【摘要】： 實驗一乙酰膽堿(ACh)對離體人心房肌電生理特性的影響 目的:研究迷走神經(jīng)遞質(zhì)乙酰膽堿(ACh)對離體人心房肌電生理特性的影響 方法:選擇20例先天性心臟病手術(shù)患者,手術(shù)中切取患者右心耳組織,采用標準玻璃微電極技術(shù)及張力換能器,檢測灌注乙酰膽堿(ACh)前后患者右心房細胞靜息膜電位(RMP),動作電位達90%復極的時程(APD90),自發(fā)動作電位及收縮力的改變。 結(jié)果:乙酰膽堿能顯著提高人心房肌肉靜息電位(RMP)(54.7±2.19mv vs 61.4±1.8mv),顯著縮短APD90(406.3±14.61ms vs 316.2±15.40ms),P0.05。乙酰膽堿能明顯抑制人心房肌自發(fā)動作電位及收縮力(60.5±3.2次/分vs 0次/分),P0.05。并且以上效應隨時間變化逐漸減弱。 結(jié)論:乙酰膽堿能顯著提高人心房肌靜息電位和縮短動作電位時程,明顯抑制人心房肌自發(fā)動作電位及收縮力,并且以上效應存在脫敏現(xiàn)象。 實驗二乙酰膽堿(ACh)對人心房肌作用的脫敏機制研究 目的:研究迷走神經(jīng)遞質(zhì)乙酰膽堿(ACh)對離體人心房肌作用的脫敏機制 方法:選擇20例先天性心臟病手術(shù)患者,手術(shù)中切取患者右心耳組織,采用全細胞膜片鉗技術(shù)及Western Blotting免疫印跡技術(shù)分別記錄人心房肌細胞IK,Ach通道電流密度變化以及灌流前后心房肌組織Kir3.4蛋白質(zhì)的表達。 結(jié)果:乙酰膽堿能激活人心房肌細胞上的IK,Ach通道產(chǎn)生電流,而且此電流存在明顯的脫敏現(xiàn)象。灌流前后心房肌組織Kir3.4蛋白質(zhì)的表達無明顯差異。 結(jié)論:乙酰膽堿對人心房肌作用的脫敏現(xiàn)象可能與人心房肌IK,Ach通道電流的脫敏有關(guān),而與IK,Ach通道蛋白表達無明顯關(guān)系。
[Abstract]:Effect of acetylcholine (ACh) on electrophysiological characteristics of isolated human atrial myography objective: to study the effect of vagus neurotransmitter acetylcholine (ACh) on the electrophysiological characteristics of human atrial myograph in vitro Methods: twenty patients with congenital heart disease were selected. The tissue of the right atrial appendage was removed during the operation, and the standard glass microelectrode technique and tension transducer were used. The time course (APD90) of resting membrane potential (RMP),) of right atrial cells before and after perfusion of acetylcholine (ACh) to 90% repolarization and the changes of spontaneous action potential and contractility were measured. Results: acetylcholine significantly increased the resting potential of human atrial muscle (RMP) (54.7 鹵2.19mv vs 61.4 鹵1.8mv), shortened APD90 (406.3 鹵14.61ms vs 316.2 鹵15.40ms), and significantly shortened APD90 (P 0.05). Acetylcholine could significantly inhibit the spontaneous action potential and contractility of human atrial muscle (60.5 鹵3.2 times / min vs 0 times / min, P 0.05). And the above effects gradually weaken with time. Conclusion: acetylcholine can significantly increase the resting potential of human atrial muscle and shorten the duration of action potential, inhibit the spontaneous action potential and contractility of human atrial muscle, and the above effects have desensitization phenomenon. Desensitization of human atrial muscle by diacetylcholine (ACh) objective: to study the desensitization mechanism of vagus neurotransmitter acetylcholine (ACh) on human atrial muscle in vitro Methods: twenty patients with congenital heart disease were selected. The right atrial appendage tissue was removed. The changes of IK,Ach channel current density in human atrial myocytes and the expression of Kir3.4 protein in human atrial myocytes before and after perfusion were recorded by whole-cell patch clamp technique and Western Blotting Western blotting technique. Results: acetylcholine could activate the IK,Ach channel in human atrial myocytes, and this current had obvious desensitization phenomenon. There was no significant difference in the expression of Kir3.4 protein in atrial muscle before and after perfusion. Conclusion: the desensitization of acetylcholine on human atrial muscle may be related to the desensitization of IK,Ach channel current in human atrial muscle, but not to the expression of IK,Ach channel protein.
【學位授予單位】：華中科技大學
【學位級別】：碩士
【學位授予年份】：2008
【分類號】：R331

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1 張昌偉;乙酰膽堿（ACh）對離體人心房肌電生理特性的影響及其脫敏機制研究[D];華中科技大學;2008年

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