CAJ | 학술논문

目的:研究迷走神经递质乙酰胆碱(ACh)对离体豚鼠心房肌细胞动作电位(AP)的影响及其对心房肌的脱敏,探讨脱敏可能发生的机制.方法:采用标准玻璃微电极细胞内记录方法,观察不同浓度(0.01,0.1,1 μmol/L) ACh对心房肌细胞AP的影响及对动作电位时程( APD)和收缩力的脱敏现象,并观察了受体或通道水平的阻断剂阿托品、氯化铯 (CsCl)对ACh所致的心房肌APD脱敏的影响.结果:①0.01,0.1,1 μm ol/L ACh分别缩短APD的变化率为(6.02±1.04)%,(14.20±3.79)%,(30.20±3.65)%.②0. 01μm ol/L ACh对心房肌细胞没有脱敏;0.1 μmol/L ACh对心房肌细胞APD有轻微脱敏,脱敏持续时间为1 min;而1 μmol/L ACh对心房肌细胞APD脱敏明显,脱敏持续时间为5 min.③1 μ mol /L阿托品与20 mmol/L CsCl并不能阻断1 μmol/L ACh对心房肌细胞APD的脱敏.结论:ACh缩短 APD的作用随浓度增大而增大;ACh对离体豚鼠心房肌细胞APD的脱敏有浓度依赖性与时间依赖性;脱敏的发生可能与毒蕈碱型胆碱能受体及Ik,ACh电流有关.
목적:연구미주신경체질을선담감(ACh)대리체돈서심방기세포동작전위(AP)적영향급기대심방기적탈민,탐토탈민가능발생적궤제.방법:채용표준파리미전겁세포내기록방법,관찰불동농도(0.01,0.1,1 μmol/L) ACh대심방기세포AP적영향급대동작전위시정( APD)화수축력적탈민현상,병관찰료수체혹통도수평적조단제아탁품、록화색 (CsCl)대ACh소치적심방기APD탈민적영향.결과:①0.01,0.1,1 μm ol/L ACh분별축단APD적변화솔위(6.02±1.04)%,(14.20±3.79)%,(30.20±3.65)%.②0. 01μm ol/L ACh대심방기세포몰유탈민;0.1 μmol/L ACh대심방기세포APD유경미탈민,탈민지속시간위1 min;이1 μmol/L ACh대심방기세포APD탈민명현,탈민지속시간위5 min.③1 μ mol /L아탁품여20 mmol/L CsCl병불능조단1 μmol/L ACh대심방기세포APD적탈민.결론:ACh축단 APD적작용수농도증대이증대;ACh대리체돈서심방기세포APD적탈민유농도의뢰성여시간의뢰성;탈민적발생가능여독심감형담감능수체급Ik,ACh전류유관.
AIM: To investigate the mechanism underlying the effects of ACh on desensitization of action potential in guinea-pigs a t rial muscles. METHODS: Using standard microelectrodes and force tr ansducer we rec orded the effects and desensitization of ACh (0.01,0.1,1μmol/L) and blo ckers (such as atropine, CsCl) on the action potential duration(APD) and force c ontract ion in atrial muscles. RESULTS:①0.01,0.1,1μmol/L ACh shortened the APD by (6. 02±1.04)%,(14.20±3.79)% and (30.20±3.65)% respectively. ②0.01μmol/L ACh has no desensitization and the time of desensitization at 0.1 and 1 μmol/L ACh lasted 1 min and 5 min, respectively. ③The desensitization at 1 μmol/L Ac h could not be blocked by 1 μmol/L atropine,20 mmol/L CsCl. But atropine or CsC l cou ld decrease the effect of shortening APD caused by ACh. CONCLUSION: T he effect of desensitization on APD to ACh in atrial cells is concentration-and time-dependent, these effects may be relate d to the change of the muscarinic receptor and the potassium channel.