The endocardial unipolar paced evoked response has excited a great deal of interest due to its possible use in the measurement of the metabolic state of the body and other pacer-related areas. Although rate-responsive pacing utilizing this signal has been clinically evaluated, little is known regarding the behavior of the components of this waveform under normal physiological conditions. We have developed an electronic circuit which allows the recording of the evoked response within a few milliseconds of a pacing stimulus of 5 V and 0.5 ms duration being applied using a single unipolar, smooth platinum electrode of 14 mm2 surface area. The paced evoked response was measured using a total of 20 isolated rabbit heart preparations. Five were run for 8 hours and the remaining fifteen were run for 5 hours. Our results indicate that the waveform components of the evoked response remain stable while the preparation is viable, but that two of the time-related measurements change with loss of viability. A significant lengthening of the stimulus-R interval was seen together with a dramatic shortening of the R-T period. The net result of these changes was an overall reduction of 17% in the complex duration. In addition, we found the R-T shortening to be a sensitive measure of myocardial integrity. We conclude that the combination of our interface charge elimination circuit and the isolated heart preparation has proved a useful system for the investigation of the paced evoked potential. Furthermore, the loss of myocardial viability has a complex action on this response.
BACKGROUND: Palmitoyl carnitine accumulation during ischemia causes profound electrophysiological changes, resulting in arrhythmias. We studied the electrophysiological and contractile effects of palmitoyl carnitine. METHODS AND RESULTS: Extracellular recordings made by using the endocardial unipolar paced evoked response (PER) in isolated perfused rabbit hearts were compared with action potentials (AP) recorded from septal artery perfused rabbit papillary muscle. Left ventricular pressure was monitored in isolated hearts. In perfused hearts palmitoyl carnitine (30 µmol/L, 30 minutes) significantly (P <.001) increased the latency of activation (St-R interval) by 58% +/- 8% and reduced repolarization time (R-E interval) by 39% +/- 4%. PER duration (St-E interval), was reduced by 30% +/- 3%. Palmitoyl carnitine (30 µmol/L) significantly (P <.001) decreased resting membrane potential (19 +/- 2 mV) of AP, reduced peak amplitude (33.5 +/- 8 mV) and rate of rise of phase 0 (41 +/- 8 V/s). Significant reductions (P <.001) in the action potential duration 50% (129.4 +/- 28 ms) and 90% (139.8 +/- 32 ms) were also observed. An initial positive inotropic effect, which declined as irreversible contracture developed, was also observed. Verapamil (1 µmol/L), nifedipine (1 µmol/L), and caffeine (10 mmol/L) failed to abolish the positive inotropy. CONCLUSIONS: We suggest that palmitoyl carnitine disrupts intracellular calcium homeostasis leading to disturbances in electrical and contractile activity. Its accumulation during myocardial ischemia could contribute to calcium overloading and initiate lethal arrhythmias.
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