A new model for evaluation of thrombosis and ischaemia/reperfusion injury

Introduction

Experimental studies on ischaemia/reperfusion injury have traditionally focused on the isolated effect following simple occlusion of the nutrient artery. In myocardial infarction the reperfusion injury is further complicated by the presence of a thrombogenic area in the coronary artery that may cause repetitive episodes of re-occlusion and embolization.

Methods

In eight pigs a thrombogenic area was created in the left anterior descending artery (LAD) by exposure of adventitia into the lumen. The LAD was occluded proximal to the lesion for 50 min, followed by 4 h of reperfusion. Troponin-T (TNT), creatine kinase (CK), and collagen-induced platelet aggregation (CPA) were measured 4 times during the experiment Indium-labeled platelets were given 30 min prior to harvesting of the hearts.

Results

The infarct size/area at risk was 40 (35–63)% in the present study. TNT and CK increased significantly to 1.7 (0.6–3.5) μg/l (P < 0.001) and 1480 (1105–2249) U/l (P < 0.02), respectively. Infarct size correlated significantly with TNT-3h (ρ=0.85, P < 0.002), but not with CK-3h. Platelet aggregation decreased by 34% (P < 0.05) 15 min of reperfusion, but returned to base-line. Platelet accumulation in the left ventricle was significantly higher in area at risk [194 (157–206)%] compared to area not at risk (100%), and to the right ventricle [137 (120–142)%]; (P < 0.05).

Conclusion

In the present study Troponin-T showed a better correlation with infarct size than CK. A decreased reactivity of circulating platelets was observed after reperfusion and significantly more platelets were found in the area at risk. These results indicate that activated platelets become entrapped in the myocardium and may aggravate the reperfusion injury.