Ischemia/reperfusion (IR) during organ procurement contributes significantly to tissue injury and may cause early organ dysfunction after transplantation. The molecular markers associated with innate immunity are prime activators of early inflammatory responses to an allograft that lead to host-induced inflammation and organ rejection. This study was undertaken to investigate the possible release of molecular markers during cardiac IR in a rat model of the left anterior descending artery (LAD) occlusion. Adult Sprague-Dawley rats randomly assigned to five groups of control; 30 min LAD occlusion; 60 min LAD occlusion; 30 min LAD occlusion/10 min reperfusion and 30 min LAD occlusion/60 min reperfusion. The LAD was occluded to generate ischemia in left ventricle (LV) of the heart. Blood and cardiac tissues were tested for the presence of Toll-like receptor 2 and -4 (TLR-2 and TLR-4) at different time intervals. TLR mRNA transcripts were significantly increased in a time dependent- manner after IR. These markers were upregulated as early as 10 minutes after reperfusion and further they were increased several-fold after 60 minutes of reperfusion in tissue and peripheral blood cells as compared to the control group. The TLR-2 levels were greater in blood samples, whereas, the TLR-4 levels were greater in cardiac LV after 30 min LADI/60 min reperfusion. The method was an effective approach to generate a localized cardiac IR in the rat, which allowed examination of the molecular markers associated with IR in peripheral blood and cardiac tissues. Key words: Cardiac, innate immunity, ischemia, LAD, myocardium, rat, reperfusion, toll-like receptors.
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