The Effects of Dexmedetomidine and Ketamine on Oxidative Injuries and Histological Changes Following Blunt Chest Trauma.

BACKGROUND: The objective of this research was to evaluate the oxidative and histopathological effects of dexmedetomidine and ketamine on the pulmonary contusion model resulting from blunt chest trauma. METHODS: Rats were randomly assigned to 5 equal groups (n=6): control group (Group C), pulmonary contusion group (Group PC), PC-dexmedetomidine group (Group PC-D), PC-ketamine group (Group PC-K), and PC-dexmedetomidine + ketamine (Group PC-D+K). The PC was performed by dropping a weight of 500 g (2.45 Joules) from a height of 50 cm. In Group PC-D, after chest trauma, dexmedetomidine (100 µg/kg) was administered intraperitoneally. In Group PC-K, after chest trauma, ketamine (100 mg/kg) was administered intraperitoneally. In Group PC-D+K, dexmedetomidine and ketamine were administered together. At the end of the 6th hour, rats were sacrificed. Malondialdehyde (MDA) level, superoxide dismutase (SOD) enzyme activities, neutrophil infiltration/aggregation, and thickness of the alveolar wall were evaluated. RESULTS: MDA levels were significantly higher in Group PC than Groups C, PC-D, and PC-D+K. SOD enzyme activity was significantly higher in Group PC than Groups C, PC-D, and PC-D+K. In addition, neutrophil infiltration/aggregation and total pulmonary injury scores were significantly higher in Group PC than in other groups, and the thickness of the alveolar wall was significantly higher in Group PC compared to Groups C, PC-D, and PC-D+K. MDA level, SOD enzyme activities, neutrophil infiltration/aggregation, and thickness of alveolar wall were similar in PC-D and PC-D+K groups. CONCLUSION: Dexmedetomidine and dexmedetomidine+ketamine have protective effects on blunt chest trauma but no protective effect was observed when ketamine was administered alone. We concluded that the administration of dexmedetomidine and ketamine after contusion is beneficial against pulmonary injury in rats.

Protective effect of chlorogenic acid on renal ischemia/reperfusion injury in rats.

OBJECTIVES: Ischemia/reperfusion (I/R) injury is a common cause of renal injury and to date, many pharmacological agents have been identified to decrease I/R injury. One of the potential compound that can target I/R injury is chlorogenic acid (CGA). It has potent antiinflammatory, antibacterial, anti-oxidant, analgesic and antipyretic activities in in vitro experiments and in vivo animal models. The aim of the study was to investigate the protective characteristic of CGA on renal I/R injury. MATERIAL AND METHODS: 24 rats were randomly allocated to three groups (n = 8): Sham, I/R+CGA and I/R groups. CGA was administered intraperitoneally at a dose of 20 mg/kg, 10 min before reperfusion. I/R injury was achieved by clamping the left renal artery for 45 minutes, followed by reperfusion for 4 hours. The left kidneys of the rats were examined for tissue damage by histopathological and biochemical examination. For histological evaluation, EGTI scoring system was used. For biochemical examination total oxidant status, total antioxidant status and oxidative stress index were used. The power analysis indicated that 8 subjects per group would be required to produce 80% chance of achieving statistical significance at p < 0.05 level. The results are expressed as mean ± SD. Mann- Whitney U was performed for statistical analysis. RESULTS: Histopathological examination of the tissue damage revealed that all kidneys in the sham group were normal. I-R group had significantly higher histopathological scores than other groups. Histopathological improvement was seen after CGA treatment. TAS, TOS and OSI values of I-R group were significantly higher than sham group (0.88 vs 0.76 (p: 0.004), 13.8 vs 7.04 (p: 0.021) and 0.15 vs 0.09 (p: 0.034), respectively). In CGA treated group TAS, TOS and OSI levels were 0.84, 6.47 and 0.07, respectively. CGA treatment resulted in significant improvement in TOS and OSI parameters. CONCLUSIONS: CGA treatment provided marked improvement in renal histology and suppressed oxidative stress. Thus, CGA may have a protective effect in renal tissue against I/R injury.