Cardiac electrophysiological effects of isoprenaline, phenylephrine, and noradrenaline on normal and mildly "ischaemic" sheep Purkinje fibers.

The aim of this study was to examine the electrophysiological effects of isoprenaline, phenylephrine, and noradrenaline on sheep Purkinje fibers in vitro, superfused either with a normal or with a modified physiological salt solution (PSS) designed to mimic some of the conditions occurring during mild myocardial ischemia (hyperkalemia, hypoxia, and acidosis). Intracellular microelectrode recording techniques were used to record resting and action potentials. Noradrenaline (10(-7) to 10(-5) M) and phenylephrine (10(-7) to 10(-5) M) prolonged the action potential of normal fibers in a concentration-dependent manner, the effect of phenylephrine being greater than that of noradrenaline. The only effect of isoprenaline (10(-7) to 10(-5) M) was a slight hyperpolarization. The modified PSS caused marked reductions in resting membrane potential, upstroke, and duration of the action potential. On these depressed fibers isoprenaline, noradrenaline, and phenylephrine all prolonged the action potential, and in the case of noradrenaline the duration of the abbreviated action potential was restored beyond control. This effect of noradrenaline and isoprenaline was more marked under ischemic than normal conditions, whereas the opposite was true of phenylephrine. In the presence of effective alpha- or beta-adrenoceptor blockade, the noradrenaline-induced prolongation of the "ischemia"-abbreviated action potential was attenuated. In some of the preparations exposed to simulated ischemia, noradrenaline caused inexcitability. In conclusion, isoprenaline, phenylephrine, and noradrenaline exhibited different electrophysiological effects on mildly "ischemic" sheep Purkinje fibers compared to their effects on normal fibers.