Jila Haghi
1, Tahereh Eteraf-Oskouei
2, Moslem Najafi
2*1 Student Research Committee, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.
2 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract
Purpose: In the present study, postconditioning effect of
fructose against ischemia/reperfusion (I/R)-induced arrhythmias and infarct
size were investigated in isolated rat heart.
Methods: The
isolated hearts were divided into 7 groups, mounted on a Langendorff apparatus
at constant pressure then subjected to 30 min zero flow global ischemia
followed by 120 min reperfusion. In the control group, normal Krebs–Henseleit
(K/H) solution was perfused into the hearts throughout the experiment. In two
separate sets of experiments, the treatment groups received 12, 24 and 48 mM of
fructose with/without normal glucose in K/H solution for 20 min at the
beginning of reperfusion. Cardiac arrhythmias including number of ventricular
tachycardia (VT), total ventricular ectopic beats, incidence and duration of
VT, reversible and irreversible ventricular fibrillation were recorded and
analyzed during the first 30 min of reperfusion. Computerized planimetry method
was used to determine volume and percentage of infarct size.
Results: Administration
of fructose as a postconditioning agent clearly reduced volume and percentage
of infarct size in the all treatment groups. The effect was statistically
significant especially in the hearts that treated by fructose plus glucose
(P<0.05). However, fructose alone or its co-administration with glucose had
no significant inhibitory effect against reperfusion arrhythmias.
Conclusion: The results showed that perfusion of high
concentration of fructose alone or coincident with glucose in globally
ischemic-reperfused isolated rat hearts can reduce infarct size without
inhibitory effect against reperfusion arrhythmias. Probably, fructose by
providing adequate ATP for cardiac functions may inhibit necrosis and death of
cardiomyocytes during I/R.