Submitted on July 4, 2007
Accepted on August 30, 2007
Heat shock treatment results in increased recruitment of labeled PMN following myocardial infarction
Jean-Francois Legare1*, Adam Oxner1, Olivier Heimrath1, Tanya Myers1, and R. William Currie2
1 Surgery, Dalhousie University, Halifax, Canada
2 Anatomyand Neurobiology, Dalhousie University, Halifax, Canada
* To whom correspondence should be addressed. E-mail: jean.legare{at}cdha.nshealth.ca.
Background: One of the proposed mechanisms for the myocardial protective effects of Heat shock (HS) treatment has been a reduction in the inflammatory response seen in animals treated by HS. The objective of the present study was to evaluate the impact of HS treatment in an established model of PMN migration post myocardial infarction.
Methods: Isolated purified PMN (10 x 106 cells) labeled with Cr51 were injected into Lewis rats following a left thoracotomy and ligation of the left anterior descending coronary artery causing myocardial infarction (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 minutes 24 hr prior to MI. An additional group of control animals underwent sham thoracotomy (n = 5). All animals were sacrificed at 24 hr after MI and gamma counts were obtained to estimate PMN migration. ICAM-1 expression was assessed by Western blot.
Results: Myocardial injury was confirmed in all experimental animals by histology and in a subgroup of animals by echocardiography. The serum Troponin I was significantly higher in HS+MI (14 ± 6 pg/ml) and MI group (14 ± 7 pg/ml) compared with sham controls suggesting similar infarct size. Labeled PMN migration was significantly higher in HS+MI animals (14.3x104 ± 3.7x104 PMN) compared to MI group (9.5x104 ± 3.6x104; 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 10 ng/ml). ICAM-1 myocardial expression was not significantly increased in HS+MI compared to MI group suggesting that the increased early PMN recruitment was not ICAM-1 dependent.
Conclusions: Our findings suggest that HS treatment results in increased PMN migration into myocardium following MI, appears to be myocardial specific and ICAM-1 indedendent. These findings suggest that the proposed cardio-protective effect of HS may not be entirely due to a down-regulation of myocardial inflammation as previously proposed.
