MAGNESIUM - A PROFIBRILLATORY OR ANTIFIBRILLATORY DRUG DEPENDING ON PLASMA-CONCENTRATION, HEART-RATE AND MYOCARDIAL PERFUSION

Background: The opinions on the efficacy of magnesium as an antiarrhyt hmic drug vary considerably. The action of magnesium on vulnerability to fibrillation was therefore investigated in anaesthetized, open-ches t pigs under different conditions as regards plasma concentration, hea rt rate and myocardial perfusion. Methods: Vulnerability to fibrillati on was assessed by electrical fibrillation threshold (EFT), measured w ith 100-ms duration diastolic impulses. These stimuli were delivered t o the heart normally perfused, at a usual (90 and 120 beats/min) or ac celerated (180 beats/min) rate. Vulnerability to fibrillation was also assessed at the high rate (180 beats/min) in the heart made ischaemic by complete occlusion of the left anterior descending coronary artery near its origin. EFT was then measured at the end of occlusion period s which were of increasing duration (30, 60, 90, 120 s). Monophasic ac tion potential (MAP) duration, intraventricular conduction time, left ventricular dP/dt max (LVdP/dt max) and mean blood pressure were concu rrently measured. Results: In the absence of ischaemia, 5 mu mol . kg- 1 . min-1 magnesium i.v. infusion, which raised plasma concentration t o 1.78+/-0.14 mmol/L, lowered EFT, measured at the rate of 116 beats/m in, from 14.0+/-1.1 to 6.8+/-1.0 mA (P<0.001) without significant vari ation of the other parameters. Administered as previously or in a mark edly higher dose (400 mu mol . kg(-1) loading dose and 10 mu mol . kg( -1) . min(-1) infusion) which raised plasma concentration up to 4.84+/ -0.52 mmol/L, magnesium significantly influenced neither EFT nor MAP d uration, reduced by the high rate (180 beats/min) to 6.2-6.7 mA and 21 2-220 ms respectively. Under the same conditions, at the same 180 beat s/min rate, ischaemia brings about a fall of EFT, from 6.9 down to nea rly 0 mA, with occurrence of fibrillation, in approximately 120 s. Mag nesium failed to slow this fall and to delay the onset of fibrillation . In contrast, within the minutes following the end of occlusion, magn esium increased EFT to a great extent (from 7.1+/-0.4 to 13.5+/-0.7 mA , P<0.001), with a significant prolongation of MAP duration (212+/-6 t o 234+/-8 ms, P<0.01). Conclusion: Magnesium may develop profibrillato ry or antifibrillatory effects depending on plasma concentration, hear t rate and myocardial perfusion. (C) Acta Anaesthesiologica Scandinavi ca 41 (1997).