本文關(guān)鍵詞： α7nAChR 擠壓綜合征 山莨菪堿 高K+血癥 雌二醇 胰島素敏感性　出處：《第二軍醫(yī)大學(xué)》2017年博士論文　論文類型：學(xué)位論文

【摘要】：研究目的擠壓傷指的是軀干或四肢受到擠壓,導(dǎo)致被擠壓部位肌肉腫脹和/或神經(jīng)功能失常。擠壓傷多發(fā)生于地震、車禍等。擠壓綜合癥則是指當(dāng)擠壓時(shí)間過長,被擠壓部位肌肉大量壞死,當(dāng)解除擠壓后,大量的細(xì)胞內(nèi)物質(zhì)從壞死肌肉釋放入血,導(dǎo)致代謝性酸中毒、高血K~+癥、以及其他代謝性紊亂。同時(shí)壞死的肌肉組織吸收大量的水分,導(dǎo)致水鈉在局部潴留,從而引發(fā)低血容量性休克。擠壓綜合癥患者如果不及時(shí)治療,后期會(huì)出現(xiàn)腎衰竭。大地震時(shí),擠壓綜合征的發(fā)生率約為2~15%,是除了外傷以外導(dǎo)致死亡最主要的原因。高達(dá)20%的擠壓綜合癥患者死因是高血K~+癥引起的心律失�；蛘叩脱萘啃孕菘恕５且�?yàn)樵呵皵D壓綜合征的診斷比較難,臨床缺乏降低擠壓綜合征患者早期死亡安全有效的藥物。山莨菪堿是一種傳統(tǒng)的抗休克藥物,可以提高血液的微循環(huán),臨床上多用于治療伴有血流障礙性的疾病,比如膿毒性休克和彌散性血管內(nèi)凝血障礙。我們既往的研究發(fā)現(xiàn)山莨菪堿的抗休克作用主要是通過作用于M受體,使乙酰膽堿更多的和α7nAChR相結(jié)合,提高血壓而不改變心率,從而發(fā)揮抗炎抗休克作用。胰島素在臨床上和葡萄糖合用,可以通過激活Na+/K~+-ATPase促進(jìn)血K~+進(jìn)入細(xì)胞而降低血K~+濃度。有研究報(bào)道N受體激動(dòng)劑尼古丁可以激活α7nAChR進(jìn)而提高胰島素的敏感性,那么山莨菪堿能否通過α7nAChR的激活用于擠壓綜合征的預(yù)防給藥或者治療呢?另外文獻(xiàn)報(bào)道擠壓傷發(fā)生時(shí),高K~+血癥主要見于成年男性,而E_2可以降低血清K~+濃度。E_2可以通過作用于胰島素信號(hào)通路提高心肌細(xì)胞Na~+/K~+-ATPase的表達(dá)和活性。但是,擠壓綜合征中E_2和高K~+血癥,E_2和胰島素敏感性的關(guān)系未見報(bào)道。本實(shí)驗(yàn)的目的在于通過一系列的實(shí)驗(yàn)探索:1、α7nAChR激活對(duì)擠壓綜合征死亡率的影響及其機(jī)制研究;2、E_2在α7nAChR激活對(duì)擠壓綜合征的預(yù)防作用中扮演的角色。研究方法1、山莨菪堿對(duì)擠壓綜合征大鼠死亡率及血生化和電解質(zhì)指標(biāo)的影響用SD大鼠制做擠壓綜合征模型。正常組:生理鹽水;對(duì)照組:擠壓+生理鹽水;預(yù)防給藥組:解除擠壓前30min給予山莨菪堿;治療給藥組:解除擠壓后1h給予山莨菪堿。解除擠壓后觀察SD大鼠24h死亡率。另外造模,解除擠壓后6h眶靜脈叢取血,靜置、離心得到血清,檢測(cè)血清K~+、Na~+、Cl~-、Scr、CK、CK-MB和BUN水平。2、山莨菪堿對(duì)擠壓綜合征大鼠胰島素敏感性的影響用SD大鼠制做擠壓綜合征模型。正常組:生理鹽水;對(duì)照組:擠壓+生理鹽水;預(yù)防給藥組:解除擠壓前30min給予山莨菪堿。解除擠壓后6h眶靜脈叢取血,靜置、離心得到血清,檢測(cè)血清胰島素和葡萄糖水平。3、α7nAChR參與了山莨菪堿對(duì)擠壓綜合征死亡率、血清K~+和胰島素敏感性的作用工具藥:α7nAChR激動(dòng)劑PUN和抑制劑MLA。用C57BL/6小鼠制做擠壓綜合征模型。對(duì)照組:造擠壓綜合征模型并給予等量的生理鹽水;預(yù)防給藥組:解除擠壓前30min給予山莨菪堿。MLA組:解除擠壓前30min給予MLA;山莨菪堿+MLA:解除擠壓前1h給予MLA,解除擠壓前30min給予山莨菪堿;PUN組:解除擠壓前30min給予PUN。解除擠壓后觀察C57BL/624h死亡情況。另外同樣的五組,解除擠壓后6h取血,靜置、離心得到血清,檢測(cè)血清K~+,胰島素和葡萄糖水平。同時(shí)檢測(cè)正常小鼠血清K~+,胰島素和葡萄糖水平。4、用α7nAChR-/-小鼠驗(yàn)證α7nAChR參與了山莨菪堿對(duì)擠壓綜合征死亡率、血清K~+和胰島素敏感性的作用用α7nAChR+/+和α7nAChR-/-小鼠制做擠壓綜合征模型。野生型和純合子各分為兩組,對(duì)照組:造擠壓綜合征模型并給予等量的生理鹽水;預(yù)防給藥組:解除擠壓前30min給予山莨菪堿。解除擠壓后6h取血,靜置、離心得到血清,檢測(cè)血清K~+,胰島素和葡萄糖水平。另外同樣的四組,解除擠壓后觀察24h死亡情況。5、山莨菪堿對(duì)高K~+血癥大鼠死亡率和血清K~+的作用對(duì)照組:生理鹽水,30min后給予KCl;實(shí)驗(yàn)組:給予山莨菪堿,30min后給予同樣的KCl。30min后取血,檢測(cè)血清K~+濃度。同樣的另外兩組觀察24h死亡情況。6、α7nAChR參與了山莨菪堿對(duì)細(xì)胞外高K~+的作用成肌細(xì)胞分成五組:山莨菪堿組,乙酰膽堿組,山莨菪堿+乙酰膽堿組,尼古丁組和PUN組。在細(xì)胞培養(yǎng)基中加入外源性K~+造高K~+模型。給藥時(shí)間在加入K~+之前30min。K~+加入6h后取培養(yǎng)基檢測(cè)K~+和葡萄糖濃度。同樣的用n受體抑制劑Mec和除α7nAChR以外的N受體阻斷劑hex探究α7nAChR的作用。7、胰島素信號(hào)通路介導(dǎo)山莨菪堿降低細(xì)胞外高K~+的作用HNMPA-(AM)3:胰島素受體抑制劑。C2C12骨骼肌成纖維細(xì)胞分成五組:正常組,對(duì)照組,山莨菪堿+乙酰膽堿,HNMPA-(AM)3和山莨菪堿+乙酰膽堿+HNMPA-(AM)3組。免疫熒光檢測(cè)HNMPA-(AM)3對(duì)Na~+/K~+-ATPase在細(xì)胞膜表面分布的影響。使用胰島素受體抑制劑HNMPA-(AM)3、mTOR抑制劑雷帕霉素、pi3k抑制劑LY294002、轉(zhuǎn)錄活化因子Stat3抑制劑Stattic和Na~+/K~+-ATPase抑制劑哇巴因探究胰島素/Na~+/K~+-ATPase通路對(duì)細(xì)胞外高K~+的作用。8、擠壓綜合征死亡率、雌激素、胰島素敏感性和血清K~+的性別差異雌雄小鼠各半造擠壓綜合征模型,觀察24h小鼠死亡情況。另外造模,解除擠壓后6h取血,測(cè)量雌雄小鼠E_2、血清K~+、胰島素和葡萄糖水平。9、α7nAChR的激活對(duì)擠壓綜合征小鼠血清K~+和E_2的影響工具藥:α7nAChR抑制劑MLA。用C57BL/6小鼠制做擠壓綜合征模型。對(duì)照組:造擠壓綜合征模型并給予等量的生理鹽水;預(yù)防給藥組:解除擠壓前30min給予山莨菪堿。MLA組:解除擠壓前30min給予MLA;山莨菪堿+MLA:解除擠壓前1h給予MLA,解除擠壓前30min給予山莨菪堿。解除擠壓后6h取血,靜置、離心得到血清,檢測(cè)血清K~+濃度、胰島素和葡萄糖水平。同時(shí)檢測(cè)正常小鼠血清K~+濃度、胰島素和葡萄糖水平。10、卵巢摘除術(shù)對(duì)擠壓綜合征小鼠血清K~+、E_2和胰島素敏感性的影響假手術(shù)組和手術(shù)組各分成四組:正常組、擠壓組、山莨菪堿組和E_2組。后三組均擠壓。取血,檢測(cè)血清K~+和E_2水平。另外假手術(shù)組和手術(shù)組各再造模分組:擠壓組、山莨菪堿組和E_2組。11、E_2對(duì)擠壓綜合征小鼠死亡率的影響假手術(shù)組和手術(shù)組各再造模分組:擠壓組、山莨菪堿組和E_2組。監(jiān)測(cè)解除擠壓后24h死亡情況。12、探究山莨菪堿對(duì)擠壓綜合征大鼠血壓的影響以及α7nAChR在其中發(fā)揮的作用SD大鼠分成五組:正常組、對(duì)照組、MLA組、山莨菪堿組和MLA+山莨菪堿組。后四組接受擠壓。解除擠壓前,各組先測(cè)量一段大鼠血壓和心率,解除擠壓后持續(xù)監(jiān)測(cè)3.5h再停止測(cè)量。記錄分析。實(shí)驗(yàn)結(jié)果1、和不給藥組相比,解除擠壓前30min和解除擠壓后1h給予山莨菪堿可以顯著降低擠壓綜合征大鼠24h死亡率以及擠壓綜合征大鼠血清K~+、scr、ck、ck-mb和bun水平2、和不給藥組相比,給予山莨菪堿可以提高擠壓綜合征大鼠胰島素敏感性。3、山莨菪堿降低擠壓綜合征小鼠24 h死亡率的作用可以被α7nAChR抑制劑MLA阻斷。而α7nAChR激動(dòng)劑PNU可以顯著降低擠壓綜合征小鼠24 h死亡率。PNU提高擠壓綜合征小鼠胰島素敏感性,MLA降低擠壓綜合征小鼠胰島素敏感性。4、山莨菪堿可以降低野生型擠壓綜合征小鼠24 h死亡率,但是對(duì)純合子擠壓綜合征小鼠24 h死亡率沒有顯著作用。5、山莨菪堿預(yù)防給藥可以通過降低血K~+降低高血K~+癥大鼠死亡率。6山莨菪堿單用、山莨菪堿和乙酰膽堿合用均可降低細(xì)胞外高K~+和葡萄糖濃度。山莨菪堿和乙酰膽堿合用比山莨菪堿單用效果更明顯。Mec和MLA可以阻斷這一作用。尼古丁和PNU單用均可以降低細(xì)胞外高K~+和葡萄糖濃度。7、山莨菪堿+乙酰膽堿使更多的Na+/K~+-ATPase磷酸化,而胰島素受體抑制劑HNMPA-(AM)3可以阻斷這一作用。HNMPA-(AM)3、雷帕霉素、LY294002、Stattic和哇巴因可阻斷山莨菪堿和乙酰膽堿降低細(xì)胞外高K~+的作用。8、擠壓綜合征雌性小鼠和雄性小鼠死亡率差異無統(tǒng)計(jì)學(xué)意義,但是擠壓以后雌性小鼠血清K~+低于雄性小鼠,E_2水平高于雄性小鼠,胰島素敏感性高于雄性小鼠。9、α7nACh R的激活可以降低擠壓綜合征小鼠血清K~+濃度及提高血清E_2的濃度。10、卵巢摘除術(shù)可以提高擠壓綜合征小鼠血清K~+濃度,降低胰島素敏感性,降低血清E_2濃度。11、E_2可以降低擠壓綜合征小鼠死亡率。12、山莨菪堿升高擠壓綜合征大鼠血壓,MLA可以阻斷山莨菪山莨菪堿的這一作用。山莨菪堿對(duì)擠壓綜合征大鼠心率沒有影響。研究結(jié)論:α7nAChR的激活可以降低擠壓綜合癥早期死亡率,這種作用部分是通過胰島素/Na+/K~+-ATPase信號(hào)通路介導(dǎo)的血K~+降低來實(shí)現(xiàn)的,并且雌激素在其中發(fā)揮重要作用;部分作用可能是通過升高血壓來實(shí)現(xiàn)的。激活α7nAChR的藥物(如山莨菪堿)以及E_2,有望成為降低擠壓綜合癥早期死亡率的有效藥物。
[Abstract]:The purpose of the study is to crush injury refers to the trunk or limbs caused by extrusion, extrusion parts of muscle swelling and / or nerve dysfunction. Crush injuries occurred in earthquake accident. Crush syndrome refers to when the extrusion time is too long, crushed muscle necrosis, when lifting pressure, a lot of material within the cell release from necrotic muscle into the blood, leading to metabolic acidosis, high blood K~+ disease and other metabolic disorders. At the same time, necrosis of muscle tissue to absorb a large amount of water, resulting in the local water and sodium retention, causing hypovolemic shock. Crush syndrome patients without treatment, the latter will appear kidney failure. Earthquake, crush syndrome incidence is about 2~15%, in addition to outside trauma resulting in the death of the main reasons. The causes of death in patients with crush syndrome is high up to 20% K~+ blood diseases caused by arrhythmia or low blood volume Shock. But because the pre hospital diagnosis of crush syndrome is difficult, lack of clinical lower crush syndrome early death in patients with safe and effective drugs. Anisodamine is a traditional anti shock drug can improve the blood microcirculation, clinical for the treatment of many diseases associated with blood disorders, such as septic shock and diffusion intravascular coagulation disorders. Our previous studies found that anisodamine anti shock function is mainly mediated by M receptors, make more acetylcholine and alpha 7nAChR combined with the increase in blood pressure without changing heart rate, so as to exert anti-inflammatory anti shock effects. Insulin in clinical and can reduce blood glucose, the concentration of K~+ by the activation of Na+/K~+-ATPase promotes blood K~+ into cells. Studies have reported that N receptor agonist nicotine can activate alpha 7nAChR and improve insulin sensitivity, so anisodustanguticus Alkali can through the activation of alpha 7nAChR for prevention of crush syndrome to medicine or treatment? Also reported crush injury occurs, high K~+ hyperlipidemia mainly in adult males, while E_2 can reduce the concentration of serum K~+.E_2 can act on the insulin signaling pathway to improve the expression and activity of Na~+/K~+-ATPase in myocardial cell. However, E_2 and high K~+ hyperlipidemia crush syndrome, E_2 and insulin sensitivity is not reported. The purpose of this experiment is that through a series of experiments: 1, alpha 7nAChR activation effect on mortality of crush syndrome and its mechanism study; 2, E_2 in alpha 7nAChR activation on play preventive effect of crush syndrome in the role. Study on the 1 methods, the model effect of anisodamine on crush syndrome rat mortality and blood biochemical and electrolyte index for SD rats made of crush syndrome. Normal group: saline control group: Extrusion + saline; preventive treatment group: treated with Anisodamine before pressure release 30min; treatment group: treated with Anisodamine 1h after pressure release. Release of SD rats was observed. In addition, the mortality of 24h after extrusion molding, extrusion after release 6h orbital venous plexus blood, static, centrifuged to obtain serum detection serum K~+, Na~+, Cl~-, Scr, CK, CK-MB and BUN level of.2, the protective effects of anisodamine on insulin sensitivity in rats with crush syndrome with SD rat model made of crush syndrome. Normal group: normal saline; control group: extrusion + saline; preventive treatment group: in addition to 30min prior to extrusion solution anisodamine. Lift after extrusion 6h orbital venous plexus blood, static, centrifuged to obtain serum, serum glucose and insulin levels of.3 alpha, 7nAChR in anisodamine on mortality of crush syndrome, serum K~+ and function of insulin sensitivity: 7nAChR alpha agonist and inhibitor PUN Model C57BL/6 mice made MLA. crush syndrome. Control group: saline made crush syndrome model and given the same amount; drug prevention group: 30min before pressure release anisodamine group.MLA: remove extrusion 30min prior to MLA; anisodamine +MLA: pressure release 1H prior to MLA, 30min treated with Anisodamine before pressure release; group PUN: pressure release given before 30min PUN. released C57BL/624h observation of death after extrusion. In the same five groups, 6h after blood pressure release, static, centrifuged to obtain serum, serum K~+, insulin and glucose levels. At the same time detection of normal mice serum K~+, insulin and glucose levels of.4 alpha 7nAChR-/- mice alpha 7nAChR is involved in the verification of anisodamine on mortality of crush syndrome, model with a 7nAChR+/+ and a 7nAChR-/- mouse made serum K~+ and insulin sensitivity in the role of crush syndrome in wild type and pure. Zygotes were divided into two groups, control group: saline made crush syndrome model and given the same amount; drug prevention group: 30min treated with Anisodamine before pressure release. After 6h blood pressure release, static, centrifuged to obtain serum, serum K~+, insulin and glucose levels. The other four groups of the same lift, after extrusion to observe 24h death.5. The effect of anisodamine on high K~+ hyperlipidemia rat mortality and serum K~+ in control group: normal saline, 30min after administration of KCl; experimental group: treated with anisodamine, 30min after giving the same KCl.30min blood serum K~+ concentrations were detected. The same in two groups 24h the death of.6, alpha 7nAChR in anisodamine on high extracellular K~+ function into muscle cells were divided into five groups: anisodamine group, acetylcholine group, anisodamine + group acetylcholine, nicotine group and PUN group. In the cell culture medium with exogenous K~+ high K + model. Time of administration before joining K~+ 30min.K~+ after joining 6h based detection of K~+ and glucose concentration in culture. The same with the N receptor inhibitor Mec and besides alpha 7nAChR N receptor blocking agent hex.7 explore alpha 7nAChR, insulin signaling pathway mediated by anisodamine reduce the effects of extracellular K~+ (HNMPA- high AM) 3: insulin receptor inhibitor.C2C12 in skeletal muscle fibroblasts were divided into five groups: normal group, control group, anisodamine + acetylcholine, HNMPA- (AM) 3 and anisodamine + +HNMPA- acetylcholine (AM) 3 groups. Immunofluorescence detection of HNMPA- (AM) 3 to Na~+ /K~+-ATPase in influencing the distribution of cell membrane. Insulin receptor inhibitor HNMPA- (AM) 3, mTOR inhibitor rapamycin, PI3K inhibitor LY294002, Stat3 inhibitor and activator of transcription factor Stattic inhibitor Na~+/K~+-ATPase /Na~+/K~+-ATPase on insulin ouabain on high extracellular K~+ The role of.8, crush syndrome mortality, estrogen, male and female mice were sex differences in insulin sensitivity and serum K~+ of crush syndrome model, to observe the 24h model mice death. In addition, 6h after blood pressure release, measurement of male and female mice E_2, serum K~+, insulin and glucose levels.9, activation of alpha 7nAChR drug effects on serum K~+ and E_2 mice of crush syndrome: model C57BL/6 mice produced alpha 7nAChR inhibitor MLA. crush syndrome. Control group: saline made crush syndrome model and given the same amount; drug prevention group: 30min before pressure release anisodamine group.MLA: remove extrusion 30min prior to MLA; anisodamine +MLA: pressure release 1H prior to MLA, 30min treated with Anisodamine before pressure release. After 6h blood pressure release, static, centrifuged to obtain serum, serum K~+ concentration, insulin and glucose levels at the same time. Detection of normal mice serum K~+ concentrations, insulin and glucose levels.10, enucleation on serum K~+ crush syndrome ovary, E_2 and insulin sensitivity of the sham operation group and operation group were divided into four groups: normal group, crush group, anisodamine group and E_2 group. The three groups after extrusion. Blood serum the K~+ and E_2 level detection. In sham operation group and operation group, model group: extrusion reconstruction group, anisodamine group and E_2 group of.11, the effect of E_2 on the mortality of mice with crush syndrome in sham operation group and operation group the model group: reconstruction crush group, anisodamine group and E_2 group. The monitoring release after extrusion 24h the death of.12, SD rats to explore the influence of anisodamine on blood pressure in rats of crush syndrome and alpha 7nAChR in the play is divided into five groups: normal group, control group, MLA group, MLA+ group and anisodamine anisodamine group. The four groups after extrusion. Lift the squeeze The pressure before the first measurement of a rat heart rate and blood pressure, remove stop measuring continuous monitoring of 3.5H extrusion. The experimental results were recorded and analyzed. 1, compared with no drug group, pressure release 30min before and after removal of crush 1H treated with Anisodamine can significantly reduce the mortality of 24h rats with crush syndrome and serum K~+. Crush syndrome rat SCR, CK, CK-MB and BUN levels of 2, compared with no drug group, treated with Anisodamine can improve the insulin sensitivity of.3 rats with crush syndrome, anisodamine reduced mice crush syndrome 24 h mortality effect can be a 7nAChR inhibitor MLA and 7nAChR alpha agonist PNU could significantly to reduce the mortality rate of 24 h mice of crush syndrome.PNU improves insulin sensitivity in mice crush syndrome, MLA syndrome mice reduce extrusion.4 insulin sensitivity, anisodamine can reduce the wild type crush syndrome mice 24 h death Rate, but significant.5 has no effect on mice homozygous crush syndrome 24 h mortality, anisodamine prophylactically can reduce blood K~+ reduce the level of blood K~+ in the rat mortality.6? Anisodamine alone, anisodamine and acetylcholine in combination can reduce the extracellular K~+ and high glucose concentration combined with Anisodamine and acetylcholine. Anisodamine than single effect more obvious.Mec and MLA can block the effect of nicotine. And PNU could both reduce the extracellular K~+ and high glucose concentration.7, anisodamine + acetylcholine phosphorylates Na+/K~+-ATPase more, and insulin receptor (AM) inhibitor HNMPA- 3 can inhibit the effect of.HNMPA- (AM) 3 rapamycin, LY294002, Stattic, and the resulting block wow anisodamine and reduce the effects of acetylcholine.8 high K~+ cells, crush syndrome and mortality in female mice and male mice had no statistical difference Learn the meaning, but after extrusion female mice serum K~+ was lower than that of male mice, E_2 level is higher than that of male mice, insulin sensitivity is higher than that of male mice.9 alpha 7nACh activation of R can reduce the crush syndrome in mice serum K~+ concentration and higher.10 concentration of serum E_2, ovariectomy can increase the serum K~+ concentration of crush syndrome, reduce insulin the sensitivity of serum concentration of E_2.11, E_2 can reduce the mortality of mice.12 crush syndrome, anisodamine increased blood pressure in rats of crush syndrome, MLA can inhibit the action of anisodamine anisodamine. Anisodamine has no effect on heart rate in rats with crush syndrome. Conclusion: alpha activation of 7nAChR can reduce the early mortality of extrusion this syndrome, partly through insulin /Na+/K~+-ATPase signaling mediated by decreased serum K~+ to achieve, and estrogen plays Some important effects may be achieved by increasing the blood pressure. Activation of alpha 7nAChR drugs (such as anisodamine) and E_2 is expected to become an effective drug to reduce the early mortality of crush syndrome.

【學(xué)位授予單位】：第二軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2017
【分類號(hào)】：R96

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