Myocardial extracellular K + and H + increase and noradrenaline release as possible cause of early arrhythmias following acute coronary artery occlusion in pigs

Abstract

Listen

Translate article

In 22 young domestic pigs, after thoracotomy, the distal half of the ramus descendens anterior of the left coronary artery was occluded. This caused an ischemia affecting about 14% w w of both ventricles. The extracellular K + concentration ([K +]e) the extracellular H + activity ([H +]e, pH e) and the coronary arteriovenous noradrenaline differences were measured before and during coronary artery occlusion. [K +]e was measured with K +-selective PVC liquid membrane electrodes which were sewn on the epicardium of the left ventricle, pH e was measured using pH-selective bulb-type glass mini-electrodes which were fixed at a depth of 5 to 7 mm below the surface of the left ventricle. Plasma noradrenaline concentration was measured fluorimetrically using the trihydroxyindole method. About 10 s after the onset of occlusion [K +]e started to increase from a control value of 4.2 ± 0.7 meq/l. In 13 pigs after 2.5 ± 1.0 min at a [K +]e of 10.7 ± 1.9 meq/l a first early phase of ventricular arrhythmias (VA) began and ventricular fibrillation (VF) started after 3.2 ± 1.8 min of ischemia at 12.4 ± 2.8 meq/l. In 9 pigs after 3.4 ± 1.2 min at a [K +]e of 12.6 ± 3.8 meq/l the first early phase of VA started which ended after 8.3 ± 3.1 min at a [K +]e of 14.0 ± 2.9 meq/l without VF. In these 9 pigs after a period without any VA after 20.5 ± 7.5 min of ischemia at a [K +] e of 15.5 ± 2.9 meq/l the second early phase of VA began. It ended after 25.3 ± 12.3 min at a [K +)e of 17.7 ± 3.9 meq/l in 7 pigs with VE. Two pigs survived for some hours without VF. Noradrenaline was released into the coronary venous blood only during the first early phase of arrhythmia. Extracellular [H +] ([H +]e) started to increase 5 to 10 s after the onset of occlusion from a control value of 40 neq/l (pH 7.4) with an average rate of change of 50 to 60 neq/l/min reaching about 3000 neq/l (pH 5.5) after about 50 min of ischemia. Thereafter [H +]e further increased at a much lower rate. These data support the view that electrical inhomogeneity, known to induce arrhythmias following myocardial ischemia during the first early phase of VA, might be caused by a combined effect of [K +]e increase in the ischemic myocardium and noradrenaline release from the ischemic and non-ischemic myocardium, while during the second early phase the further [K +]e increase possibly in the border zone seems to be the main reason. The [H +]e increase does not seem to play an important rule in causing VA.