PROLONGATION AND SHORTENING OF ACTION-POTENTIALS BY ELECTRICAL SHOCKS IN FROG VENTRICULAR MUSCLE

被引:30
作者
KNISLEY, SB
SMITH, WM
IDEKER, RE
机构
[1] DUKE UNIV, MED CTR, DEPT PATHOL, DURHAM, NC 27710 USA
[2] DUKE UNIV, SCH ENGN, DEPT BIOMED ENGN, DURHAM, NC 27710 USA
[3] DUKE UNIV, SCH ENGN, ENGN RES CTR EMERGING CARDIOVASC TECHNOL, DURHAM, NC 27710 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1994年 / 266卷 / 06期
关键词
VENTRICULAR ACTION POTENTIAL; VENTRICULAR REFRACTORY PERIOD; CALCIUM; POTASSIUM; CONTRACTILITY; ELECTRICAL COUNTERSHOCK; DEFIBRILLATION; CARDIOVERSION; ELECTROPORATION;
D O I
10.1152/ajpheart.1994.266.6.H2348
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Effects of electrical shocks on myocardium are important for defibrillation. We measured effects of shocks (5 ms, 1-40 V/cm) in isolated frog ventricular strips. We recorded contraction strength and intracellular action potential (AP) with a shock-voltage cancellation technique to allow recordings immediately after shocks. Shocks of 15 V/cm produced a dose- and latency dependent prolongation of the AP ongoing during the shock. Stronger shocks of 28-40 V/cm decreased the duration, maximum diastolic potential, amplitude, and maximum rate of rise of the phase zero depolarization of paced APs that began after the shock. The contraction strength increased 43 and 59% during the 10 s after the stronger shocks. The transmembrane potential was shifted toward 0 mV immediately after the stronger shocks. We concluded that weak or strong shocks prolong the AP ongoing during the shock, whereas sufficiently strong shocks also shorten APs that begin after the shock. AP prolongation and shortening may be important for defibrillation and acceleration of tachycardia after failed cardioversion shocks.
引用
收藏
页码:H2348 / H2358
页数:11
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