Arsenic trioxide (As2O3) is used clinically in the management of acute promyelocytic leukemia, and the use of electrocardiogram (ECG) in this management is important as arsenic use may cause distortion of the electrical properties with its attendant sequel. We studied the effect of As2O3 on vasomotion in rat aortic rings using isometric tension recordings and ECG in anesthetized rats. The results showed that As2O3 (10(-5) M) significantly (p < 0.01) reduced the frequency of acetylcholine (10(-5) M ACh)- and KCl (10 mM)-induced vasomotion, and it also increased the relaxation time (R t) of vasomotion. This effect was restored by 10(-8) M sodium nitroprusside (nitric oxide donor). ACh-induced NO release in the aorta was blunted in the presence of As2O3. The corrected QT interval (QTc) of the ECG, and time dilation (T d) of the pulse wave in the tail artery of the anesthetized rat were significantly (p < 0.05) increased in the arsenic-treated group (50 ppb As) versus control. In conclusion, data suggest that arsenic-induced reduction in vasomotion frequency of the isolated aortic rings is associated with a decreased bioavailability of NO, an increase in QTc and a decrease in the frequency of the pulse wave generated by the cardiac cycle in anesthetized rats.
Keywords: Aorta rat; Arsenic; Electrocardiogram; K+ channels; Nitric oxide; Pulse wave; Vasomotion.