Effect of melatonin on antioxidant capacity, inflammation and apoptotic cell death in lung tissue of diabetic rats

Abstract Purpose: To investigate the effects of melatonin on antioxidant capacity, inflammation and apoptotic cell death (through expression of cleaved-caspase 3) in lung tissue samples of diabetic rats. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups. Group 1 (control group) was made up of healthy rats. Group 2 (diabetes group) received streptozotocin at a dose of 50 mg/kg/day for 5 days.Group 3 (diabetes plus melatonin group) received streptozotocin at a dose of 50 mg/kg/day for 5 days and then they received melatonin at a dose of 20 mg/kg/day between 28thand 35thdays of the study. Results: Tissue MDA and MPO levels were found to be significantly higher in diabetes group compared to control group (p<0.05) whilst administration of melatonin was found to significantly lower this increase down to normal levels (p<0.05). Bronchus associated lymphoid tissue (BALT) was more severe in diabetics whereas administration of melatonin alleviated this hyperplasia. Cleaved caspase 3 activity was severe in hyperplastic BALT in diabetic rats however in lowered down to moderate level when melatonin was administered. Conclusion: The melatonin caused an increase in antioxidant capacity and decreased the expression of cleaved-caspase 3.

A comparison of the effects of desflurane, sevoflurane and propofol on QT, QTc, and P dispersion on ECG.

The aim of this prospective, randomized, and double-blinded study was to compare the effects of desflurane, sevoflurane, propofol on both atrial and ventricular wall function by measurement of QT dispersion (QTd), corrected QT dispersion (QTcd), and P dispersion (Pd) on electrocardiogram (ECG). Forty-six patients from the American Society of Anesthesiologists class I−II undergoing noncardiac surgery, were enrolled in this study. Patients were randomly allocated to receive desflurane, sevoflurane or propofol anesthesia. ECG recordings were taken before and after 5 minutes of drug administration. Induction with desflurane significantly increased the QTd compared to baseline (38 ± 2 ms vs. 62 ± 6 ms, P < 0.05). Sevoflurane and propofol anesthesia was not associated with any changes in QTd. QTcd was increased with desflurane induction and decreased with sevoflurane and propofol induction, but this decrease was only significant in the propofol group (67 ± 5 ms vs. 45 ± 3 ms, P < 0.05). Pd was significantly increased after induction with desflurane (34 ± 3 vs. 63 ± 6 ms, P < 0.05). There was a significant increase in QTd and Pd in desflurane group, but this increment did not cause any dangerous arrhythmias. QTcd significantly decreased in propofol group. We believe that further investigations are required for using desflurane as safe as sevoflurane and propofol in noncardiac surgery patients who have high cardiac arrhythmia and ischemia risk.