Coronary Reperfusion and Cytokines View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1998

AUTHORS

Akira Matsumori , Koh Ono , Shigetake Sasayama

ABSTRACT

Elevated levels of circulating cytokines have been reported in patients with various heart diseases, and these cytokines have been shown to depress myocardial contractility in vitro and in vivo. Cardiac inflammatory responses appear to play a pivotal role in scar formation after acute myocardial infarction. Monocyte chemotactic and activating factor (MCAF)/ monocyte chemoattractant protein-1 (MCP-1) is a cytokine with chemotactic activity for mononuclear phagocytes but also for NK cells, T cells, mast cells, and basophils. To investigate the possible involvement of MCAF/MCP-1 in the pathogenesis, its course was studied in patients with acute myocardial infarction. The plasma level of MCAF/MCP-1 in myocardial infarction tended to increase at 3 h after the onset of chest pain, was significantly elevated at 9h, and remained increased during the 24-h observation period. The level of MCAF/MCP-1 correlated significantly with the plasma level of another chemokine, interleukin-8, suggesting that common stimuli mediate the release of both cytokines in myocardial infarction. The identification of MCAF/MCP-1 as an inflammatory mediator in acute myocardial infarction suggests that mononuclear phagocytes may play an important role in the early stage of the disease. We also studied serum hepatocyte growth factor (HGF) in patients with various heart diseases and found markedly increased circulating levels of serum HGF in the very early period of acute myocardial infarction. Serum HGF levels correlated well with peak levels of serum creatine kinase. These findings suggest that serum HGF reflects the severity of myocardial infarction and that HGF may play an important role in tissue repair in acute myocardial infarction. Our recent study of myocardial ischemia and reperfusion in a rat model showed that the plasma concentration of HGF began to increase within 1 h after reperfusion following 1 h of ischemia. The peak level was reached at 3 h after reperfusion. Northern blotting revealed that HGF mRNA expression in the heart was augmented at 24 h after the myocardium was reperfused. The signal for mRNA of c-met, the high-affinity HGF receptor, was also upregulated parallel to that for HGF. These results indicated that HGF/c-Met plays a role in capillary endothelial cell regeneration in the ischemically injured heart. More... »

PAGES

157-177

Book

TITLE

Protection Against Ischemia/Reperfusion Damage of the Heart

ISBN

978-4-431-68484-8
978-4-431-68482-4

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-4-431-68482-4_11

DOI

http://dx.doi.org/10.1007/978-4-431-68482-4_11

DIMENSIONS

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