Background: The two main factors concerned with the experimental generation of reperfusion damage are oxygen-derived free radicals and cytosolic calcium overload. The pineal hormone, melatonin, is known to be a potent free radical scavenger and its pharmacological concentrations have been shown to reduce the ischemia-reperfusion-induced necrosis in isolated rat hearts. However, the physiological role of melatonin in the prevention of these damage is unknown. This study was designed to investigate the effects of physiological concentrations of melatonin on the ischemia-reperfusion-induced necrosis in an in vivo rat model.

Material and Method: Rats were pinealectomized or sham-operated (control) two months before the ischemia-reperfusion studies. To produce necrosis, left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. This study was designed to investigate the effects of physiological concentrations of melatonin on the ischemia-reperfusion-induced necrosis in an in vivo rat model. To examine this, we used pinealectomized (Px) and sham-operated (non-Px) rats in the study.

Results: Infarct size was found significantly higher in pinealectomized rats (49±3.4 %) than control group (34±3.6 %), analyzed by one-way ANOVA.

Conclusions: These results show that physiological melatonin concentrations would seem important to reduce the ischemia-reperfusion-induced infarct size. Since melatonin levels have been reported to decrease with age, melatonin replacement therapy may attenuate reperfüzyon injury especially in older patients.