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Nitric oxide-releasing aspirin decreases vascular injury by reducing inflammation and promoting apoptosis.

Abstract
Endothelial dysfunction, defined as a deficit in the bioavailability of nitric oxide (NO), occurs as sequelae of many vascular diseases; however, the utility of supplementing NO to obviate the extent of disease is understudied. Here, we examined if prolonged treatment with an NO-releasing form of aspirin (NO-ASA) can influence neointimal remodeling of femoral arteries of hypercholesterolemic ApoE (-/-) mice. Treatment of ApoE (-/-) mice with NO-ASA, but not aspirin (ASA), improved neointimal remodeling post-injury. NO-ASA treatment increased lumen diameters and reduced intimal-to-medial ratios of injured femoral arteries compared with ASA- or vehicle-treated mice. The reduction in lumen diameter in NO-ASA-treated mice was associated with a marked reduction in CD45-positive inflammatory cells and an increased number of TUNEL-positive cells. Thus, NO-ASA, by virtue of releasing NO, can reduce vascular inflammation and promote apoptosis during vascular remodeling associated with neointimal thickening.
AuthorsJun Yu, Radu Daniel Rudic, William C Sessa
JournalLaboratory investigation; a journal of technical methods and pathology (Lab Invest) Vol. 82 Issue 7 Pg. 825-32 (Jul 2002) ISSN: 0023-6837 [Print] United States
PMID12118084 (Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Apolipoproteins E
  • Platelet Aggregation Inhibitors
  • nitroxy-butyl-acetylsalicylic acid
  • Cholesterol
  • Aspirin
Topics
  • Animals
  • Apolipoproteins E (deficiency)
  • Apoptosis (drug effects)
  • Aspirin (analogs & derivatives, pharmacology, therapeutic use)
  • Cholesterol (blood)
  • Disease Models, Animal
  • Femoral Artery (drug effects, pathology)
  • Humans
  • Inflammation (prevention & control)
  • Male
  • Mice
  • Mice, Knockout
  • Muscle, Smooth, Vascular (drug effects, pathology)
  • Platelet Aggregation Inhibitors (therapeutic use)

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