60 min in each group was measured to reflect the oxidative stress. The degree of phosphorylation of ERK 1 / 2 was measured by.Western blotting, and the content of nicotinamide adenine dinucleotide (NAD+) was measured to reflect the opening of mPTP.
2, the rat model was established by ligation of the left anterior descending branch of the coronary artery (LAD). After 6 weeks, the heart was taken out of the chest and perfused in vitro with K-H buffer. The ischemia reperfusion injury model was established after 30 min of the whole heart ischemia. The heart of the sevoflurane ischemic post treatment group was perfused with the K-H buffer saturated with 3% sevoflurane at the beginning of ischemia reperfusion after ischemia. The role of PKB/Akt and ERK 1 / 2 in the post-treatment of sevoflurane ischemia was given separately or with the specific inhibitor LY294002 (15 M) and PD98059 (20 micron M) given to the two kinase of sevoflurane respectively. The hemodynamics, myocardial infarction area, and the level of LDH and CK-MB in the coronary outflow fluid were compared between each group. The Western blotting was used for the determination of 15 min P. The phosphorylation of KB/Akt and ERK 1/2 was measured. The NAD+ content in myocardium was measured to reflect the opening of mPTP.
3, after perfusion of 10 min in the balance period of the isolated heart of healthy adult rats, they were randomly divided into 4 groups: control (CTRL) group: after continuous perfusion of 25 min, 30 min whole heart ischemia, and then reperfusion 120 min, no other drug intervention was given, sevoflurane ischemic preconditioning (SpreC) group: before ischemia, 3% sevoflurane 15 min were given after 15 min to wash 10 min Preconditioning, sevoflurane ischemic postconditioning (SpostC) group: 3% sevoflurane was given at the first 15 min after ischemia, and sevoflurane ischemic preconditioning combined with sevoflurane ischemic postconditioning (SpreC+SpostC) group: the combined use of SpreC and SpostC groups. Index. After the experiment, TTC staining was used to compare the area of myocardial infarction. LDH and CK-MB in the flow of coronary flow were measured at the balance stage and 120 min as the index of myocardial injury. The dynamic change trend of the difference of PKB/Akt and ERK 1/2 in the experiment was observed by the Western blot (WB). The content of NAD+ in the 15 min myocardium was measured to reflect the mP. In addition, the gene expression profiles of left ventricular myocardium were analyzed at 120 min after reperfusion for TP.
4, the computer retrieves foreign literature databases such as Pubmed, EMBASE, Chinese biomedical literature database, Chinese Journal Network and other Chinese databases, and with manual retrieval of the full text of all the documents. The related data are extracted by two authors respectively, including the general situation of the patients, the operation situation and the cardiac exclusion index after cardiopulmonary bypass (CI), after the operation. Cardiac troponin I level (cTnI), postoperative mechanical ventilation time, positive inotropic drug support and other index parameters, ICU and time of hospitalization, mortality, myocardial infarction, myocardial ischemia and atrial fibrillation, were followed by a meta-analysis of RevMan 5.
Result:
1, compared with the ISCH group, 3% sevoflurane at the beginning of reinjection could significantly improve cardiac function (increased left ventricular development pressure, maximum left ventricular systolic / diastolic velocity, coronary flow rate, heart rate, and lower left ventricular end diastolic pressure), lower myocardial infarction area and reduction of LDH and CK-MB release (P0.05). The myocardial protection of sevoflurane also showed a decrease in deficiency. MDA content (P0.05) of myocardium after blood reperfusion injury. However, giving NAC or PD98059 not only eliminates the above protective effect, but also inhibits the protective effect of sevoflurane enhanced ERK 1/2 phosphorylation and inhibition of mPTP opening (P0.05).
2, compared with the ischemia-reperfusion injury group, 3% sevoflurane at the early stage of reperfusion could significantly improve cardiac function (increased left ventricular development pressure, left ventricular maximum contraction / diastolic velocity, coronary flow rate, heart rate, and lower left ventricular end diastolic pressure), reduced infarct size and reduced LDH and CK-MB release (P0.05). However, LY or PD was given to inhibit PKB/, respectively. After Akt or ERK 1/2 phosphorylation, the protective effect (P0.05) was eliminated, and the NAD+ content of myocardium decreased (P0.05).
3, compared with group CTRL, 3 groups of sevoflurane treated (SpreC, SpostC, and SpreC+SpostC) improved cardiac function after ischemia reperfusion injury (LVDP, +dp/dt, -dp/dt, CF and HR increase and LVEDP decrease), infarct size, LDH and CK-MB release decreased. The above indicators were compared in the group of 3 sevoflurane treatment groups: The protective effect of reC+SpostC was the best (P0.05), while the difference between SpreC and SpostC was not statistically significant (P0.05).WB analysis showed that the degree of phosphorylation of PKB/Akt and ERK-1/2 after ischemia and reperfusion in the CTRL group was stronger than that in the equilibrium phase (P0.05), and both SpreC and SpreC+SpostC groups had a dual phase and phosphorylation enhancement (respectively). The difference was that the PKB/Akt and ERK-1/2 phosphorylation enhanced (after treatment) in the SpostC group only. Comparison between groups: the enhancement of the phosphorylation of PKB/Akt and ERK-1/2 by SpreC and SpostC in the SpreC+SpostC group was 15 min and 120 min in the complex irrigation of 15 min. The NAD+ content of myocardium was the lowest (P0.05) and the highest (P0.05) in group SpreC+SpostC (P0.05), suggesting that the effect of SpreC and SpostC on the inhibition of mPTP opening could also be accumulative. Gene differential expression analysis of myocardial and untreated ischemia reperfusion injury after 3 sevoflurane ischemic treatment was carried out with a small number of genes. At the same time, SpreC, SpostC and SpreC+SpostC are regulated in the same direction.
4, the meta-analysis was included in 13 prospective randomized controlled studies (RCT), including 696 patients, of which 402 were sevoflurane and 294 in the propofol group. The results showed that there were no significant differences in mechanical ventilation time, positive inotropic drug support, mortality, myocardial infarction and atrial fibrillation in the two groups (P0.05). Compared with the patients in the sevoflurane group, the CI increased (P=0.003) after cardiopulmonary bypass, and the postoperative cTnI decreased (P0.00001), the incidence of myocardial ischemia was reduced (P=0.02), and the time of ICU and hospitalization were shortened (P=0.24 and P=0.21).
Conclusion:
1,3% sevoflurane ischemic postconditioning can protect the isolated rat heart from ischemia-reperfusion injury through ROS-ERK 1/2-mPTP signaling pathway.
2,3% sevoflurane is treated by ischemic postconditioning by activating PI3K-PKB/Akt and MEK 1/2-ERK 1/2 pathway and inhibiting the opening of mPTP, thus providing protection for ischemic reperfusion injury in the isolated heart of chronic infarcted rats.
The protective effect of 3,3%'s SpreC and SpostC on myocardial ischemia and reperfusion injury in isolated heart is similar, mainly in improving cardiac function, reducing infarct size, reducing myocardial damage, promoting protective kinase activation and inhibiting the opening of mPTP. Combined use of SpreC and SpostC can provide additional myocardial protection effect. Three kinds of sevoflurane ischemic place There is a great difference in the gene expression profiles of the posterior myocardium.
4, available evidence shows that sevoflurane is better than propofol for coronary protection in patients undergoing coronary artery bypass grafting.
【學(xué)位授予單位】：中國協(xié)和醫(yī)科大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2010
【分類號】：R363

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