Background: Alcohol-induced lung damage may be associated with increased oxidative stress. Objective: Our aim was to investigate alcohol-induced changes in the biochemistry and histopathology of the lung. Methods: Rats were divided into two groups, a control group and an ethanol group. The ethanol group received 2 g/kg ethanol (total: 3 ml) intraperitoneally. The controls were given the same amount of saline via the same route. Three hours later, the rats were sacrificed, and blood and lung tissue samples were obtained. Oxidative stress was assessed by measuring the levels of erythrocyte reduced glutathione (GSH), tissue malondialdehyde (MDA), myeloperoxidase (MPO) and Na⁺-K⁺ ATPase. Histopathologic evaluation of the lung tissues was also performed. Results: In the ethanol group, serum and tissue MDA levels and MPO activities were increased (p = 0.007, p = 0.001 and p = 0.000), and lung tissue Na⁺-K⁺ ATPase activities and erythrocyte GSH were decreased (p = 0.001 and p = 0.000) compared to the controls. Histopathologic examination demonstrated alveolocapillary thickening, alveolar degeneration, leukocyte infiltration and erythrocyte extravasation in the lungs of the ethanol group (p < 0.05). Conclusion: These results suggest that high-doseacute alcohol administration aggravates systemic and local oxidative stress leading to acute lung injury, ranging from mild pulmonary dysfunction to severe lung injury. It should be borne in mind that rapid onset of the acute respiratory distress syndrome (ARDS) may also be due to increased oxidative stress following alcohol abuse, especially when ischemic disturbances, e.g. coronary heart disease, acute ischemia of the extremities and traumatic accidents, are concomitantly present. Therefore, precautions against ARDS may prevent morbidity and mortality in alcohol-induced lung damage in at-risk patients.

Treatment with levosimendan provided better cardioprotection with cold cardioplegic arrest followed by global hypothermic ischaemia in isolated rat hearts.

The present study was performed to investigate the effect of trapidil on ischemic damage of cells after spinal cord injury. The injury was produced by extradural clip compression of the exposed spinal cord in rats according to Rivlin and Tator. The ten rats in group 1 were used to determine normal findings without any surgery or medication. On the 15 rats in group 2, only six-level laminectomy was performed to determine the influence of the total laminectomy on the biochemical factors measured and the, light and ultrastructural findings. The 15 rats each in groups 3 and 4 were used as trauma and trapidil (40 mg/kg) treatment groups, respectively. The injury actually produced a significant decrease in Na+-K+/Mg+2 ATPase activity of the injured segments as early as 10 min after trauma. Trapidil attenuated Na+-K+/Mg+2 ATPase inactivation in the traumatized rats for 120 min after treatment (P<0.05) and significantly reduced the malone dialdehyde content below that in the traumatized group at all determined times (P<0.05). Light and electron microscopic findings supported the biochemical results.

No abstract

No abstract