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In the present study, we investigated the effects of simvastatin, a 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitor, on lipid metabolism, lipid peroxidation, antioxidant enzyme activities and ultrastructure of diabetic rat lung. Diabetes was induced by a single injection of streptozotocin (45 mg kg(-1), i.p.). After 8 weeks induction of diabetes, some control and diabetic rats were treated with simvastatin (10 mg kg(-1) rat day(-1); orally) for 4 weeks. Diabetes resulted in significantly high levels of blood glucose and plasma lipids. Malondialdehyde levels were unchanged after 12-week-old diabetic rats, whereas catalase activity significantly decreased in the lung. Glutathione peroxidase activity and nitric oxide level were significantly elevated in the diabetic lung. Histological analysis of the diabetic lung revealed some deterioration in the structure. Simvastatin treatment reduced plasma lipid levels and partially decreased the severity of hyperglycaemia. Catalase, glutathione peroxidase activities and nitric oxide levels were partially restored and accompanied by improved structure in diabetic lung by the simvastatin treatment. These results suggest that structural disturbances and alteration of antioxidative enzyme activities occurred in diabetic lung. Simvastatin treatment may provide some benefits in the maintenance of antioxidant status and structural organization of diabetes-induced injury of lung., (Copyright (c) 2004 John Wiley & Sons, Ltd.)

Corticosteroids are used to reduce the oedema and prevent scar tissue formation of the upper airways by their ability to inhibit influx of inflammatory cells, limit capillary permeability and block collagen synthesis in the early stages of wound healing. Triazolopyrimidine (Trapidil) is an antiplatelet agent that acts in part as a phosphodiesterase inhibitor and as a competitive inhibitor of the platelet-derived growth factor (PDGF) receptor. Trapidil, with its vasodilator and NO releasing effect may have some potential to diminish the tissue injury. This study was carried out to evaluate the effects of trapidil (triazolopyrimidine) on lipid peroxidation and nitric oxide in the corticosteroid-impaired healing of tracheal anastomoses. Thirty-four adult Wistar rats were divided into five groups. The animals underwent tracheal transection and primary anastomoses. The groups were assigned as follows: group I, control, (GI, n = 6); group II, sham, (GII, n = 6); group III, dexamethasone, 0.1 mg kg(-1) twice daily intramuscularly, (GIII, n = 8); group IV, trapidil, 6 mg kg(-1) twice daily intraperitoneally (GIV, n = 7); group V, dexamethasone, 0.1 mg kg(-1) plus trapidil, 6 mg kg(-1) twice daily (GV, n = 7), for 1 week. After 1 week, anastomotic healing was assessed by measurement of bursting pressure, evaluation of histopathology, measurement of MDA and nitrite/nitrate levels. In GIII, GIV and GV bursting pressures resulted in significantly reduced anastomotic strength compared to the controls (p < 0.001 for all groups). The difference between bursting pressures of GIII and GIV was not found to be statistically significant (p = 0.966). In regard to fibroblast proliferation and collagen content, a significant difference was found between GIII and GI (p < 0.01), A significant difference was also found when GIV and GV were compared to GIII (p < 0.01). MDA and nitrite/nitrate levels were found to be higher in GIII when compared to all other groups. MDA levels of GIV and GV rats were found to be lower than GIII (p < 0.001, for both groups). The nitrite/nitrate levels of GIV and GV rats were found to be lower than GIII (p < 0.05), and higher than GI (p < 0.001). Trapidil may be useful for its preventive effects on lipid peroxidation and possible increases in NO in cases with corticosteroid-impaired healing of trachea anastomoses.

Objectives: Cerebral hypoperfusion in the contralateral cerebellar hemisphere after stroke is interpreted as a functional and metabolic depression, possibly caused by a loss of excitatory afferent inputs on the corticopontocerebellar pathway terminating in the cerebellar gray matter. This phenomenon is defined as crossed cerebellar diaschisis and can be diagnosed clinically by positron emission tomography, single-photon emission computed tomography, brain magnetic resonance imaging and electroencephalography in terms of regional cerebral blood flow or metabolic rate of oxygen measurements., Materials and Methods: In the present study, nitric oxide indicators (nitrite and cyclic guanosine monophosphate) and lipid peroxidation products (malondialdehyde and conjugated dienes) were measured in rat cerebral cortices and cerebella after permanent right middle cerebral artery occlusion in order to assess the crossed cerebellar diaschisis., Results: Nitrite values in ipsilateral cortex were significantly higher than those in contralateral cortex at 10 (P < 0.001) and 60 (P < 0.05) min of ischemia but no significant changes were observed in both cerebellum compared to the 0 min values. In both cerebral cortex and cerebellum cGMP levels at 10 and 60 min were significantly increased (P < 0.001). This increase was marked in ipsilateral cortex and contralateral cerebellum when compared with opposite cortex and cerebellum (P < 0.001). MDA values in ipsilateral cortex were significantly higher than those in contralateral cortex at 60 min of ischemia (P < 0.05). Contralateral cerebellar MDA values were found significantly higher than those in ipsilateral cerebellum at 0 (P<0.001) and 60 (P < 0.05) min of ischemia. In ipsilateral cortex, conjugated diene values at 0, 10, 60 min of ischemia were higher than those in contralateral cortex. On the other hand 0, 10, 60 min conjugated diene levels in contralateral cerebellum were significantly higher than those in ipsilateral cerebellum (P < 0.001)., Conclusion: These findings support the interruption of the corticopontocerebellar tract as the mechanism of the crossed cerebellar diaschisis.

Aim Alpha-thalassaemia is known to reduce intra-erythrocyte Hb S (sickle haemoglobin) concentration in sickle cell trait ( SCT) subjects. Because Hb S was shown to increase oxidative stress, the purpose of this study was to assess the effects of the coexistence of α-thalassaemia and SCT on oxidative stress markers and nitric oxide ( NO) metabolism after an acute physical exercise. Methods Forty subjects (age: 23.5 ± 2.21 years), SCT carriers ( Hb AS) or healthy subjects ( Hb AA), with (-α T) or without (- Nα T) an associated α-thalassaemia took part in the study. Plasma markers of oxidative stress [advanced oxidation protein products ( AOPP), protein carbonyl, malondialdehyde ( MDA) and nitrotyrosine], anti-oxidant defences and NO metabolism ( NOx) were measured at rest ( Trest), immediately following an incremental maximal exercise test ( Tex) and during recovery ( T1h, T2h and T24h). Results Malondialdehyde expressed as the percentage of changes from baseline was significantly higher in the Hb AS- Nα T compared with Hb AS-α T during recovery (+36.3 ± 14.1% vs. −1.8 ± 13.2% at T1h, P = 0.02; +36.6 ± 13.4% vs. −11.4 ± 12.5% at T2h, P = 0.004 and +24.1 ± 12.3% vs. −14.4 ± 11.5% at T24h, P = 0.02 in Hb AS- Nα T vs. Hb AS-α T). Compared with Hb AS- Nα T, Hb AS-α T had a higher NOx change from baseline at Tex (−23.4 ± 20.6% vs. +57.7 ± 19.3%, respectively; P = 0.005) and lower nitrotyrosine change from baseline at T1h (+7.2 ± 22.2% vs. +93.5%±29.3%, respectively; P = 0.04). Conclusion All these data suggest that the presence of α-thalassaemia may blunt the higher level of oxidative stress and the impaired bioavailability of NO observed in the SCT carriers. [ABSTRACT FROM AUTHOR]