本文選題：人類心室模型　切入點(diǎn)：后除極　出處：《廣西師范大學(xué)》2017年碩士論文

【摘要】：竇房結(jié)是心臟的起博器,它產(chǎn)生的激發(fā)波在心肌組織中以靶波的形式傳播,當(dāng)心肌缺陷導(dǎo)致靶波失穩(wěn)時(shí),靶波可能轉(zhuǎn)變?yōu)楦哳l螺旋波,導(dǎo)致心臟心動(dòng)過(guò)速:如果螺旋波破碎成時(shí)空混沌,這種混沌的電信號(hào)就會(huì)導(dǎo)致心顫發(fā)生,使得心臟不能進(jìn)行正常的收縮與舒張,引起心臟供血障礙,進(jìn)而發(fā)生猝死,因此當(dāng)心臟出現(xiàn)螺旋波和時(shí)空混沌電信號(hào),就需要及時(shí)控制。眾所周知,突然的心臟死亡常常由心臟的心律失常引起,心臟出現(xiàn)螺旋波只是其中一種心律失常,此外心律失常常與后除極化有關(guān),因此心律失常產(chǎn)生的潛在機(jī)制及控制受到科學(xué)家們極大的關(guān)注。在本文中采用人類心室TNNP模型,研究了在二維心臟組織中螺旋波如何導(dǎo)致后除極化,以及如何控制心臟中的螺旋波和時(shí)空混沌。本文的內(nèi)容安排:第一章為綜述部分,在這部分我們主要介紹了兩種反應(yīng)擴(kuò)散系統(tǒng)、幾個(gè)心臟的電生理模型、螺旋波破碎的機(jī)制、螺旋波的控制、心臟老化等。在第二章,我們采用人類心臟模型研究了二維心肌組織中存在螺旋波或其他二維波下后除極化的發(fā)生,通過(guò)改變L型鈣電導(dǎo)和快鉀電導(dǎo)讓螺旋波演化,觀察后除極化在空間的分布。我們發(fā)現(xiàn):(1)在單細(xì)胞和一維不出現(xiàn)后除極化的情況下,螺旋波可導(dǎo)致相Ⅱ型和相Ⅲ型早期后除極化、延遲后除極化、增強(qiáng)的自動(dòng)性以及延時(shí)激發(fā)和延時(shí)增強(qiáng)自動(dòng)性的出現(xiàn);此外還觀察到螺旋波導(dǎo)致膜電位在膜電位Ⅰ期出現(xiàn)弱振蕩;(2)后除極化一般出現(xiàn)在螺旋波波核區(qū)域,它是由螺旋波的相奇異點(diǎn)引起。(3)后除極化也可以分布在更大的范圍,當(dāng)參數(shù)選取適當(dāng)時(shí),出現(xiàn)早期后除極化、延遲后除極化、增強(qiáng)自動(dòng)性的空間點(diǎn)在空間呈螺旋線分布,展示記憶效應(yīng)。(4)當(dāng)激發(fā)細(xì)胞的鈉電流很小時(shí)可誘發(fā)L型鈣電流、鈉鈣交換電流的增大和慢鉀電流、快鉀電流的減少,導(dǎo)致各種后除極化的產(chǎn)生,因此增大鈉電流可有效抑制后除極化的發(fā)生。在第三章,我們?nèi)圆捎萌祟愋呐K模型研究了用晚鈉電流控制二維心臟組織中的螺旋波和時(shí)空混沌,我們提出這樣的控制策略來(lái)產(chǎn)生晚鈉電流:讓慢失活門始終等于0.7,同時(shí)實(shí)時(shí)調(diào)節(jié)鈉電流的快失活門變量的閾值電壓,即先讓閾值電壓經(jīng)過(guò)T1時(shí)間從71.55mV均勻減少到50.55 mV,然后經(jīng)過(guò)T2時(shí)間再?gòu)?0.55 mV均勻增加到71.55 mV,當(dāng)閾值電壓回到71.55 mV,鈉電流的快、慢失活門變量恢復(fù)正常變化。數(shù)值模擬結(jié)果表明:只要適當(dāng)選擇控制時(shí)間,不論心肌細(xì)胞是否存在自發(fā)的晚鈉電流,使用晚鈉電流都可以有效抑制螺旋波和時(shí)空混沌,而且控制產(chǎn)生的晚鈉電流都很小,需要的控制時(shí)間很短,因?yàn)槁菪ê蜁r(shí)空混沌消失主要是通過(guò)傳導(dǎo)障礙消失,此外,還觀察到時(shí)空混沌還有通過(guò)轉(zhuǎn)變?yōu)榘胁ê笙У默F(xiàn)象。第四章是總結(jié)與展望,在本章里我們指出了研究的創(chuàng)新點(diǎn),歸納了得到的重要結(jié)論,指出了今后研究的方向及可能的成果。
[Abstract]:The sinoatrial node is the pacemaker of the heart. The excitation wave is transmitted in the form of target wave in myocardial tissue. When the target wave is unstable due to myocardial defect, the target wave may be transformed into high frequency spiral wave. Cause cardiac tachycardia: if the helical waves are broken into spatio-temporal chaos, this chaotic electrical signal causes cardiac fibrillation, causing the heart to fail to contract and dilate normally, causing the heart to lose blood supply, and then sudden death. So when the heart has helical waves and space-time chaotic electrical signals, it needs to be controlled in time. As we all know, sudden cardiac death is often caused by cardiac arrhythmia, and the occurrence of spiral waves in the heart is just one kind of arrhythmia. In addition, arrhythmia is often related to depolarization, so the potential mechanism and control of arrhythmia have attracted great attention of scientists. In this paper, the human ventricular TNNP model is used. This paper studies how helical waves lead to depolarization and how to control helical waves and spatiotemporal chaos in two-dimensional heart tissue. In this part, we mainly introduce two kinds of reaction-diffusion systems, several electrophysiological models of the heart, the mechanism of helical wave fragmentation, the control of spiral wave, the aging of heart, etc. We used the human heart model to study the occurrence of depolarization under helical waves or other two-dimensional waves in two-dimensional myocardial tissue, which evolved by changing L-type calcium conductance and fast potassium conductance. We find that in the case of single cell and one-dimensional depolarization, the helical wave can lead to the early depolarization and delayed depolarization of phase 鈪，

本文編號(hào)：1670687