Akademik Veri Yönetim Sistemi
16th World Congress on Basic and Clinical Pharmacology, Kobenhavn, Danimarka, 17 - 23 Temmuz 2010, cilt.170, sa.839, ss.4
This study was designed to clarify the role of
adenosine receptors on mechanism of citalopraminduced cardiovascular toxic effects. The
cardiovascular toxic dose of the citalopram was
found as 4mg/kg/min (n=18). Rats were
randomized into four groups. After the
stabilization period, sodium cromoglycate (A3
receptor antagonist, 20mg/kg, i.v) was
administered to all groups. 5% dextrose (n=7),
DPCPX (selective adenosine A1 receptor
antagonist, 20µg/kg/dk, n=7), CSC (selective
adenosine A2a receptor antagonist, 24 µg/kg/min,
n=7) or 10% DMSO (n=3) was administered for
20 minutes, respectively. Following the infusions,
we administered citalopram (4mg/kg/min/60
minutes). Mean arterial pressure (MAP), heart rate
(HR), QT and QRS durations were recorded. In
the dextrose group, citalopram infusion caused a
significant decrease in the MAP (P<0.001) and
HR (P<0.01) after the 20th minute and caused a
significant prolongation in the QRS (P<0.05) and
QT durations (P<0.01) after the 30th minute. The
citalopram infusion in the DPCPX group, caused a
significant decrease in the MAP after the 20th
minute (P<0.001) and caused a significant decrease in the HR after the 30th minute
(P<0.01). It caused a significant prolongation in
the QRS duration at the 60th minute (P<0.05). It
did not cause any significant difference in the QT
duration. DPCPX infusion significantly prevented
the prolongation of the QT duration induced by
citalopram after the 20th minute when compared
to the control group (P<0.05). In the CSC and
DMSO groups, there was not any significant
change in citalopram-induced cardiovascular
effects. The adenosine A1 receptor stimulation
may be responsible for the citalopram-induced QT
prolongation.