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This Article Full Text Full Text (PDF) All Versions of this Article: 293/5/H3210    most recent 00773.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Légaré, J.-F. Articles by Currie, R. W. Search for Related Content PubMed PubMed Citation Articles by Légaré, J.-F. Articles by Currie, R. W.

Heat shock treatment results in increased recruitment of labeled PMN following myocardial infarction

Departments of ¹Surgery, ²Microbiology and Immunology, and ³Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada

Submitted 4 July 2007 ; accepted in final form 30 August 2007

One of the proposed mechanisms for the myocardial protective effects of heat shock (HS) treatment has been a reduction in the inflammatory response. The objective of the present study was to evaluate the impact of HS treatment in an established model of polymorphonuclear cell (PMN) migration following myocardial infarction (MI). Isolated purified PMNs (10 x 10⁶ cells) labeled with ⁵¹Cr were injected into Lewis rats following a left thoracotomy and ligation of the left anterior descending coronary artery causing MI. Two experimental groups of animals were created: MI group (n = 11) and HS+MI group (n = 7). HS treatment consisted of an elevation in core temperature to 42°C for 15 min 24 h prior to MI. An additional group of control animals underwent sham thoracotomy (n = 5). All animals were euthanized at 24 h after MI, and gamma counts were obtained to estimate PMN migration. Myocardial injury was confirmed in all experimental animals (histology and echocardiography). The serum troponin I and infarct size (triphenyltetrazolium chloride) were similar in both groups. Labeled PMN migration was significantly higher in HS+MI animals (14.3 x 10⁴ ± 3.7 x 10⁴ PMN) compared with MI group (9.5 x 10⁴ ± 3.6 x 10⁴; P = 0.01), suggesting increased PMN migration as a result of HS treatment. HS treatment did not affect PMN migration to positive skin control sites (LPS). ICAM-1 myocardial expression was not significantly increased in HS+MI compared with MI group. In summary, HS treatment results in increased PMN migration into myocardium following MI independent of ICAM-1. These findings suggest that the proposed cardioprotective effect of HS may not be entirely due to a downregulation of myocardial inflammation as previously proposed.

myocardial protection; inflammation; polymorphonuclear cells