Increased Serum Malondialdehyde and Decreased Nitric Oxide within 24 hours of Thrombotic Stroke Onset

Abstract

ABSTRACT
Background and purpose: Ischaemia/reperfusion generates free oxygen radicals, that react with the unsaturated lipids of biomembranes resulting in the generation of 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 to the brain parenchyma, could be a sensor for non-flow phenomenon. Thereby, the purpose of this research was to evaluate the behavior of MDA and NO within the first 24 hours after the stroke onset. Methods: Fifteen patients aged between 49 and 87 years, admitted to the emergency of University Hospital and Chiquinquirá Hospital in Maracaibo, Venezuela, were examined by a neurologist and underwent 12-lead ECG and brain 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 first 24 hours after the stroke onset. Results: MDA for patients with stroke had a significant increase (p<0.001) when compared with 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 with the group control (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. Conclusions: MDA increases and NO diminishes within the first 24 hours after the thrombotic stroke onset. This suggests that the 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.