MODERATE STRESS BY CARDIAC PACING MAY INDUCE BOTH SHORT-TERM AND LONG-TERM CARDIOPROTECTION

Objective: The aim was to investigate whether moderate ischaemic stres s induced by brief periods of cardiac pacing to twice the normal heart rate protects the heart from the electrophysiological and haemodynami c consequences of subsequent periods of rapid pacing. Methods: Conscio us rabbits with implanted right ventricular electrodes and a permanent catheter in the left ventricular cavity were studied. Hearts were pac ed at a rate of 500.min-1 for 5 min. The resulting transient ST segmen t elevation in the intracavital electrogram, the ventricular effective refractory period, and the left ventricular end diastolic pressure we re measured. Results: After discontinuation of pacing, a shortlasting ST segment elevation appeared in the endocardial electrogram, together with a transient rise in left ventricular end diastolic pressure. The se changes were significantly reduced after a second pacing provided t hat this was applied not later than 30 min after the first pacing; max imum protection occurred when there was a 5 min interval between these pacing periods. Serial stimulation (10 pacing periods with a 5 min in terval between each) gave a similar protection to that resulting from a single pacing period. The protection was lost after 1 h; however, 24 h and 48 h (but not 72 h) after the end of serial stimulation there w as again a reduction in postpacing ST segment and left ventricular end diastolic pressure elevation. At these times the ventricular effectiv e refractory period was prolonged. The cyclo-oxygenase inhibitor sodiu m meclofenamate (1-2 mg.kg-1) prevented the early protection. Conclusi ons: The results suggest that brief periods of rapid pacing induce bot h short term and long term cardioprotection, as shown by reduced elect rophysiological and haemodynamic consequences of subsequent pacing per iods. Endogenous prostanoids might play a role in the short term cardi oprotection.