PROLONGATION OF VENTRICULAR REFRACTORINESS BY DEFIBRILLATION SHOCKS MAY BE DUE TO ADDITIONAL DEPOLARIZATION OF THE ACTION-POTENTIAL

被引：31

作者：

DILLON, SM

MEHRA, R

机构：

[1] Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York

[2] Medtronic, Inc., Minneapolis, Minnesota

来源：

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY | 1992年 / 3卷 / 05期

关键词：

VENTRICULAR FIBRILLATION; REFRACTORY PERIOD; RABBIT HEART; CANINE HEART; OPTICAL RECORDING;

D O I：

10.1111/j.1540-8167.1992.tb00988.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Shock-Induced Refractoriness Prolongation in Canines. Introduction: A comparison of the effects of shock timing and strength on the effective refractory periods (ERPs) of open chest canine hearts to the duration of depolarization in optically recorded action potentials from the rabbit heart was conducted in order to investigate the mechanism of ERP prolongation in the canine. Methods and Results: Studies were conducted in four open chest canines hearts and three isolated, perfused rabbit hearts. Shocks were applied during ventricular pacing and the strength and timing were varied. The shock voltage gradient was measured at the stimulating site used to assess the ERP in the canine and at the optical recording site in the rabbit. Shock voltage gradients ranged from 7.5 to 53 V/cm in the canine and 2 to 25 V/cm in the rabbit. Shock coupling intervals (CIs) were varied over a range of 15% to 105% of the control ERP (canine) and 10% to 115% of the control action potential duration (APD) (rabbit). Shocks prolonged the ERP in the canine and they caused an additional period of depolarization that prolonged the action potential in the rabbit. ERP and APD prolongation showed similar dependencies on the shock strength and CI: both increased with increasing shock strength and CI. Conclusion: ERP prolongation in the canine may be due to the same type of responses seen on the optically recorded action potentials in the rabbit. ERP prolongation by low-strength shocks at long CIs in the canine may be due to graded responses and premature action potentials. ERP prolongation by high-strength shocks over a range of CIs may be due to the additional depolarization time response that prolongs the action potential in rabbits.

引用

页码：442 / 456

页数：15

共 20 条

[1] Witkowski FX, Penkoske PA, Plonsey R, Mechanism of cardiac defibrillation in open‐chest dogs with unipolar DC‐coupled simultaneous activation and shock potential recordings, Circulation, 82, pp. 244-260, (1990)
[2] Chen PS, Wolf PD, Melnick SD, Et al., Comparison of activation during ventricular fibrillation and following unsuccessful defibrillation shocks in open‐chest dogs, Circ Res, 66, pp. 1544-1560, (1990)
[3] Dillon SM, Optical recordings in the rabbit heart show that defibrillation strength shocks prolong the duration of depolarization and the refractory period, Circ Res, 69, pp. 842-856, (1991)
[4] Mehra R, Dillon SM, DeGroot P, Et al., Effect of high voltage stimuli on effective refractory period of the canine ventricle, (Abstract) PACE, 13, (1990)
[5] Frazier DW, Krassowska W, Chen PS, Et al., Extracellular field required for excitation in three‐dimensional anisotropic canine myocardium, Circ Res, 63, pp. 147-164, (1988)
[6] Lepeschkin E, Jones JL, Rush S, Et al., Local potential gradients as a unifying measure for thresholds of stimulation, standstill, tachyarrhythmia and fibrillation appearing after strong capacitor discharges, Adv Cardiol, 21, pp. 268-278, (1978)
[7] Chen PS, Wolf PD, Claydon FJ, Et al., The potential gradient field created by epicardial defibrillation electrodes in dogs, Circulation, 74, pp. 626-636, (1986)
[8] Lu FC, The optimum pressure for perfusing the isolated rabbit's heart, Rev Can Biol, 10, pp. 42-47, (1951)
[9] Gupta RK, Salzberg BM, Grinvald A, Et al., Improvements in optical methods for measuring rapid changes in membrane potential, J Membr Biol, 58, pp. 123-137, (1981)
[10] George EB, Nyirjesy P, Basson M, Et al., Impermeant potential‐sensitive oxonol dyes. I. Evidence for an ‘On‐Off’ mechanism, J Membr Biol, 103, pp. 245-253, (1988)

← 1 2 →