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机构地区:[1]河北北方学院生理教研室,河北张家口075000
出 处:《河北北方学院学报(医学版)》2005年第5期17-19,共3页Journal of Hebei North University:Medical Edition
摘 要:目的:探讨高血压大鼠左室流出道自发性慢反应电位0相和4相去极离子流中Ca2+的作用。方法:利用自发性高血压大鼠(SHR)的离体心脏,常规玻璃微电极细胞内记录方法和Ca2+离子通道阻断剂维拉帕米(VER),观测最大舒张电位(MDP)、0相除极幅度(APA)、0相最大除极速度(Vmax)、4相自动除极速度(VDD)、复极50%(APD50)和90%(APD90)的时间以及自发放电频率(RPF)。结果:1.0μmol/L维拉帕米可使该慢电位的APA、Vmax、VDD明显减小,RPF减慢(P<0.01);APD、APD90延长(P<0.05)。结论:(1)该区域的自发慢电位0相去极离子流主要为Ca2+内流。(2)4相去极离子流中,Ca2+内流起部分作用。Objective:To analysis the function of Ca^2+ in the ionic mechanism underlying the phase 0 and phase 4 in the slow-response action of left ventricular outflow tract of spontaneous hypertensive rats. Methods:Spontaneous slow action potentials of the left ventricular outflow tract in heart were intracellularlly recorded with conventional manner. Electrophysiological parameters examined are: maximal diastolic potential (MDP), amplitude of action potential(APA),maximal rate of depolarization of phase 0 (Vmax),velocity of diastolic depolarization of phase 4(VDD),duration of 50% and 90% repolarization(APD50 and APD90 )and rate of pacemaker firing (RPF). Results: It was found that: 1.0μmol/L verapamil (VER) significantly decreased APA ,Vmax,VDD and RPF, (P〈0. 01) ,but APD and APD90 were significantly prolonged. Conclusion:The above results suggest that:(1)Generation of 0 phase in depolarization of slow-response activity in aortic vestibule from spontaneous hypertensive rats is contributed mainly to Ca^2+ current. (2)In addition,the inward Ca^2+ current plays some role in phase 4 depolarization.
关 键 词:维拉帕米 自发性高血压大鼠 左心室流出道 自发慢电位
分 类 号:R331.3[医药卫生—人体生理学]
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