Mustafa Arslan

Dexmedetomidine decreases emergence agitation in pediatric patients after sevoflurane anesthesia without surgery

Background:  The purpose of the present study was to determine whether prophylactic use of 1 μg·kg−1 dexmedetomidine affected the incidence of emergence agitation (EA) after sevoflurane based anesthesia without surgery in children.

Effects of ovariectomy and ascorbic acid supplement on oxidative stress parameters and bone mineral density in rats.

Objectives The aim of this study is to investigate the effects of ovariectomy on bone mineral density (BMD) and oxidative state in rats, and the alterations in these effects that vitamin C supplementation may produce. Materials and methods Twenty female Wistar albino rats were randomly divided into three groups: control (C, n=6); ovariectomy (O, n=7); and ovariectomy + vitamin C supplement (OV, n=7). Oxidative stress (OS) was assessed 100 days postovariectomy by measuring the activity of several enzymes, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase, as well as the concentrations of malondialdehyde (MDA), nitric oxide (NO), and total sulfhydryl groups in plasma and bone homogenates. Results A significant decrease in BMD was observed in O group compared with C group (p = 0.015), and a significant increase was observed in OV compared with O group (p=0.003). When groups were compared with respect to parameters of OS, MDA and NO levels in bone tissue were significantly higher in O than in C (p=0.032, p=0.022) and were significantly lower in OV than in O (p=0.025, p=0.018). SOD activity was significantly higher in O than in C (p=0.032). In plasma, MDA activity was significantly higher in O than in C (p = 0.022) and NO level was significantly higher in O than in C and OV (p=0.017, p=0.018). Conclusions Our results suggest that ovariectomy may produce osteoporosis and OS in females, and vitamin C supplementation may provide alterations regarding improvement in OS and BMD values. We assume that studies including more subjects are needed to make a decisive conclusion about OS–BMD relation.

The pre-emptive analgesic effect of intra-articular bupivacaine in arthroscopic knee surgery.

Background:  The purpose of this study was to determine whether intra‐articular injection of bupivacaine prior to surgery provided better pain control after arthroscopic meniscectomy as compared with post‐operative administration of bupivacaine.

Dexmedetomidine protects from post-myocardial ischaemia reperfusion lung damage in diabetic rats

Objective Diabetic complications and lipid peroxidation are known to have a close association. Lipid peroxidation commonly occurs at sites exposed to ischaemia, but distant organs and tissues also get damaged during ischaemia/reperfusion (I/R). Some of these targets are vital organs, such as the lung, liver, and kidney; the lung is the most frequently affected. The aim of our study was to investigate the effects of dexmedetomidine on I/R damage in lung tissue and on the oxidant/anti-oxidant system in diabetic rats. Material and methods Diabetes was induced with streptozotocin (55 mg/kg) in 18 Wistar Albino rats, which were then randomly divided into three groups (diabetes control (DC), diabetes plus ischaemia-reperfusion (DIR), and diabetes plus dexmedetomidine-ischaemia/reperfusion (DIRD)) after the effects of diabetes were clearly evident. The rats underwent a left thoracotomy and then ischaemia was produced in the myocardium muscle by a left anterior descending artery ligation for 30 min in the DIR and DIRD groups. I/R was performed for 120 min. The DIRD group received a single intraperitoneal dose of dexmedetomidine (100 µg/kg); the DIR group received no dexmedetomidine. Group DC was evaluated as the diabetic control group and also included six rats (C group) in which diabetes was not induced. These mice underwent only left thoracotomy and were closed without undergoing myocardial ischaemia. Histopathological changes, activities of catalase (CAT) and glutathione-S-transferase anti-oxidant enzymes, and malondialdehyde (MDA) levels were evaluated in the lung tissues of all rats. Results Neutrophil infiltration/aggregation was higher in the DIR group than in the C, DC, and DIRD groups (p=0.001, p=0.013, and p=0.042, respectively). The lung injury score was significantly higher in the DIR group than in the C and DC groups (p<0.0001 and p=0.024, respectively). The levels of MDA were significantly higher in the DIR group than in the C and DIRD groups. CAT activity was significantly higher in the DIR group than in the DIRD and C groups. Conclusion Our results confirm that dexmedetomidine has protective effects against the lung damage resulting from I/R in diabetic rats. Future studies conducted to evaluate the effects of the use of dexmedetomidine on damage to various organs following different I/R durations may help understanding possible protective effects of dexmedetomidine and underlying mechanisms in tissue damage related to I/R injury.Objective Diabetic complications and lipid peroxidation are known to have a close association. Lipid peroxidation commonly occurs at sites exposed to ischaemia, but distant organs and tissues also get damaged during ischaemia/reperfusion (I/R). Some of these targets are vital organs, such as the lung, liver, and kidney; the lung is the most frequently affected. The aim of our study was to investigate the effects of dexmedetomidine on I/R damage in lung tissue and on the oxidant/anti-oxidant system in diabetic rats. Material and methods Diabetes was induced with streptozotocin (55 mg/kg) in 18 Wistar Albino rats, which were then randomly divided into three groups (diabetes control (DC), diabetes plus ischaemia-reperfusion (DIR), and diabetes plus dexmedetomidine-ischaemia/reperfusion (DIRD)) after the effects of diabetes were clearly evident. The rats underwent a left thoracotomy and then ischaemia was produced in the myocardium muscle by a left anterior descending artery ligation for 30 min in the DIR and DIRD groups. I/R was performed for 120 min. The DIRD group received a single intraperitoneal dose of dexmedetomidine (100 µg/kg); the DIR group received no dexmedetomidine. Group DC was evaluated as the diabetic control group and also included six rats (C group) in which diabetes was not induced. These mice underwent only left thoracotomy and were closed without undergoing myocardial ischaemia. Histopathological changes, activities of catalase (CAT) and glutathione-S-transferase anti-oxidant enzymes, and malondialdehyde (MDA) levels were evaluated in the lung tissues of all rats. Results Neutrophil infiltration/aggregation was higher in the DIR group than in the C, DC, and DIRD groups (p=0.001, p=0.013, and p=0.042, respectively). The lung injury score was significantly higher in the DIR group than in the C and DC groups (p<0.0001 and p=0.024, respectively). The levels of MDA were significantly higher in the DIR group than in the C and DIRD groups. CAT activity was significantly higher in the DIR group than in the DIRD and C groups. Conclusion Our results confirm that dexmedetomidine has protective effects against the lung damage resulting from I/R in diabetic rats. Future studies conducted to evaluate the effects of the use of dexmedetomidine on damage to various organs following different I/R durations may help understanding possible protective effects of dexmedetomidine and underlying mechanisms in tissue damage related to I/R injury.

Dexmedetomidine protects against lipid peroxidation and erythrocyte deformability alterations in experimental hepatic ischemia reperfusion injury.

Background : Hepatic ischemia–reperfusion injury is a common clinical problem in hepatic surgery and transplantation. Several cellular and tissue structural and functional alterations are observed in such injury. The aim of this study was to evaluate the effect of dexmedetomidine on lipid peroxidation and erythrocyte deformability during ischemia–reperfusion injury in rats. Methods : Twenty-four Wistar Albino rats were randomly separated into three groups as control (C), ischemia–reperfusion injury (I/R) and dexmedetomidine group (I/R-D). Ischemia was induced with portal clampage for 45 min and reperfusion period was 45 min after declampage. Group I/R-D received dexmedetomidine 100 µg/kg i.p. 30 min before portal clampage. Serum malondialdehyde and superoxide dismutase activities to document lipid peroxidation and erythrocyte deformability index were investigated. Results : Serum superoxide dismutase and malondialdehyde activity levels were significantly higher and erythrocyte deformability index was decreased in hepatic ischemia–reperfusion group. However, these changes were observed to be prevented with dexmedetomidine treatment when given before portal clampage. Conclusion : These findings clearly indicate that erythrocyte deformability index is decreased in hepatic ischemia reperfusion injury and has a potential role to prevent these alterations. The protective effect of dexmedetomidine on hepatic I/R injury is also decreased lipid peroxidation. Further experimental and clinical investigations may clarify the molecular mechanisms and clinical significance of these findings.

Effect of dexmedetomidine on erythrocyte deformability during ischemia-reperfusion injury of liver in diabetic rats.

UNLABELLED The aim of this study is to evaluate the effect of dexmedetomidine on erythrocyte deformability during IR heart injury in diabetic rats. METHODS Eighteen Wistar Albino rats were included in the study after streptozocin (55 mg/kg) treatment for four weeks. In the Group C and DC (sham-control group), the coronary artery was not occluded or reperfused in the control rats. In the Group DIR, a branch of the left coronary artery was occluded for 30 minutes followed by two hours of reperfusion to produce IR. In the Group DIRD, a branch of the left coronary artery was occluded for 30 minutes followed by two hours of reperfusion to produce IR, and dexmedetomidine was administrated via 100 µg/kg IP route 30 minutes before ligating the left coronary artery. Deformability measurements were performed in erythrocyte suspensions containing Htc 5 % in a PBS buffer. RESULTS The deformability index was significantly increased in diabetic rats; however, it was similar in the Group DC and DIRD. It was significantly increased in the Group DIR when compared to the Group C, DIRD and DC. The relative resistance was increased in IR models. CONCLUSION Erythrocyte deformability was decreased in rats having diabetes and IR injury. This injury might lead to further problems in microcirculation. It was shown that dexmedetomidine might be useful in enhancing the adverse effects of this type of injury (Fig. 1, Ref. 39).

Effects of adrenomedullin and vascular endothelial growth factor on ischemia/reperfusion injury in skeletal muscle in rats

BACKGROUND In this study we investigated the effects of adrenomedullin (AM) and vascular endothelial growth factor (VEGF) on skeletal muscle ischemia/reperfusion (I/R) injury in a rat model. MATERIALS AND METHODS Thirty-six Wistar rats were randomized into six groups (n = 6). Laparotomy was performed in all groups under general anesthesia. Nothing else was done in Group S (Sham). The Group I/R underwent I/R performed by clamping and declamping of the infrarenal abdominal aorta for 120 min, respectively. Group VEGF and Group AM received intravenous infusion of VEGF (0.8 μg/kg) or AM (12 μg/kg) respectively, without I/R. Group I/R + VEGF and Group I/R + AM received intravenous infusion of VEGF (0.8 μg/kg) or AM (12 μg/kg) immediately after 2 h period of ischemia, respectively. At the end of reperfusion period, skeletal muscle samples of lower extremity were taken from all groups for biochemical and histopathologic examinations. RESULTS Tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), nitric oxide (NO), and hypoxia inducible factor 1 alpha (HIF 1α) were found to be significantly higher in Group I/R than the levels in Group S (P < 0.05). Tissue levels of MDA, SOD, NO, and HIF 1α were significantly lower in Group I/R + AM compared with the levels in Group I/R (P < 0.05). In Group I/R + VEGF, tissue levels of MDA and NO were significantly lower than the levels in Group I/R (P < 0.05). No statistically significant difference was found in the tissue levels of catalase among the groups. Histologic examination revealed a larger central muscular necrosis than the peripheral necrosis, red blood cells in the lumens of capillary vessels, and a stronger atrophy and elliptical or round shape in muscle fibers in Group I/R. Terminal deoxynucleotidyl transferase mediated dUPT nick end labeling (TUNEL)-positive cell count was significantly lower in groups I/R + AM and I/R + VEGF than Group I/R (P < 0.0001, P < 0.0001, respectively). CONCLUSIONS These results indicate that AM and VEGF have protective effects on I/R injury in skeletal muscle in a rat model.

Synthesis and Pharmacological Evaluation of Some Novel Thebaine Derivatives: N-(Tetrazol-1H-5-yl)-6,14-endoethenotetrahydrothebaine Incorporating the 1,3,4-Oxadiazole or the 1,3,4-Thiadiazole Moiety

In this study, we synthesized some novel N‐(tetrazol‐1H‐5‐yl)‐6,14‐endoethenotetrahydrothebaine 7α‐substituted 1,3,4‐oxadiazole and 1,3,4‐thiadiazole derivatives as potential analgesic agents. The structures of the compounds were established on the basis of their IR, 1H NMR, 13C NMR, 2D NMR, and high‐resolution mass spectral data. The analgesic activity was evaluated by a rat‐hot plate test model and a rat tail‐flick model. Compound 12 showed analgesic activity higher than that of morphine. In addition to a histopathological and biochemical evaluation, the LD50 dose for the most active compound 12 was determined.

The age- and gender-dependent effects of desflurane and sevoflurane on rat liver

OBJECTIVE This study aimed to investigate the age- and gender-dependent effects of desflurane and sevoflurane on the liver. MATERIAL AND METHOD Upon the approval of ethics committee, 84 rats were divided into four groups as 21 young male, 21 young female, 21 old male, and 21 old female rats. Then, each group was further divided into three groups as desflurane, sevoflurane, and control groups. Maintaining the minimum alveolar concentration of 1, desflurane at 6vol% and sevoflurane at 2vol% in 6Lmin(-1) 100% O2 were administered for 2h in a transparent plastic container of 40cmx40cmx70cm. Each liver preparation was evaluated for hydropic degeneration, nuclear polymorphism, portal neutrophile infiltration, portal lymphocyte infiltration, and focal necrosis, and each preparation was assigned injury points of 0-3; thus, the number of histopathologically injured cases, total injury scores of each preparation, and the mean injury scores of each group were determined. RESULTS Desflurane and sevoflurane did not significantly increase hepatic injury in the young male rats, while both agents caused significantly more hepatic injury in the young female rats. In the old rats, both desflurane and sevoflurane inflicted more hepatic injury on both genders. In addition, desflurane caused more hepatic injury in the old female rats than in the young female or the old male rats. CONCLUSION Hepatic injury associated with desflurane and sevoflurane was mild to moderate, suggesting that both agents can be safely used in routine anaesthesia procedures.

The effect of levosimendan on lung damage after myocardial ischemia reperfusion in rats in which experimental diabetes was induced

BACKGROUND It is known that diabetic complications and lipid peroxidation are closely associated. During ischemia and reperfusion (IR), injury may occur in distant organs, as well as in tissues next to the region exposed to the ischemia, and the lungs can be one of the most affected of these organs. Therefore, this study investigated the effects of levosimendan on lung tissue and the oxidant-antioxidant system in diabetic rats. MATERIALS AND METHODS The study was conducted in 24 Wistar albino rats that were separated into four groups (C, control; DC, diabetic control; DIR, diabetic IR; and DIRL, diabetic IR levosimendan). Diabetes was induced in 18 rats using streptozotocin (55 mg/kg), and the animals were randomly separated into three groups after the effects of the diabetes became apparent. After a left thoracotomy, ischemia was performed on the myocardial muscle with the left main coronary artery (LAD) for 30 min in the DIR and DIRL groups. After ischemia, the LAD ligation was removed, and reperfusion was applied for 120 min. Single-dose intraperitoneal 12 μg/kg levosimendan was administered to group DIRL before the ischemia. Group DC was evaluated as the diabetic control group, and six rats were considered to be the control group (group C), in which thoracotomy was performed and then closed with no induction of myocardial ischemia. We measured the levels of malondialdehyde, as a lipid peroxidation end product, as well as catalase and glutathione S-transferase activities, as antioxidant enzymes in the lung tissue. Tissue samples were also examined histopathologically. RESULTS Neutrophil infiltration or aggregation in lung tissue was significantly higher in the DIR group compared with the C, DC, and DIRL groups (P = 0.003, P = 0.026, and P = 0.026, respectively). Alveolar wall thickening in lung tissue was significantly higher in the DIR group compared with the C, DC, and DIRL groups (P = 0.002, P = 0.002, and P = 0.006, respectively). In addition, the lung tissue damage score was significantly higher in the DIR group compared with the C, DC, and DIRL groups (P = 0.001, P = 0.004, and P = 0.007, respectively). Finally, catalase and glutathione S-transferase activity levels were significantly higher in the DIR group compared with those observed in the C, DC, and DIRL groups. CONCLUSIONS Although diabetes increases lipid peroxidation, it suppresses antioxidant activity. Our results showed that levosimendan had a protective effect against lung damage secondary to IR in the rats with induced diabetes. We recommend that experimental and clinical studies be conducted to examine the effects of levosimendan at different doses and different IR durations on various organs for clinical use.