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AI InsightIt did not cause anysignificant difference in QRS duration in any group.When compared to the control group, DPCPX aftercitalopram infusion shortened the prolongation of theQT interval after 40, 50 and 60 minutes (p
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Abstract
Background: Citalopram is a selective serotonin re- uptake inhibitor that requires routine cardiac monitoring to prevent a toxic dose. Prolongation of the QTinterval has been observed in acute citalopram poisoning. Our previous experimental study showed that citalopram may be lead to QT prolongation by stimulatingadenosine A1 receptors without affecting the release ofadenosine. Aims: We examined the effects of adenosine receptorantagonists in reversing the cardiovascular toxic effectsinduced by citalopram in rats. Study Design: Animal experimentation. Methods: Rats were divided into three groups ran- domly (n=7 for each group). Sodium cromoglycate (20mg/kg) was administered to all rats to inhibit adenosineA3 receptor mast cell activation. Citalopram toxicitywas achieved by citalopram infusion (4 mg/kg/min) for20 minutes. After citalopram infusion, in the controlgroup (Group 1), rats were given an infusion of dextrose solution for 60 minutes. In treatment groups, theselective adenosine A1 antagonist DPCPX (Group 2,8-cyclopentyl-1,3-dipropylxanthine, 20 μg/kg/min) orthe selective A2a antagonist CSC (Group 3, 8-(3-chlo- rostyryl)caffeine, 24 μg/kg/min) was infused for 60 minutes. Mean arterial pressure (MAP), heart rate(HR), QRS duration and QT interval measurementswere followed during the experiment period. Statistical analysis was performed by ANOVA followed byTukey s multiple comparison tests.Results: Citalopram infusion reduced MAP and HRand prolonged the QT interval. It did not cause anysignificant difference in QRS duration in any group.When compared to the control group, DPCPX aftercitalopram infusion shortened the prolongation of theQT interval after 40, 50 and 60 minutes (p