MAGNESIUM AND ISCHEMIC POSTCONDITIONING OF REPERFUSION ARRHYTHMIAS

DIEZ ED, PONCE ZUMINO AZ

Zaragoza

Simposio; II Simposio Ibérico del Mg y V Jornadas de Elementos Traza; 2010

Magnesium prevents myocardial reperfusion injury, including severe ventricular arrhythmias (VA). However, the clinical impact of magnesium administration has been controversial. Postconditioning, by brief episodes of ischemia applied at the beginning of reperfusion, reduces reperfusión arrhythmias. We decided to compare the electrophysiological effects of 3 min magnesium administration and intermittent ischemia during reperfusion. Effects of Mg2+ concentration (1.2, 2.4, and 9.6 mM) on the incidence and severity of VA and on the cellular electrical activity were studied in spontaneously beating rat hearts, and compared with 3 cycles of 30 seconds of reperfusion and 30 seconds of ischemia. The electrogram and the membrane poten¬tial were recorded during 10 min of regional ischemia and 10 min of reperfusion. All groups suffered ventricular tachycardia and/or fibrillation during reperfusion. Mg2+ did not reduced the incidence of reperfusion VA and was unable to restore sinus rhythm, but induced a delay in the occurrence of ventricular fibrillation in the higher concentration from 34 s (CI95 24-43) to 154 s (CI95 79-233) p<0.05. Postconditiong neither reduced VA incidence but restored sinus rhythm in 8/11 hearts vs 2/11 hearts of control group (p<0.05 by Fisher exact test). Both strategies reduced action potential duration and ventricular conduction, but only postconditioning induced bradycardia. Our results could explain, in part, why Mg2+ administration during a short period of time fails to protect against reperfusion arrhythmias but delays fibrillation development, probably due to action potential shortening. Mg2+and postconditioning have similar electrophysiological effects, however others mechanisms should be involved in the latter situation.