家兔急性缺血早期心室肌细胞跨膜电位的变化及迷走神经的保护作用

以在体家兔的心脏为对象,应用浮置微电极技术研究了急性缺血早期心室肌细胞跨膜电位的变化及迷走神经的保护作用。 冠状动脉的一个分支阻断后 1—5min,静息电位(RP)、动作电位振幅(APA)和 0相最大上升速率(dv/dt)_(max)均减小(P<0.01)。动作电位时程APD_(30)、APD_(50)和APD_(90)均缩短(P<0.01)。反映 2相平台时程的 APD_(30)和 APD_(50)缩短较总时程 APD_(90)的缩短更明显。 在自然心率的条件下,左颈迷走神经电刺激,可使急性缺血的心肌电位的变化有所恢复:RP、APA、(dv/dt)_(max)均增加,APD_(30)、APD_(50)、APD_(90)延长(P_均<0.01)。刺激迷走神经时缺血的心室肌细胞跨膜电位有所恢复,对防止缺血早期的室性心律失常可能具有重要作用。

CHANGES IN TRANSMEMBRANE POTENTIALS OF CARDIAC VENTRICULAR FIBERS DURING THE EARLY STAGE OF ACUTE CARDIAC ISCHEMIA AND PROTECTIVE EFFECTS OF VAGAL STIMULATION IN RABBITS

This study was carried out on rabbit hearts. Floating glass microelectrodewas used to record the transmembrane potentials of cardiac ventricular fibers insitu. Resting potential (RP), action potential amplitude (APA) and maximumupstroke velocity of phase 0 (dv /dt)_(max) were decreased (P<0.01) 1-5 min aftercoronary occlusion. The duration of action potential, especially the time requiredfor 30% and 50% of recovery (APD_(30), APD_(50)), was shortened, and the durationof the plateau was shortened even more markedly. These changes in potentials of the ventricular cells during acute ischemia wereabolished by vagal stimulation, RP, APA, and (dv /dt)_(max) were increased (P<0. 01).Vagal stimulation lengthened APD_(30),APD_(50), and APD_(90) under condition of na-tural heart rate, it was suggested that the lengthening of the APD during vagalstimulation was due to the decrease in heart rate. These results suggested that recovery of the transmembrane potentials of theischemic ventricular cells during vagal stimulation was beneficial to impulse conduc-tion in the ventricular muscles and to lengthening of the effective refractory period,which might play an important role in prevention of ventricular arrhythmia in earlystage of acute ischemia.