Volkan Hancı

Effects of dexmedetomidine or methylprednisolone on inflammatory responses in spinal cord injury

Background: The aim of this study was to compare the anti‐inflammatory response of methylprednisolone and the α2‐agonist dexmedetomidine in spinal cord injury (SCI).

Fournier's Gangrene: Overview of Prognostic Factors and Definition of New Prognostic Parameter

OBJECTIVES To identify the prognostic factors and the new parameters that might predict a worse outcome in nonsurvivors compared with survivors of Fourniers gangrene (FG) and evaluated the validity of the Fourniers Gangrene Severity Index (FGSI) in patients with FG. METHODS The medical records of 18 patients with FG who were treated and followed up in our clinic were reviewed. Data were collected in terms of medical history, symptoms, and physical examination findings. The biochemical, hematologic, and bacteriologic study (aerobic and anaeorobic wound cultures) results at admission and at the final evaluation, the physical examination findings, the timing and extent of surgical debridement, and the antibiotic therapy were also recorded. The Charlson Comorbidity Index (CCI) and FGSI were evaluated stratified by survival. RESULTS The results were evaluated for 2 groups: those who survived (n = 14) and those who did not (n = 4). The admission FGSI score was 5.00 +/- 2.91 (range 0-10) for survivors compared with 13.5 +/- 2.62 (range 9-15) for nonsurvivors (P = .001). The CCI score was 3 +/- 1.5 in survivors and 7 +/- 2.2 in nonsurvivors (P = .008). Individual laboratory parameters such as hypomagnesemia, hemoglobin, hematocrit, alkaline phosphatase, creatinine, and the heart and respiratory rates were associated with a worse prognosis. In addition, a FGSI >9, rectal involvement, colostomy diversion, and a high CCI were associated with high mortality. CONCLUSIONS Low magnesium levels might be a new parameter for a worse prognosis. High CCI and FGSI scores might be associated with a worse prognosis in patients with FG. A FGSI threshold of 9 was a predictor of mortality during the initial assessment.

Effect of Dexmedetomidine on Testicular Torsion/Detorsion Damage in Rats

Background and Objective: We assessed the antioxidant activity of dexmedetomidine (DEX) during an ischemic period in a rat model of testicular torsion/detorsion (T/DT) by using biochemical and histopathological methods. Methods: Wistar Albino male rats weighing 250–300 g were divided into three groups: sham (group S, n = 7); torsion/detorsion (group T/DT, n = 7), and DEX treatment (group DEX, n = 7). In the T/DT group, right testes were rotated 720° for 1 h. Group S served for normal basal values. Rats in group T/DT were operated to make T/DT, this group served as a control group. Group DEX received intraperitoneal DEX 10 µg · kg–1 after the 30-min torsion period. For measurement of total antioxidant enzyme activities and malondialdehyde (MDA) levels, testes of 7 animals in each group were excised after 4 h of reperfusion. Germ cell apoptosis was evaluated using the apoptosis protease-activating factor 1 (APAF-1) antibody in all groups and also on the expressions of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) were assessed within the bilateral testes. Results: Mean MDA levels in group T/DT were significantly higher than in groups S and DEX (p < 0.05). There were also significant decreases in mean total antioxidant activities in group T/DT when compared to groups S and DEX (p < 0.05). These values were significantly higher in group DEX than group T/DT. Germ cell apoptosis, eNOS and iNOS levels were significantly higher in group T/DT when compared to groups S and DEX (p < 0.05). Conclusions: DEX treatment has potential biochemical and histopathological benefits by preventing ischemia/reperfusion-related cellular damage in an experimental testicular torsion model. Preference of DEX for anesthesia during the detorsion procedure may attenuate ischemia-reperfusion injury.

Vardenafil Reduces Testicular Damage Following Ischemia/Reperfusion Injury in Rats

We investigated the effect of intraperitoneal vardenafil (1 mg/kg) administration during an ischemic period in a rat model of testicular torsion/detorsion (T/D). Twenty‐one adult Wistar rats were equally randomized into a control group, a T/D group and a vardenafil group. The control group was designed to collect basal values for biochemical and histopathological parameters. The T/D group underwent testicular torsion for 1 hour. The vardenafil group received vardenafil (1mg/kg) intraperitoneally at 30 minutes after torsion. All rats were sacrificed 4 hours after reperfusion to evaluate the tissue levels of malondialdehyde and total antioxidant status. Germ cell apoptosis was evaluated using the apoptosis protease activating factor 1 antibody in all groups. The expressions of endothelial nitric oxide synthase (NOS) and inducible NOS were also assessed in both testes of all rats. The malondialdehyde levels in the T/D group were significantly higher than in the control and vardenafil groups. There were also significant decreases in total antioxidant status in the T/D group compared with the control and vardenafil groups. Vardenafil treatment significantly reduced apoptosis protease activating factor 1, endothelial NOS and inducible NOS levels in the vardenafil group compared with the T/D group. Administration of 1 mg/kg vardenafil during testicular torsion decreased ischemia/reperfusion cellular damage. Our results indicate that the reduction in oxidative stress by vardenafil may play a major role in its cytoprotective effects.

Effect of coenzyme Q10 on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats.

BackgroundHead trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ10 in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ10 administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out.ResultsIn the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group (p < 0.05). Administration of CoQ10 after trauma was shown to be protective because it significantly lowered the increased MDA levels (p < 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ10 group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ10 and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (p < 0.05).ConclusionNeuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ10 use in rats with traumatic brain injury.

The effects of dexmedetomidine on mesenteric arterial occlusion-associated gut ischemia and reperfusion-induced gut and kidney injury in rabbits.

OBJECTIVE We assessed the antioxidant activity of dexmedetomidine (Dex) administered during the ischemic period in a rabbit model of mesenteric ischemia/reperfusion (I/R) injury using biochemical and histopathological methods. METHODS A total of 24 male New Zealand white rabbits weighing between 2.5 and 3.0 kg were randomly divided into three groups: the sham group (Group S, n = 8), the I/R group (Group I/R, n = 8), and the I/R plus Dex treatment group (Group Dex, n = 8). In the I/R group, ischemia was achieved with 60 min of mesenteric occlusion. The sham group provided normal basal values. The rabbits in Group I/R were operated to achieve I/R. Group Dex received intravenous Dex 30 min after the commencement of reperfusion (10 μg/kg Dex was infused within 10 min, and then a maintenance dose of 10 μg/kg/h Dex was infused intravenously). For the measurement of tissue malondialdehyde, total antioxidant status, total oxidant status, lipid hydroperoxide levels, superoxide dismutase, catalase, and myeloperoxidase activity levels in the renal tissue samples of animals, the rabbits in each group were sacrificed 3 h after reperfusion. The histopathological examination scores were determined using the intestinal and renal tissues. RESULTS The mean malondialdehyde, total oxidant status, myeloperoxidase, and lipid hydroperoxide levels were significantly higher in Group I/R than in Groups S and Dex (P < 0.05). There also were significant decreases in the mean total antioxidant status, catalase, and superoxide dismutase activities in Group I/R compared with Groups S and Dex (P < 0.05). The histopathological examination scores of the intestinal and renal tissues were significantly higher in Group I/R compared with Groups S and Dex (P < 0.05). CONCLUSION Dex treatment may have biochemical and histopathological benefits by preventing I/R-related cellular damage of intestinal and renal tissues as shown in an experimental mesenteric ischemia model. The preference to use Dex for anesthesia during the mesenteric ischemia procedure may attenuate I/R injury in intestinal and renal tissues.

Coenzyme Q10 treatment reduces lipid peroxidation, inducible and endothelial nitric oxide synthases, and germ cell–specific apoptosis in a rat model of testicular ischemia/reperfusion injury

In this experimental study, we assessed the preventive effects of coenzyme Q(10) (CoQ(10)) in a rat model of ischemia/reperfusion injury. The results of this study show that CoQ(10) administration before the reperfusion period of testicular torsion provides a significant decrease in testicular lipid peroxidation products and expressions of inducible nitric oxide synthase, endothelial nitric oxide synthase, and germ cell-specific apoptosis.

Effects of Fentanyl-lidocaine-propofol and Dexmedetomidine-lidocaine-propofol on Tracheal Intubation Without Use of Muscle Relaxants

The aim of this study was to compare the effects of fentanyl or dexmedetomidine when used in combination with propofol and lidocaine for tracheal intubation without using muscle relaxants. Sixty patients with American Society of Anesthesiologists stage I risk were randomized to receive 1 mg/kg dexmedetomidine (Group D, n = 30) or 2 mg/kg fentanyl (Group F, n = 30), both in combination with 1.5 mg/kg lidocaine and 3 mg/kg propofol. The requirement for intubation was determined based on mask ventilation capability, jaw motility, position of the vocal cords and the patients response to intubation and inflation of the endotracheal tube cuff. Systolic arterial pressure, mean arterial pressure, heart rate and peripheral oxygen saturation values were also recorded. Rate pressure products were calculated. Jaw relaxation, position of the vocal cords and patients response to intubation and inflation of the endotracheal tube cuff were significantly better in Group D than in Group F (p < 0.05). The intubation conditions were significantly more satisfactory in Group D than in Group F (p = 0.01). Heart rate was significantly lower in Group D than in Group F after the administration of the study drugs and intubation (p < 0.05). Mean arterial pressure was significantly lower in Group F than in Group D after propofol injection and at 3 and 5 minutes after intubation (p < 0.05). After intubation, the rate pressure product values were significantly lower in Group D than in Group F (p < 0.05). We conclude that endotracheal intubation was better with the dexmedetomidine–lidocaine–propofol combination than with the fentanyl–lidocaine–propofol combination. However, side effects such as bradycardia should be considered when using dexmedetomidine.

Protective effect of dexmedetomidine in a rat model of α-naphthylthiourea–induced acute lung injury

BACKGROUND We assessed the effects of dexmedetomidine in a rat model of α-naphthylthiourea (ANTU)-induced acute lung injury. METHODS Forty Wistar Albino male rats weighing 200-240 g were divided into 5 groups (n = 8 each), including a control group. Thus, there were one ANTU group and three dexmedetomidine groups (10-, 50-, and 100-μg/kg treatment groups), plus a control group. The control group provided the normal base values. The rats in the ANTU group were given 10 mg/kg of ANTU intraperitoneally and the three treatment groups received 10, 50, or 100 μg/kg of dexmedetomidine intraperitoneally 30 min before ANTU application. The rat body weight (BW), pleural effusion (PE), and lung weight (LW) of each group were measured 4 h after ANTU administration. The histopathologic changes were evaluated using hematoxylin-eosin staining. RESULTS The mean PE, LW, LW/BW, and PE/BW measurements in the ANTU group were significantly greater than in the control groups and all dexmedetomidine treatment groups (P < 0.05). There were also significant decreases in the mean PE, LW, LW/BW and PE/BW values in the dexmedetomidine 50-μg/kg group compared with those in the ANTU group (P < 0.01). The inflammation, hemorrhage, and edema scores in the ANTU group were significantly greater than those in the control or dexmedetomidine 50-μg/kg group (P < 0.01). CONCLUSION Dexmedetomidine treatment has demonstrated a potential benefit by preventing ANTU-induced acute lung injury in an experimental rat model. Dexmedetomidine could have a potential protective effect on acute lung injury in intensive care patients.

The effects of dexmedetomidine dosage on cerebral vasospasm in a rat subarachnoid haemorrhage model.

We investigated the effect of two different doses of dexmedetomidine on vasospasm in a rat model of subarachnoid haemorrhage (SAH). SAH was induced by injecting 0.3 mL blood into the cisterna magna in all rat groups except the control (Group C). At 1 hour and 24 hours after SAH, 5 microg/kg dexmedetomidine was given to group D5, and 10 microg/kg dexmedetomidine was given to group D10. No medication was administered to the haemorrhage group (Group H). Malondialdehyde (MDA) and paraoxonase (PON) levels were measured at 48 hours after SAH. Mean wall thickness (MWT), mean luminal diameter (MLD), and proliferating cell nuclear antigen (PCNA) expression of the basilar artery were evaluated. MDA levels and MWT were lower in the dexmedetomidine groups. The lowest MDA levels and MWT were found in Group D10. The MLD was lowest in Group H. PCNA expression was observed only in Group D10. We concluded that dexmedetomidine reduces oxidative stress and vasospasm following SAH in a dose-dependent manner.