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Inhibition of No Synthesis Induces Inflammatory Changes and Monocyte Chemoattractant Protein-1 Expression in Rat Hearts and Vessels

  1. Author:
    Tomita, H.
    Egashira, K.
    Kuboinoue, M.
    Usui, M.
    Koyanagi, M.
    Shimokawa, H.
    Takeya, M.
    Yoshimura, T.
    Takeshita, A.

  2. Author Address

    Egashira K KYUSHU UNIV SCH MED ANGIOCARDIOL RES INST FAC MED HIGASHI KU 3-1-1 MAIDASHI FUKUOKA 8128582 JAPAN KYUSHU UNIV SCH MED ANGIOCARDIOL RES INST FAC MED HIGASHI KU FUKUOKA 8128582 JAPAN KUMAMOTO UNIV SCH MED DEPT PATHOL 2 KUMAMOTO 860 JAPAN NATL CANC INST IMMUNOBIOL LAB IMMUNOPATHOL SECT FREDERICK, MD USA
    1. Year: 1998
  2. Journal: Arteriosclerosis Thrombosis and Vascular Biology
    1. 18
    2. 9
    3. Pages: 1456-1464
  4. Type of Article: Article
  1. Abstract:

    We recently showed that chronic inhibition of NO synthesis by N-omega-nitro-L-arginine methyl ester (L-NAME) causes coronary vascular remodeling (ie, vascular fibrosis and medial thickening) in rats. To test the hypothesis that the inhibition of NO synthesis induces inflammatory changes in the heart, we characterized the inflammatory lesions that occurred during L-NAME administration and determined whether inflammation involved the induction of monocyte chemoattractant protein-1 (MCP-1) in vivo. During the first week of L-NAME administration to Wistar-Kyoto rats, we observed a marked infiltration of mononuclear leukocytes (ED1-positive macrophages) and fibroblast-like cells (alpha-smooth muscle actin-positive myofibroblasts) into the coronary vessels and myocardial interstitial areas. These inflammatory changes were associated with the expression of proliferating cell nuclear antigen and MCP-1 (both mRNA and protein). The areas affected by inflammatory changes, as well as the expression of MCP-1 mRNA, declined after longer (28 days) treatment with L-NAME and were replaced by vascular and myocardial remodeling. Our results support the hypothesis that the inhibition of NO synthesis induces inflammatory changes in coronary vascular and myocardial tissues and involves MCP-1 expression. Results also suggest that the early stages of inflammatory changes are important in the development of later-stage structural changes observed in rat hearts. [References: 48]

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