Sclerostin and bone metabolism markers in hyperthyroidism before treatment and interrelations between them.

Sclerostin, which is a glycoprotein produced by osteocytes, reduces the formation of bones by inhibiting the Wnt signal pathway. Thyroid hormones are related with Wnt signal pathway and it has been reported that increased thyroid hormones in hyperthyroidism fasten epiphysis maturation in childhood, and increase the risk of bone fractures by stimulating the bone loss in adults. The aim of this study was to examine the sclerostin serum levels, the relation between sclerostin and thyroid hormones as well as the biochemical markers of the bone metabolism in patients with hyperthyroidism (including multinodular goiter and Graves' disease), whose treatments have not started yet. No difference was found in the serum sclerostin levels between the hyperthyroidism group (n=24) and the control group (n=24) (p=0.452). The serum osteocalcin levels and 24-hour urinary phosphorus excretion were found to be higher in the hyperthyroid group than in the control group (p<0.001, p=0.009). A positive correlation was determined between the sclerostin and bone alkaline phosphatase levels (p<0.001); a negative correlation between the osteocalcin and thyroid stimulating hormone (TSH) (p<0.05); a positive correlation between the osteocalcin and thyroid hormones (FT3,FT4) (p<0.001); and a positive correlation between the deoxypyridinoline and hydroxyproline (p<0.001). No correlation was determined between sclerostin and TSH,FT3,FT4 (p>0.05). Therefore, we consider that a long-term study that covers the pre-post treatment stages of hyperthyroidism, including both the destruction and construction of the skeleton would be more enlightening. Moreover, the assessment of the synthesis of sclerostin in the bone tissue and in the serum level might show differences.

Evaluation of Serum Fetuin-A and Osteoprotegerin Levels in Patients with Psoriasis.

Psoriasis patients are determined to have a high ratio of coronary artery calcification. Fetuin-A and osteoprotegerin are systemic calcification inhibitors and related to vascular calcification and cardiovascular mortality. In this study we investigated the relationship between fetuin-A and osteoprotegerin levels in psoriasis patients. The study included 40 healthy volunteers and 40 psoriasis patients. Venous blood were collected from healthy volunteers and psoriasis patients in order to search the fetuin-A and osteoprotegerin levels. Disease severity were grouped as mild, moderate and severe according to psoriasis area and severity index (PASI). The relationship between fetuin-A and osteoprotegerin levels and clinical features as sex, PASI and presence of psoriatic arthritis were analyzed. Fetuin-A levels in psoriasis patients were statistically lower than the control group (p < 0.001). In serum osteoprotegerin levels, no statistically significant difference was found in two groups (p > 0.05). Serum fetuin-A and osteoprotegerin level differences were not statistically significant between patients with psoriatic arthritis history and those without. When we grouped patients in respect of their sexes fetuin-A and osteoprotegerin levels of males and females were not significantly different (p > 0.05). No correlation was detected between the ages and PASI scores and the fetuin-A and osteoprotegerin levels of patients. As a result fetuin-A levels in psoriasis patients are found to be low but not related to disease severity. In the light of our results we concluded that fetuin-A may have a role in psoriasis pathogenesis and may contribute to the calcification process developed in psoriasis.

Leptin levels in children with obstructive sleep apnea syndrome.

INTRODUCTION: The aim of this study is to assess the effect of obstructive sleep apnea syndrome (OSAS) severity on leptin levels in children. PATIENTS AND METHODS: Children with habitual snoring underwent overnight polysomnography. Fasting venous blood samples were obtained between 8 AM and 9 AM, following the night of the sleep study. Children with an apnea-hypopnea index of ≥ 5/h were included in the moderate-to-severe OSAS group while those with an apnea-hypopnea index of < 5/h formed the mild OSAS/primary snoring group. RESULT: 47 children (51% male and 49% female; mean age 7.8 ± 2.6 years) were recruited. Twenty seven participants were diagnosed with moderate-to-severe OSAS, and twenty children who had AHI < 5 were included in the mild OSAS/primary snoring. The two groups did not differ regarding age, gender and body mass index z score (p> 0.05). Furthermore there were no differences in log serum leptin levels (p= 0.749). Log serum leptin levels correlated with the BMI z score in the whole study group (p= 0.001; r= 0.499) but they were not associated with apnea-hypopnea index, mean and lowest oxygen saturation during sleep. CONCLUSIONS: Serum leptin levels are affected by adiposity but not by OSAS severity among children with habitual snoring.

Apoptosis and necrosis in the circumventricular organs after experimental subarachnoid hemorrhage as detected with annexin V and caspase 3 immunostaining.

OBJECTIVES: The circumventricular organs (CVOs) are essential for most autonomic and endocrine functions. Trauma and bleeding can affect their function. The aim of this study was to investigate apoptosis and necrosis in CVOs in the early period after experimental subarachnoid hemorrhage (SAH) in rats, using annexin V affinity and caspase 3 immunostaining. METHODS: Three experimental groups were used: Days 1 and 2 after SAH, and a control group, seven Wistar albino rats each. Subarachnoid hemorrhage was accomplished by transclival basilar artery puncture. Rats were perfused with 0.9% NaCl and 0·1M phosphate buffer pH 7.4 until heart stoppage. Apoptosis and necrosis in CVOs were measured by flow cytometry with annexin V staining, and by caspase 3 immunostaining. RESULTS: Apoptosis in the organum vasculosum lamina terminalis (OVLT), median eminence (ME), and area postrema (AP) was significantly higher in the Day 1 group than in the control group. Apoptosis in the subfornicial organ (SFO), OVLT, ME, and AP was significantly higher in the Day 2 group than in the control group. There were significant differences between the Day 1 and Day 2 groups, except for AP. Necrosis in SFO and OVLT was significantly higher in the Day 2 group than in the Day 1 or control groups, whereas necrosis in the ME and AP did not differ between the three groups. Caspase 3-positive cell density was more intense in the Day 2 group than in the Day 1 and control groups. DISCUSSION: Prevention of apoptosis may potentially improve impaired functions of CVOs after SAH.

Ischemia modified albumin increase indicating cardiac damage after experimental subarachnoid hemorrhage.

BACKGROUND: Cardiac complications are often developed after subarachnoid hemorrhage (SAH) and may cause sudden death of the patient. There are reports in the literature addressing ischemia modified albumin (IMA) as an early and useful marker in the diagnosis of ischemic heart events. The aim of this study is to evaluate serum IMA by using the albumin cobalt binding (ACB) test in the first, second, and seventh days of experimental SAH in rats.Twenty-eight Wistar albino rats were divided into four groups each consisting of seven animals. These were classified as control group, 1st, 2nd and 7th day SAH groups. SAH was done by transclival basilar artery puncture. Blood samples were collected under anesthesia from the left ventricles of the heart using the cardiac puncture method for IMA measurement. Histopathological examinations were performed on the heart and lung tissues. Albumin with by colorimetric, creatine kinase (CK), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) were determined on an automatic analyser using the enzymatic method. IMA using by ACB test was detected with spectrophotometer. RESULTS: Serum IMA (p = 0.044) in seventh day of SAH were higher compared to the control group. Total injury scores of heart and lung tissue, also myocytolysis at day 7 were significantly higher than control group (p = 0.001, p = 0.001, p = 0.001), day 1 (p = 0.001, p = 0.001, p = 0.001) and day 2 (p = 0.001, p = 0.007, p = 0.001). A positive correlation between IMA - myocytolysis (r = 0.48, p = 0.008), and between IMA - heart tissue total injury score (r = 0.41, p = 0.029) was found. CONCLUSION: The results revealed that increased serum IMA may be related to myocardial stress after SAH.

Cystain C and neuropeptid Y levels in brain tissues after experimental subarachnoid hemorrhage.

The aim of this study was to investigate the changes in the levels of cystatin C, which protects neurodegeneration in the central nervous system with the inhibition of cysteine protease and by inducing autophagy in the pathogenesis of cerebral vasospasm and levels of vasoconstrictive neuropeptid Y (NPY) in the brain tissue homogenates of rat model of subarachnoid hemorrhage (SAH). Three experimental groups were used: Day 2 and Day 7 groups after SAH, and also a control group. There were seven Wistar albino rats in each group. SAH was accomplished by transclival basilar artery puncture. Rat cystatin C, rat NPY were determined with ELISA in brain tissue homogenates. Day 2 group showed significantly enhanced cystatin C values in comparision with the control group (P=0.048). NPY levels between the Day 2 and Day 7 groups and the control groups were not significantly different (P=0.315). In histopathological examination, there was less neuronal loss in the Day 2 group than in the Day 7 group. Regarding our results, it would be more valuable to measure NPY levels in specific brain areas. The increased cystatin C levels on the second day after SAH is probably a pathophysiologic mechanism to organize protease activity.

Determinants of plasma homocysteine in coal miners.

AIM: Several studies suggest that coal miners are under risk of severe health problems such as cardiovascular, pulmonary, neurological, renal, hematological and musculoskeletal disorders. However, there are limited data on biochemical changes in underground workers. In our study we aimed to evaluate the association between serum homocysteine (Hcy), vitamin B12, cystatin C and folate levels in the blood of underground coal miners. MATERIALS AND METHODS: Eighty one coal miners who work as underground or surface workers were recruited into our study. The study population was divided into two groups: the surface worker group (control group, n=33) and the underground worker group (n=48). The folate, vitamin B12, Hcy, cystatin C levels and body mass indexes (BMI) of both groups were measured and compared. Serum folate, Hcy and vitamin B12 levels were measured with a competitive chemiluminescence immunassay. Serum levels of cystatin C were determined by the latex particle-enhanced turbidimetric method using a cystatin C kit. Urea values were measured with a kinetic method on an automated analyzer. RESULTS: There were no statistically significant differences between the underground workers and surface workers in the urea, cystatin C and vitamin B12 levels. High serum Hcy levels and low folate levels were found in underground workers compared with those in surface workers. The correlation between Hcy and folate levels was also statistically significant. Similarly, there was also a significant correlation between Hcy and vitamin B12, and between Hcy and cystatin C levels. CONCLUSIONS: Elevated Hcy levels may be associated with underground working but further research is necessary to understand the relation between elevated Hcy and increased prevalence of health problems in coal miners.

Levels of oxidized LDL, estrogens, and progesterone in placenta tissues and serum paraoxonase activity in preeclampsia.

In vitro literature studies have suggested that atherosclerotic oxidized low density lipoprotein (OxLDL) inhibits trophoblast invasion. The objective of this study was to determine the levels of OxLDL and to examine the relationship between antioxidative estradiol, estriol, and prooxidative progestin in normal and preeclamptic placental tissues and measure the serum activity of antioxidative paraoxonase (PON1). The study included 30 preeclamptic and 32 normal pregnant women. OxLDL was determined with ELISA, estradiol, unconjugated estriol, and progesterone that were determined with chemiluminescence method in placental tissues. Serum PON1 activity was determined with spectrophotometric method. Levels of OxLDL (P = 0.027), estriol (P < 0.001), estradiol (P = 0.008), and progesterone (P = 0.009) were lower in the placental tissues of preeclamptic group compared to the normal pregnant women. Serum PON1 activity was higher in preeclamptic group (P = 0.040) and preeclamptic group without intrauterine growth restriction (P = 0.008) compared to normal pregnant women. Tissue estriol of preeclamptic group without/with IUGR (P < 0.001, P = 0.002) was lower than the normal group. Results of our study suggest that the events leading to fetoplacental insufficiency lead to a reduction in the levels of estriol limit deposition of OxLDL in placental tissues. The serum PON1 activity is probably important in the inhibition of OxLDL in preeclampsia.

Evaluation of serum lipid levels in children.

This study aimed to establish reference values for serum levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in children. The study included samples from 4,102 healthy children (2,003 boys and 2,099 girls) ages 1-18 years. The serum levels of total cholesterol, triglycerides, and HDL-C were determined using the Advia 2400 autoanalyzer. The LDL-C levels were calculated using the Friedewald equation. The mean, standard deviation, and 5th, 10th, 25th, 50th, 75th, 90th, and 95th percentile values of the biochemical parameters for boys and girls were detected. The total cholesterol and HDL-C levels were higher among the girls than among the boys in 15- to 18-year-old group. No significant difference was found for the other serum lipid levels among any of the age groups. This study provided pediatric reference intervals for the lipid parameters for children.

High mobility group B1 levels in sepsis and Disseminated Intravascular Coagulation.

Cytokines trigger coagulant and fibrinolytic systems in sepsis to result in Disseminated Intravascular Coagulation (DIC) that is an important complication and leads to disseminated hemorrhages and multi-organ failure. High Mobility Group B1 DNA Binding (HMGB1) protein is a cytokine taking part in systemic inflammatory response. The objective of this study was to investigate HMGB1 levels in groups of septic patients with and without DIC.Twenty-one septic patients without DIC and 12 septic patients with DIC from the Intensive Care Unit (ICU) were included in the study. In addition, 20 patients admitted to the ICU without sepsis or DIC and 20 healthy volunteers served as controls. Levels of HMGB1, prothrombin time, activated partial thromboplastin time, fibrinogen, D-dimer, protein C, protein S, anti-thrombin III (ATIII), platelet (thrombocyte) and leukocyte count were determined. Levels of fibrinogen, protein C, ATIII and platelet count were significantly lower and D-dimer was significantly higher in the group with sepsis plus DIC compared to the group with sepsis without DIC. Levels of HMGB1 were higher in the group with sepsis and DIC compared to the group with sepsis; however, the difference was not statistically significant and the levels of HGMB1 of both groups were significantly higher compared to ICU and healthy control groups. HMGB1 levels were not significantly different in survivor and non survivor patients. HMGB1 levels did not differ in lower respiratory tract infection (LRTI) and urinary tract infection (UTI) in regard to the etiology of sepsis.

Placental prostate-specific antigen content in preeclampsia.

Preeclampsia is a multisystem disorder that can manifest clinically with hypertension and proteinuria. Previous studies reported the presence of placental PSA in normal pregnancy but no study has been done in preeclampsia. The aim of this study was to investigate PSA content in preeclampsia. Preeclampsia was diagnosed according to the American College of Obstetricians and Gynecologists criteria. Placentas were obtained from 33 preeclamptic and 34 normotensive women. Placenta samples were homogenized and the supernatants were immediately analyzed. The tissue PSA content was measured by Immulite 2000 PSA assay. The data were analyzed with Student's t-test and Pearson correlation test. There was a significant difference in placental PSA content between preeclamptic and normotensive women. Placental content of PSA was higher in the preeclamptic group with intrauterine growth restriction (IUGR) than in the preeclamptic and normotensive pregnant without IUGR groups. No significant difference was found in this respect between preeclamptic and normotensive women without IUGR. In conclusion, we found that placental PSA content is elevated in preeclampsia and negatively correlated with infant birth weight. Further studies will be necessary to define the roles of PSA more precisely and to examine its effects on the pathophysiology of preeclampsia.

A preliminary study about the effects of warm priming solution on oxidative stress and postoperative atrial fibrillation in open heart surgery.

BACKGROUND: An important reason for production of ischemia and reperfusion injury and oxidative stress is the sudden and rapid changes in body temperature during the institution of cardiopulmonary bypass. The aim of this study was to investigate the effects of warm priming solution on oxidative stress and atrial fibrillation. METHODS: This is a preliminary prospective study on a group of 40 patients who underwent elective coronary artery bypass grafting operation using cardiopulmonary bypass. Patients were randomized into two groups, each consisting of 20 patients; one group was primed with a solution at 20 °C and the other at 36 °C initially for cardiopulmonary bypass. Blood samples from both of the groups were drawn preoperatively and at the 15th and 60th min of aortic cross clamping and 24th h following the surgery. Serum malondialdehyde levels, protein carbonyl content and total antioxidant status were detected. Patients were followed for postoperative atrial fibrillation. RESULTS: Malondialdehyde and protein carbonyl content were found to be significantly higher and total antioxidant status was concordantly lower in the cold priming group at the 15th and 60th min, recovering to the normal range postoperatively at the 24th h. Patients in the cold priming group had developed a significantly higher rate of atrial fibrillation when compared with the patients in the warm priming group during the postoperative period. CONCLUSION: In conclusion, although this study has its limitation about the sample size it may provide an insight about the probable preventive effects of 36 °C warm priming solution in oxidative stress and postoperative atrial fibrillation.

The presence of oxidized low-density lipoprotein and inducible nitric oxide synthase expression in renal damage after intestinal ischemia reperfusion.

Intestinal ischemia/reperfusion (I/R) is a complex phenomenon that causes destruction of both local and remote tissues. The objective of this study was to investigate the possible participation of oxidized low-density lipoproteins (oxLDLs) and inducible nitric oxide synthase (iNOS) expression in renal tissue damage after intestinal I/R. The superior mesenteric artery was blocked for 30 minutes, followed by 24 hours of reperfusion. At the end of the reperfusion period, renal tissues were removed; the presence of oxLDL, superoxide dismutase enzyme activity, malondialdehyde levels, and iNOS expression were evaluated. I/R resulted in positive oxLDL staining in renal tissue. Compared with control rats, tissue from the I/R group showed significantly higher malondialdehyde levels and lower superoxide dismutase enzyme activity. Strong and diffuse iNOS expression was present in the I/R group. Our findings support the hypothesis that I/R of intestinal tissue results in oxidative and nitrosative stress and enhances lipid peroxidation in the end organ. These data show that oxLDL accumulates in rat renal tissue after intestinal I/R. Antioxidant strategies may provide organ protection in patients with reperfusion injury, at least by affecting interactions with free radicals, nitric oxide, and oxLDL. This study demonstrates for the first time that oxLDL may play a role in renal tissue damage after intestinal I/R. Antioxidant strategies may be beneficial for protection from reperfusion injury.

Prostate specific antigen levels after acute myocardial infarction.

Prostate Specific Antigen (PSA), a member of kallikrein family, is a specific serine protease of prostatic tissue. In some case reports, changes in PSA levels after acute myocardial infarction (AMI) have been reported. In this study we evaluated variations in PSA levels post-AMI. Twenty-six male patients who had PSA levels within reference limits were included in the study. The diagnosis of AMI was confirmed by clinical findings, ECG (electrocardiogram) and cardiac marker studies. Serum total PSA (tPSA) and free PSA (fPSA) levels were measured at days 0 (day of admission), 1, 2 and 3 after AMI. PSA/albumin ratio was also calculated in order to evaluate the effect of dilution. A statistical analysis of the results of all patients revealed significant decrease in tPSA levels and tPSA/Albumin ratio at day 2 when compared to days 0 and 3, which showed a similar pattern. Changes of fPSA and fPSA/ Albumin ratio according to days were not found significant. In only four patients we found increased levels of tPSA and increased fPSA levels in three of them. These patients displayed severe problems such as renal failure, cardiac failure, ventricular aneurysm and cerebral ischemia due to cardiac arrest. The lower tPSA levels on day 2 suggest that tPSA can be eliminated rapidly from the circulation on days 1 and 2, probably through the formation of complexes of tPSA with acute phase proteins.

Inflammatory markers in preeclamptic patients.

BACKGROUND: Preeclampsia is characterized by hypertension and proteinuria that begins in the second half of pregnancy. Endothelial dysfunction and trophoblastic hypoperfusion seen in preeclampsia suggested to be part of an increased maternal inflammatory response to pregnancy. In this study, we aimed to evaluate some inflammatory markers in pre-eclamptic and normotensive pregnants. METHODS: The study included 36 cases with mild preeclamp-sia, 36 cases with severe preeclampsia and 33 cases of normotensive pregnant. High sensitive C-reactive protein (hsCRP) and serum amyloid A (SAA) were measured by enzyme-linked immunosorbent assays, serum procalcitonin was measured by enzyme-linked fluorescent immunassay. Mean arterial pressure (MAP) was used as an indicator of the severity of the disease. RESULTS: In severe preeclampsia group hsCRP, serum amyloid A and procalcitonin levels were significantly higher than mild preeclamptic and normotensive groups. SAA and hsCRP levels were higher in mild preeclamptic group when compared with normotensive pregnant but no significant difference was found in procalcitonin between these groups. There were significant correlations betweeen hsCRP, SAA, procalcitonin and MAP. CONCLUSIONS: The results confirm that inflammatory reactions are closely associated with preeclampsia.

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

BACKGROUND: Head 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. RESULTS: In 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). CONCLUSION: Neuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ10 use in rats with traumatic brain injury.

Clinical characterization of patients with macroprolactinemia and monomeric hyperprolactinemia.

Macroprolactinemia is often a cause of misdiagnosis, unnecessary expensive investigation, and unsuitable treatment. The aim of the present study was to investigate the clinical findings and the concentrations of macroprolactin in patients with hyperprolactinemia in our region. Eighty-four female hyperprolactinemic patients were screened for macroprolactinemia. Prolactin was measured by chemiluminescence method on an Immulite 2000 analyzer (Siemens Health Diagnostics, Deerfield, IL, USA). Recoveries less than or equal to 40% after polyethylene glycol precipitation were indicative of macroprolactinemia. Clinical features and biochemical values were compared in true hyperprolactinemic and macroprolactinemic patients. Macroprolactinemia was detected in 31 patients (36.9%), with 84 hyperprolactinemic female patients. There was no difference in frequency of galactorrhea and oligomenorrhea/amenorrhea between the two groups. When we evaluated the clinical features of patients according to prolactin levels, no significant difference was found between the groups. In conclusion, our initial data show that no clinical features could reliably differentiate macroprolactinemic from true hyperprolactinemic patients, but at least one of these symptoms was present in most macroprolactinemic patients.

Effect of vardenafil on cerebral vasospasm following experimental subarachnoid hemorrhage in rats.

We examined the effects of the phosphodiesterase 5 (PDE-5) inhibitor vardenafil on cerebral vasospasm in an experimental rat subarachnoid hemorrhage (SAH) model. Thirty-two albino Wistar rats were divided into five groups: G1, no experimental intervention; G2, administered subarachnoid physiological saline after sham surgery; G3, subjected to SAH; G4, subjected to SAH and administered low-dose (0.5 mg/kg) vardenafil treatment; and G5, subjected to SAH and administered high-dose (5 mg/kg) vardenafil treatment. For animals in G3, G4 and G5, SAH was induced by an injection of autologous non-heparinized blood into the cisterna magna. Immediately after SAH, for animals in G4 and G5, vardenafil was administered by gavage at intervals of 8 hours for 2 days. The rats were then decapitated, and basilar arteries and blood samples were taken for biochemical and histopathological examination. Malonyldialdehyde values in G2 (p = 0.004) and G3 (p = 0.002) were significantly higher than those in G1. G4 and G5 had significantly lower values than G2 and G3 (p = 0.014, G4 v. G2; p = 0.005, G4 v. G3; p = 0.005, G5 v. G2; p = 0.002, G5 v. G3). Total antioxidant capacity (TAC) values in G3 were significantly lower than those in G1 (p = 0.041). TAC values in G4 and G5 were significantly higher than those in G3 (p = 0.043). Mean luminal diameter in G3 was significantly smaller compared with G1 and G2 (p = 0.002), but larger in G4 (p = 0.002) and G5 (p = 0.001) compared with G3. Mean luminal diameter was also significantly larger in G5 than in G2 (p = 0.008) and G4 (p = 0.038). Mean wall thickness in G2 (p = 0.015) and G3 (p = 0.002) was significantly thicker compared with G1. Wall thickness was significantly thinner in G4 and G5 compared with G2 and G3 (p = 0.008, G4 v. G2; p = 0.001, G4 v. G3; p = 0.005, G5 v. G2; p = 0.001, G5 v. G3). Our results confirm that vardenafil may induce vasodilatation and provide potential benefits in SAH therapy by preventing vasospasm.

Effects of ebselen versus nimodipine on cerebral vasospasm subsequent to experimental subarachnoid hemorrhage in rats.

We investigated the effect of ebselen relative to nimodipine in an animal model of subarachnoid hemorrhage. Thirty Wistar albino rats were divided into 5 groups: G1, no intervention; G2, sham surgery without subarachnoid hemorrhage (SAH); G3, SAH only; G4, SAH plus nimodipine treatment; G5, SAH plus ebselen treatment. For G2 animals, physiological saline (0.9% NaCl) was injected into the cisterna magna. For G3, G4 and G5 animals, SAH was induced by injecting autologous non-heparinized blood into the cisterna magna. One hour after injection, G4 animals received nimodipine at 6-hour intervals and G5 animals received ebselen twice a day for 48 hours. After treatment, brain tissue and blood samples were taken for biochemical and histopathological examination. Mean malonyldialdehyde concentration was significantly higher in G3 than in G1 (p<0.0001), G2 (p=0.01), G4 (p=0.002) and G5 (p=0.014), and significantly higher in G5 than in G1 (p=0.013). Mean superoxide dismutase activity was significantly lower in G4 than in both G1 (p=0.025) and G2 (p=0.02). Mean wall thickness was significantly greater in G3 than in G1 (p<0.0001), G2 (p=0.01), G4 (p<0.0001) and G5 (p<0.0001). Mean wall thickness was also significantly greater in both G1 and G2 than in G4 (p<0.0014 and p<0.0001) and G5 (p<0.0001 and p<0.0001). Mean luminal diameter of the basilar artery was significantly smaller in G3 than in G2 (p=0.02), G4 (p<0.018) and G5 (p<0.001). Our results confirm that ebselen may have neuroprotective effects by acting to prevent vasospasm.

The effectiveness of dexmedetomidine in experimental spinal cord injury compared to methylprednisolone in rats.

The present study aimed to investigate the neuroprotective efficacy of dexmedetomidine in a rat experimental spinal cord injury model. The rats (n=40) were equally divided into four groups: G1, G2, G3, and G4. Rats in the G1 group underwent a laminectomy only. For the rats in the G2, G3, and G4 groups, spinal cord injury was induced by placing an aneurysm clip extradurally for 60 s at T10. The rats in G2 did not receive any post-injury treatment. Immediately after trauma was induced, rats in G3 were given methylprednisolone (30 mg/kg) and in G4, dexmedetomidine (10 microg/kg), both intraperitoneally. The rats were sacrificed under anesthesia 24 hours later and 1.5 cm lengths of injured spinal cord were obtained. Malonyldialdehyde values were significantly increased in G2 compared to G1, G3 and G4 (p<0.05). The neuronal cell count in G1 was significantly higher than in G2 and G3 (p=0.0001; p=0.007). G4 had higher cell counts compared to G2 and G3 (p=0.0001; p=0.05). These findings indicated that dexmedetomidine might have neuroprotective effects in spinal cord injury.