本文選題：乙酰膽堿 + 洗脫��； 參考：《石河子大學(xué)》2008年碩士論文

【摘要】： 目的:研究乙酰膽堿(acetylcholine, ACh)灌注并迅速洗脫后所致離體兔心正性肌力作用的規(guī)律及其可能機制,探討ACh灌注與洗脫對離體家兔右心房復(fù)極時限及跨壁復(fù)極離散度(transmural dispersion of repolarization, TDR)的影響。 方法:采用Langendorff離體心臟灌流技術(shù),觀察對照組與實驗組共28例在給予ACh并洗脫后離體兔心的心肌收縮力變化;采用單相動作電位(MAP)記錄技術(shù),同步且同部位記錄9例家兔右房心外膜心肌、中層心肌和心內(nèi)膜心肌MAP,測量并計算ACh(1×10-5 mol/L,0.3 ml/kg)灌注及洗脫后,心房肌MAP復(fù)極達50%與90%的時間(MAPD50與MAPD90)及其TDR。 結(jié)果:10-8~10-3 mol/L濃度的ACh灌注并立即洗脫后所致心肌收縮力的最大反跳率分別為2.22%±1.70%、6.71%±3.40%、9.18%±3.54%、14.16%±3.27%、4.37%±5.86%、1.03%±6.86%;腎上腺素組的最大反跳率為29.25%±5.83%,普萘洛爾組最大反跳率為5.15%±4.45%,二者與對照組同濃度ACh (1×10-5 mol/L)相比,均有顯著統(tǒng)計學(xué)差異(P0.05, n=7);維拉帕米組持續(xù)800 s未出現(xiàn)反跳現(xiàn)象。ACh灌注時,三層心房肌的MAPD50、MAPD90及MAPD90-50值較ACh灌注前延長(P0.05,給藥后30±5 s; n=9),TDR50、TDR90和TDR90-50值較給藥前增加(P0.05,給藥后30±5 s; n=9);在ACh洗脫后,三層右房心肌MAPD50、MAPD90、MAPD90-50及其TDR值的變化,較灌注ACh前無顯著差異(P0.05,給藥后100±5 s; n=9)。 結(jié)論:在離體兔心,我們可以觀察到ACh灌注并迅速洗脫后出現(xiàn)的負性與正性肌力作用;ACh洗脫后所致的正性肌力作用與心肌Ca2+通道、β受體的活性有關(guān);ACh洗脫后與高濃度ACh時引起正性肌力作用的機制可能存在不同;ACh灌注時與洗脫后在右房復(fù)極方面存在明顯不同的電生理變化,它們所致心律失常的機制有必要從多角度進行進一步研究。
[Abstract]:Objective: To study the regularities and possible mechanisms of positive inotropic action of the isolated rabbit heart after acetylcholine (ACh) perfusion and rapid elution, and to explore the effect of ACh perfusion and elution on the repolarization time limit of right atrium and transmural dispersion of repolarization (TDR) in the right atrium of rabbit in vitro.
Methods: Langendorff isolated heart perfusion technique was used to observe the changes of myocardial contractility in 28 cases of the isolated rabbit heart after ACh and elution in the control group and the experimental group. The single phase action potential (MAP) recording technique was used to record the right atrial epicardial myocardium in 9 rabbits, the middle myocardium and the cardiac endomyocardial MAP were recorded simultaneously and in the same site. The ACh (1 x) was measured and calculated. After 10-5 mol/L, 0.3 ml/kg perfusion and elution, the MAP repolarization of atrial muscle reached 50% and 90% (MAPD50 and MAPD90) and TDR. respectively.
Results: the maximum rebound rate of myocardial contractility induced by ACh perfusion and immediate elution of 10-8~10-3 mol/L was 2.22% + 1.70%, 6.71% + 3.40%, 9.18% + 3.54%, 14.16% + 3.27%, 4.37% + 5.86%, 1.03% + 6.86%, and the maximum rebound rate of epinephrine group was 29.25% + 5.83%, and the maximum rebound rate of propranolol group was Compared with the same concentration of ACh (1 x 10-5 mol/L), there were significant statistical differences (P0.05, n=7), while the MAPD50, MAPD90 and MAPD90-50 values of three layers of atrial muscle were prolonged (P0.05, 30 + 5 s,) in the Vera Pammy group sustained 800 s without the phenomenon of reverse jump.ACh perfusion (30 + 5 after administration). (n=9); after ACh elution, the changes of MAPD50, MAPD90, MAPD90-50 and TDR values in the three layers of right atrial myocardium were not significantly different from those before perfusion ACh (P0.05, 100 + 5 s after administration; n=9).
Conclusion: in the isolated rabbit heart, we can observe the negative and positive inotropic action after ACh perfusion and rapid elution. The positive inotropic action after ACh elution is related to the myocardial Ca2+ channel, the activity of beta receptor, and the mechanism of positive inotropic action may be different from the high concentration ACh after ACh elution; ACh perfusion and elution after elution. There are obvious electrophysiological changes in the repolarization of right atrium. The mechanism of arrhythmia induced by them is necessary to further study from multiple angles.

【學(xué)位授予單位】：石河子大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2008
【分類號】：R33

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