【摘要】：休克是一個(gè)復(fù)雜的病理過程，根據(jù)其嚴(yán)重程度分為可逆性休克和不可逆性休克(重癥難治性休克)。重癥休克的發(fā)生是眾多創(chuàng)傷及感染性疾病發(fā)展的共同歸宿，是導(dǎo)致病人死亡率居高不下的直接原由。當(dāng)進(jìn)入重癥難治性階段，微血管對(duì)升壓藥物反應(yīng)性喪失致使休克病人出現(xiàn)頑固性低血壓，并對(duì)所有的治療措施均處于無反應(yīng)狀態(tài)。因此，解決微血管的低反應(yīng)性問題是治愈休克的關(guān)鍵。 近期的實(shí)驗(yàn)證明，失血性休克2小時(shí)后，血管平滑肌鉀通道(BK_(Ca)和K_(ATP))大量開放，電流增加，細(xì)胞內(nèi)鈣依賴性發(fā)生變化，導(dǎo)致細(xì)動(dòng)脈平滑肌細(xì)胞(arteriolar smooth muscle cells，ASMC)發(fā)生超極化。鈣通道、鈣釋放通道、鈉通道的抑制，鉀通道活動(dòng)的增強(qiáng)均可導(dǎo)致細(xì)胞膜超極化。其中，L型鈣通道(L-type calcium channels，L-Ca)調(diào)節(jié)大部分可興奮性和非興奮性細(xì)胞的活動(dòng)，是細(xì)胞膜外鈣離子的內(nèi)流的主要途徑。本室的工作證明，休克時(shí)ASMCs超極化。給予升壓藥物(NE)刺激后，細(xì)胞內(nèi)鈣離子濃度升高僅為正常時(shí)的50％，而且主要是外鈣的內(nèi)流受到抑制。所以我們推測(cè)在休克后期，，細(xì)胞膜的超極化抑制了ASMCs上的L-Ca通道，但沒有直接測(cè)定過此通道的變化。本課題采用膜片鉗與熒光探針技術(shù)研究休克后期平滑肌細(xì)胞L-Ca的變化及其與血管平滑肌反應(yīng)性下降的關(guān)系，用實(shí)驗(yàn)證明以上推測(cè)，為休克的臨床治療提供進(jìn)一步的理論依據(jù)。
[Abstract]:Shock is a complicated pathological process, which can be divided into reversible shock and irreversible shock according to its severity. The occurrence of severe shock is the common destination for the development of many trauma and infectious diseases and the direct cause of high mortality. When the severe refractory phase was reached, the loss of microvascular reactivity to pressor drugs caused intractable hypotension in shock patients, and no response to all treatment measures was observed. Therefore, to solve the problem of microvascular hyporesponsiveness is the key to cure shock. Recent experiments have shown that after hemorrhagic shock for 2 hours, the potassium channels (BK_ (Ca) and K _ (ATP) of vascular smooth muscle were opened, the current increased, and the intracellular calcium dependence changed, which resulted in (arteriolar smooth muscle cells, of arteriolar smooth muscle cells. ASMC) hyperpolarization. The inhibition of calcium channel, calcium release channel, sodium channel and enhancement of potassium channel activity can lead to cell membrane hyperpolarization. L-type calcium channel (L-type calcium channels,L-Ca) regulates the activity of most excitable and non-excitatory cells and is the main pathway of extracellular calcium influx. Our work proves that ASMCs hyperpolarization occurs during shock. After (NE) stimulation, the increase of intracellular calcium concentration was only 50% of the normal level, and the inward flow of extracellular calcium was inhibited. So we speculated that in the late stage of shock, the hyperpolarization of cell membrane inhibited the L-Ca channel on ASMCs, but we did not measure the change of this channel directly. In this study, patch clamp and fluorescence probe technique were used to study the changes of L-Ca in smooth muscle cells and its relationship with vascular smooth muscle reactivity in the late stage of shock. To provide further theoretical basis for the clinical treatment of shock.
【學(xué)位授予單位】：第一軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2006
【分類號(hào)】：R363

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本文編號(hào)：2354608