nitrogen-dioxide and Aneurysm

The relationship between air pollutants, including fine particles (particulate matter [PM] < 10 μm and < 2.5 μm), and aneurysmal subarachnoid hemorrhage (SAH) has been inadequately studied, and the results remain inconclusive. In this study, we attempted to investigate the relationship between air pollutant levels and aneurysmal SAH.. Ninety-two patients diagnosed with aneurysmal SAH were retrospectively included in the study. Medical records were reviewed, and levels of pollutants, including those of sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and PM with an aerodynamic diameter < 10 and 2.5 μm (PM10 and PM2.5), were collected from the open-source Air Korea website for a period of 4 days. Independent t-tests were conducted to identify the difference in the pollutant levels between the data obtained on the day of aneurysm rupture (D-0) and the other 3 days (D-7, D-2, and D-1).. A majority (40.2%) of the patients experienced aneurysm rupture during the fall season when the mean daily pollutant levels were 0.004 ± 0.001 (ppm, SO2), 0.517 ± 0.218 (ppm, CO), 0.02056 ± 0.012 (ppm, O3), 0.02628 ± 0.015 (ppm, NO2), 36.36957 ± 24.538 (μg/m3, PM10), and 19.75581 ± 13.494 (μg/m3, PM2.5), respectively. The level of NO2 was significantly higher on the day of aneurysm rupture (P = .035) than on the other days, while the levels of CO and O3 were nonsignificantly higher (P = .081, P = .055, respectively) on the day of aneurysm rupture than on the other days. There was no significant differences in the PM levels between the 4 days.. A relationship between PM levels and aneurysm rupture was not identified. Only the levels of classic air pollutant (CO, O3, and NO2) were higher on the aneurysm rupture day than on the other days.

Topics: Air Pollutants; Aneurysm; Environmental Pollutants; Humans; Nitrogen Dioxide; Ozone; Particulate Matter; Retrospective Studies; Subarachnoid Hemorrhage; Sulfur Dioxide

Marfan syndrome (MS) is an autosomal dominant disorder of connective tissue that is caused by mutations in the fibrillin-1 (FBN-1) gene that cause degeneration of the artery. It is accompanied by endothelial dysfunction. The potential transient receptor of the vanilloid subfamily 1 (TRPV1) ion channel plays an important role in endothelial vascular functioning. Here we determine the association of the presence TRPV1 in aortic aneurysm with dilation and dissection of the artery in MS patients. Histological sections of aortic aneurysm tissue obtained by the surgical procedure of Bentall and De Bono or David, were processed by immunohistochemistry with antibodies against ICAM, VCAM, iNOS, eNOS, TRPV1 and TNF-α and the immunolabelling area was determined. We also measured the NO₃⁻/NO₂⁻ ratio in the aortic tissue. C-reactive protein and HDL in plasma were quantified. A significant increase in iNOS, TRPV1, VCAM (p≤0.05), NO₃⁻/NO₂⁻ ratio (p=0.002) and a significant decrease in eNOS (p=0.04) and HDL in plasma (p=0.02) in the MS vs. the C group were found. Conclusion: TRPV1 is over-expressed in aortic tissue from MS patients and can be associated with increases in iNOS, VCAM and a decrease in eNOS. These changes might contribute to the progression and rupture of the thoracic aneurysm.

Topics: Adult; Aneurysm; Aortic Aneurysm, Thoracic; C-Reactive Protein; Disease Progression; Female; Fibrillin-1; Gene Expression Regulation; Humans; Immunohistochemistry; Inflammation; Intercellular Adhesion Molecule-1; Lipoproteins, HDL; Male; Marfan Syndrome; Middle Aged; Nitric Oxide Synthase Type III; Nitrogen Dioxide; Nitrogen Oxides; Phenotype; TRPV Cation Channels; Vascular Cell Adhesion Molecule-1