| Literature DB >> 9507563 |
K Kaneko1, T Kanda, T Yokoyama, Y Nakazato, T Iwasaki, I Kobayashi, R Nagai.
Abstract
While an overproduction of interleukin-6 (IL-6) has been observed in patients with acute myocardial infarction (AMI), its clinical significance and localization in the ischemic myocardium have not been elucidated. We examined immunohistochemically the expression of IL-6 in 12 autopsied patients with AMI who had died within seven days of the infarction. Twenty sections of ischemic myocardium and nine of the coronary arteries involved were stained with anti-IL-6 and anti-atrial natriuretic peptide (ANP). The diameter of the myocardium was analyzed. The greatest expression of IL-6 in the infarcted myocardium occurred in patients who had died three to four days after the onset (2.7 +/- 0.4), as judged by a scheme for grading IL-6 expression. Patients who died within one to two days (1.0 +/- 0.3) or five to eight days (0.6 +/- 0.4) less frequently showed an overproduction of IL-6. The IL-6-positive myocardium co-expressed ANP and was significantly (p < 0.05) hypertrophied, when compared with the IL-6-negative myocardium. The diameter of IL-6-positive myocardial myocytes was significantly (p < 0.02) increased in patients who died within one to two days (1.6 +/- 0.2), three to four days (1.8 +/- 0.3), or five to eight days (2.0 +/- 0.2) after the AMI. The involved coronary arteries expressed IL-6 in the intimal and smooth muscle cells, as did atherosclerotic coronary arteries not involved in AMI. An overproduction of IL-6 was confirmed in the injured myocardium with hypertrophy in patients who died of AMI within seven days after onset. The hypertrophied injured myocardium co-expressed IL-6 and ANP. The expression of IL-6 in the myocardium in AMI appears to be associated with the mechanism of cardiac hypertrophy.Entities:
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Year: 1997 PMID: 9507563
Source DB: PubMed Journal: Res Commun Mol Pathol Pharmacol ISSN: 1078-0297