I
f was shown to be present in adult
human atrial and ventricular myocytes but data obtained from
infant myocytes are lacking. We have studied
I
f in isolated ventricular myocytes from
children undergoing surgical correction of tetralogy of Fallot
(TOF; n = 5; mean age: 15.3 months). All recordings were made
with the patch clamp technique in the whole cell mode at a
temperature of 36–37 °C. A modi

ed Tyrode solution containing 25
mM KCl was used to amplify I
f.
Considering I
f to be present when its
current density at –120 mV was greater than 0.5 pA/pF,
I
f could be found in 28 out of 32
myocytes (88%). The mean current density was –2.01 ± 0.3 pA/pF
(mean ± S.E.M.). First current activation occurred at –70 mV and
I
f could be reversibly inhibited by
superfusing the myocytes with CsCl (2 mM). Half maximal
activation (V
1/2) of
I
f was at –80.3 ± 1.0 mV (n = 28).
Beta-adrenergic receptor stimulation with isoproterenol (1 µM)
caused an acceleration of current activation and a shift of
V
1/2 by 7.88 ± 1.8 mV (n = 10) to less
negative potentials. This study provides

rst evidence that the
hyperpolarization-activated pacemaker current
I
f is present in infant human ventricular
myocytes. Our results suggest that I
f in
ventricle of infants suffering from TOF has similar properties
as I
f in adult ventricle.
Key words
Infant ventricular myocytes - tetralogy of Fallot - patch clamp - ion channel - pacemaker current