At high plasma concentrations (472 ± 68 ng ml−1 ≈ 1.82 μ m), additional shortening of the endocardial MAP duration and QTc interval was observed, beyond that seen at low plasma propranolol concentrations (104 ± 17 ng ml−1 ≈ 0.57 μ m) (Duff et al. 1983).
Computer modelling predicts that this small but significant change in Ito can largely explain the effects of voluntary exercise on the APD of single myocytes [ 27] and the MAP duration at the EPI surface of excised, intact hearts.
MAP duration (MAPD) was assessed at 25 %, 50 and 90% and 90%isation (MAPD25, MAPD50 and MAPD90, repolarisationusing Chart v5 (ADInstruMAPD25Ltd,).
When the ventricles of extrinsically paced, isolated working trout hearts were dilated by increasing afterload, monophasic action potential (MAP) duration was significantly shortened at 25% repolarisation, unaltered at 50% repolarisation and significantly lengthened at 90% repolarisation.
MAP duration (MAPd) was measured, at 90% levels of repolarization.
We observed a significant prolongation of EPI MAP duration in TRN hearts (Fig. 2).
MAP duration was assessed from the time to reach 90% repolarization (APD90).
The observation that MAP duration from the epicardial surface of trained hearts was lengthened shows that the electrical remodelling we have previously reported in single myocytes [ 27] persists in whole hearts, paced at a physiological frequency and is not cancelled by the electronic loading of cell neighbours in the multicellular environment [ 41].
Local activation time is the time measured from the point of electrical stimulus to the maximal amplitude of the AP repolarization time is obtained by the addition of local activation times to MAP duration; however, in the present study we only observed insignificant changes in local activation time in the presence of reduced [K+]o (data not shown).
One explanation for longer mapping durations is that via the retrograde approach, it may sometimes be difficult to pass through the aortic valve, particularly in patients with arteriosclerosis.
