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(Circulation Research. 1995;77:593-602.)
© 1995 American Heart Association, Inc.

Articles

Optical Transmembrane Potential Measurements During Defibrillation-Strength Shocks in Perfused Rabbit Hearts

Xiaohong Zhou, Raymond E. Ideker, Timothy F. Blitchington, William M. Smith, Stephen B. Knisley

From the Departments of Medicine and Pathology, Duke University Medical Center, and the Engineering Research Center in Emerging Cardiovascular Technologies, School of Engineering, Duke University, Durham, NC.

Correspondence to Xiaohong Zhou, MD, G82A Volker Hall, Box 201, UAB Station, Birmingham, AL 35294-0019. E-mail xhz@dukebar.crml.uab.edu.

Abstract To study the optical transmembrane potential change (F) induced during shocks, optical recordings were obtained in 15 isolated perfused rabbit hearts treated with the potentiometric dye di-4-ANEPPS and diacetyl monoxime. Shock electrodes were sutured on the right and left ventricles. A laser beam 30 µm in diameter was used to optically excite di-4-ANEPPS. Fluorescence from a region 150 µm in diameter was recorded during a shock. In the macroscopic study (six animals), there were nine recording spots that were 3 mm apart between the two shock electrodes. In the microscopic study, there were three recording regions that were 3 mm away from either shock electrode and midway between them, with nine recording spots that were 30 µm (three animals), 100 µm (three animals), and 300 µm (three animals) apart in each region. After 20 S₁ stimuli, a 10-ms truncated exponential S₂ shock of defibrillation-threshold strength was given during the plateau of the last S₁ action potential. In the microscopic study, shocks were also given during diastole, with F recordings at the three recording regions. Shocks of both polarities were tested. F during the shock was expressed as a percentage of the fluorescence change during the S₁ upstroke action potential amplitude (the S₁ F_apa), ie, F/F_apa%. In the macroscopic study, the magnitudes of F/F_apa% from recording spots 1 to 9, numbered from the left to the right ventricular electrodes, were 77±41%, 46±32%, 32±27%, 28±20%, 37±25%, 24±20%, 33±22%, 37±25%, and 59±29%, respectively (P<.05 among the nine spots). Depolarization or hyperpolarization could occur near either shock electrode with both shock polarities, but the magnitude of hyperpolarization was 1.8±0.9 times that of depolarization at the same recording spot when the shock polarity was reversed (P<.01). In the microscopic study, the change in F/F_apa% varied significantly over the microscopic regions examined. The maximum values of F/F_apa% for hyperpolarizing shocks during diastole reached only 7±10% of those for shocks during the plateau (P<.01). During diastole, the time until a new action potential occurred after the beginning of the shock was shorter when the membrane was depolarized (1.1±0.5 ms) than when it was hyperpolarized (12.8±9.1 ms, P<.01). Conclusions are as follows: (1) A shock can induce either hyperpolarization or depolarization. (2) Hyperpolarization or depolarization during a shock can occur near either the anodal or cathodal shock electrode. (3) Variation of F/F_apa% exists within a microscopic region. (4) The effects of a shock during an action potential plateau are different from those during diastole. (5) The different responses of the F during a shock affect the excitation latency during diastole.

Key Words: action potential duration • di-4-ANEPPS • electrical defibrillation • optical transmembrane potential

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