ISOPRENALINE AUGMENTS TOTAL MYOCARDIAL K+ INFLUX OF THE INSITU BEATING PORCINE HEART

To determine the total rate of K+ flux into myocardial cells of the in-situ beating heart and how this influx is affected by β-adrenoceptor stimulation, we measured 42K+ content in myocardial biopsies taken at intervals after an intra-atrial infusion of 42K+ before and during an i.v. isoprenaline infusion (20 μg min-1) in six anaesthetized, open-chest pigs. Determination of the total K+ influx during β-adrenoceptor stimulation was initiated 10 min after the start of isoprenaline infusion, when the transient net myocardial K+ uptake had subsided. Total K+ influx increased from a control value of 414 ± 42 to 1086 ± 246 μmol 100 g-1 min-1 during isoprenaline infusion. A quantitatively smaller increase in K+ influx carried by the Na+-K+ pump has previously been demonstrated during isoprenaline infusion. Left ventricular dP/dt rose from 1350 ± 146 to 4833 ± 150 mmHg s-1, stroke volume remained unchanged, but heart rate and peak left ventricular systolic pressure rose as expected, by 52 ± 4 and 32 ± 4% respectively during isoprenaline stimulation. All haemodynamic parameters, total plasma K+ concentration and plasma 42K+ activity remained stable throughout each experimental period. The number of ouabain binding sites was 65.5 ± 1.0 before and 66.9 ± 1.6 nmol 100 g-1 during isoprenaline infusion (difference n.s.). The present data indicate that not only the K+ influx carried by the ouabain-sensitive Na+-K+ pump but also the influx through ouabain-insensitive pathways is increased during β-adrenoceptor stimulation of the in-situ beating pig heart.