Author + information
- Received October 6, 1982
- Revision received November 30, 1982
- Accepted December 3, 1982
- Published online May 1, 1983.
- Gary J. Anderson, MD, FACC*,
- John Swartz, MD,
- Steven C. Dennis, PhD and
- Joseph Reiser, PhD
- ↵*Address for reprints: Gary J. Anderson, MD, Likoff Cardiovascular Institute, Hahnemann University, 230 North Broad Street, Philadelphia, Pennsylvania 19102.
The electrophysiologic effects of insulin (40 mU/ml) and elevated potassium (4 to 6 mM) on glucose-superfused normal and infarcting tissue from 24 hour coronary artery ligated canine myocardium were studied. With standard intracellular microelectrode techniques, it was observed that insulin infusion for 30 minutes produced an increase in resting membrane potential and a prolongation of action potential duration. In the normal myocardium, the hyperpolarization and the repolarization delay were minimal, but in infarcting tissue with depressed electrophysiologic function, resting membrane potential and action potential duration were significantly improved. This was particularly evident in the presence of an increased potassium concentration (6 mM) when insulin hyperpolarized infarcting cells (n = 8) from 73 ± 6 to 85 ± 7 mV (p < 0.01). In the same studies, action potential amplitudes were increased from 75 ± 7 to 95 ± 11 mV (p < 0.01). In addition, action potential durations at 40 and 80% repolarization were extended from 64 ± 25 and 141 ± 46 ms to 132 ± 34 and 198 ± 27 ms, respectively (p < 0.01). Thus, these data are in accord with the reduced ST segment elevation observed in patients treated with glucose-insulin-potassium and support the use of this intervention in the management of acute infarction.
- Received October 6, 1982.
- Revision received November 30, 1982.
- Accepted December 3, 1982.
- American College of Cardiology Foundation