Increased serum malondialdehyde and decreased nitric oxide within 24 hours of thrombotic stroke onset

Abstract

Ischaemia/reperfusion generates free oxygen radicals, that react with the unsaturated lipids of biomembranes resulting in the generation products such as malondialdehyde (MDA). MDA could be a sensor for tissue damage and reperfusion. Nitric oxide (NO), released due to the early arrival of leukocytes in the brain parenchyma, could be a sensor for non-flow phenomenon. Thereby, the purpose of this research was to evaluate the behaviour of MDA and NO within the 24 hours after the stroke onset. Fifteen patients up to an age of 49 years, admitted to the emergency of University Hospital and Chiquinquira Hospital in Maracaibo, Venezuela, were examined by a neurologist and underwent 12-lead ECG and CT Scan for the diagnosis of thrombotic stroke. Serum MDA and NO were measured as thiobarbituric acid adducts and total nitrites. Data were collected within the 24 hours after the stroke onset. MDA for patients with stroke had a significant increase (p<0.001) when compared to healthy controls (47.9 ± 7.1 vs. 1.7 ± 0.2 mmol/L). Conversely, serum NO for patients with stroke had a significant decrease (p<0.001), when compared to the control group (14.5 ± 1,4 vs. 41,3 ± 3,7 mmol/L). The lowest values of MDA and the highest values of NO were observed in two patients, who died. We conclude that MDA increases and NO diminishes within 24 hours after the thrombotic stroke onset which suggests that MDA could be used as a potential reliable and sensitive sensor for reperfusion, whereas NO could acts as a potential biochemical sensor for non-reflow phenomenon.