nitrogen-dioxide and Infarction--Middle-Cerebral-Artery

Here the correlativity between NO(2), a representative pollutant of vehicle exhaust, and ischemic stroke was first determined under experimental conditions following some epidemiological reports. First, we found that blood viscosity, red blood cell (RBC) aggregation-, electrophoresis- and rigidity-index in healthy rats were increased after exposure to 5mg/m(3) NO(2) for one- and three-month. Based on this, we set up stroke rat model and exposed them to NO(2) at the same concentration for one week, and found that NO(2) exposure time-dependently delayed neurological structure and function recovery of MCAO (middle cerebral artery occlusion) rat, and worsened pathological injuries and apoptosis induced by MCAO operation. Endothelial and inflammatory responses, two common cellular pathomechanisms involved in ischemic brain damage, were induced in cortex by MCAO treatment and exacerbated by followed NO(2) inhalation. Expression of the endothelial and inflammatory biomarkers in stroke displayed the same tendency in healthy rats after sub-acute and sub-chronic NO(2) exposure as in MCAO model in a concentration-dependent manner. Our data provide evidence that environmental NO(2) is an important inducer, and also a promoter of ischemic stroke, with endothelial nitric oxide synthase (eNOS), cyclooxygenase-2 (COX-2) and intercellular adhesion molecule 1 (ICAM-1) being potential indicators of this effect.

Topics: Air Pollutants; Animals; Cyclooxygenase 2; Infarction, Middle Cerebral Artery; Intercellular Adhesion Molecule-1; Male; Nitric Oxide Synthase Type III; Nitrogen Dioxide; Random Allocation; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; RNA; Specific Pathogen-Free Organisms; Stroke