A pilot study for determination of anxiety related SLC6A4 promoter "S" and "L" alleles in healthy Turkish athletes.

We aimed to analyze the allelic distribution of solute carrier family-6 member-4 promoter region in Turkish athletes. Recent studies showed the association of lesser expressing "S" allele with anxiety. Genotype percentages for LL, LS and SS genotypes were found as 46, 35 and 19, respectively. 38% of the males had LL, %38 had LS and 24% had SS genotypes. Percentages of LL, LS and SS genotypes were 54, 31 and 15 in females, respectively. 15 (58%) male and 18 (69%) females had L, 11 (42%) male and 8 (31%) females had S alleles. Variations in the association of the SLC6A4 alleles with neuropsychiatric disorders according to different nationalities have been reported. This is the first report showing that LL genotype and L allele in Turkish athletes was more frequent than SS genotype and S allele.

Acute lung injury following thermal insult to the skin: a light and transmission electron microscopial study.

Oxygen radicals are involved in the development of burn shock and distant organ injury in animal models of trauma. Neutrophils are likely the source of reactive oxygen metabolites as a result of the systemic inflammatory reaction to a local burn insult. The aim of the present study was to assess the role of neutrophils in the development of lung injury related to second degree skin burn in rats. Rats were decapitated at two hours following burn injury. Lung tissue samples were removed and examined biochemically and histologically. Tissue-associated myeloperoxidase (MPO) activity, which is an index of neutrophil infiltration, was increased considerably in lung tissue at 2 h after burn injury. Disturbance of alveolar structure, intraalveolar hemorrhage and prominent neutrophil infiltration indicated lung parenchymal injury. Ultrastructural examination of the lung revealed that pneumocytes type I, pneumocytes type II and capillary endothelial cells were degenerated. The data presented here suggest that neutrophil accumulation in the lung is involved in pathogenesis of this distant organ after burn injury.

Oxidative organ damage in a rat model of thermal injury: the effect of cyclosporin A.

Animal models of thermal trauma implicate oxygen radicals as a causative agent in local wound response, development of burn shock and distant organ injury. It has been proposed that the source of reactive oxygen metabolites could be neutrophils sequestered in systemic organs as a result of the systemic inflammatory reaction to a local burn insult. Recent studies have suggested that cyclosporin A (CsA), a potent immunosuppressive drug, may have effects on neutrophils by modulating the rate of their accumulation during acute inflammatory reactions. This study aimed to assess the role of neutrophils in the early and late phases of burn injury in rats with second-degree skin burn. We also aimed to determine whether CsA has protective effects on organs remote from the thermal injury. The results demonstrate that there is significant neutrophil accumulation in the gastric mucosa, liver and lung tissues during the early phase of a burn injury and that CsA failed to protect these organs. In conclusion, the data of this study suggest that neutrophil accumulation in liver, lung and gastric mucosa following burn injury may be involved in the pathogenesis of remote organ damage. The results also indicate that CsA failed to reduce the severity of damage in these organs, probably due to its own toxic effects.

Role of neutrophils in indomethacin-induced gastric mucosal lesions in rats.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause clinically important gastric damage by several mechanisms. In order to evaluate the role of neutrophil infiltration in lesion formation, tissue myeloperoxidase activities were assessed in different gastric layers of the stomach both in rats with normal neutrophil levels and in neutropenic rats. Sprague-Dawley rats were treated either with indomethacin (Indo; 25 mg/kg, s.c.) or the vehicle. A group of rats were made neutropenic by administration of methotrexate (MTX; 2.5 mg/kg i.p.) once a day for 3 days. The stomachs were removed for the determination of lesion index, glutathione, lipid peroxide levels, protein oxidation and tissue myeloperoxidase activities. MTX treatment appeared to reduce neutrophil infiltration significantly while producing insignificant effects on eosinophils and macrophages. Indo administration caused multiple gastric lesions and treatment with MTX significantly reduced lesion index. In rats treated with Indo, neither glutathione nor LP levels showed any significant changes but the protein oxidation was significantly higher than that of other groups. The MPO level of gastric mucosa was increased in Indo-treated rats and reversed by MTX pretreatment. The results of the present study indicate that neutrophil infiltration in the gastric mucosa of rats may be involved in the pathogenesis of NSAID-induced gastric mucosal injury, but no correlation was found between lesion formation and protein oxidation in the gastric mucosa.

The effect of nitric oxide synthase blockade and indomethacin on gastric emptying and gastric contractility.

The aim of the present study was to investigate the effect of nitric oxide (NO) synthase inhibition on gastric emptying rate in conscious rats and on gastric muscle contractility. The involvement of NO was also investigated in indometacin-induced (25 mg/kg, s.c.) changes in gastric emptying rate and smooth muscle contractility. L-NAME (NG-nitro-L-arginine methyl ester; 10 mg/kg, i.v.) inhibited the gastric emptying rate compared to controls and this effect was abolished by L-arginine (300 mg/kg, i.v.). Similarly, indometacin treatment led to a significant delay of gastric emptying rate with respect to vehicle-treated rats. Gastric longitudinal and circular muscle strips of L-NAME or indometacin-treated rats showed a reduction in contractile responses to carbachol. The results demonstrate that NO synthase blockade and indometacin treatment delay gastric emptying in conscious rats, concomitant with reduced responsiveness to carbachol, in vitro.

Influence of gallopamil on the gastric effects of stress in conscious rats.

The influence of the calcium-channel blocker gallopamil on cold-restraint stress (CRS)-induced gastric effects was investigated in conscious rats with gastric cannula. CRS, while leading to multiple gastric lesions, reduced gastric acid output and mast cell count, but increased the gastric emptying rate of acid solutions. Intraperitoneally injected gallopamil (1 mg/kg), given 1 h before CRS administration, prevented gastric lesion formation and partially reversed mast cell count and the emptying of acid solutions, but had no further effect on acid output. However, gallopamil in unrestrained rats did not significantly affect acid emptying or mast cell count. Regarding calcium involvement in the pathophysiology of stress-induced gastric lesions, the possible antiulcer actions of gallopamil involved in the prevention of CRS-induced lesion formation may be attributed to its putative stabilizing effect on mast cells and gastric emptying.