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

• Published in: APMIS : acta pathologica, microbiologica et immunologica Scandinavica Vol. 108; no. 5; pp. 373 - 379
• Main Authors: Ravn, Hanne B., MøLdrup, Ulla, Ilkjær, Lars B., Chew, Michelle, Jensen, Liselotte, Johnsen, SøRen, Birk-SøRensen, Lene, TøNnesen, Else, Hjortdal, VIbeke E.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-05-2000; Blackwell
• Subjects: Animals; Biological and medical sciences; Blood Platelets - physiology; Cardiology. Vascular system; Coronary heart disease; Coronary Thrombosis - diagnosis; Creatine Kinase - biosynthesis; Heart; infarct size; ischaemic markers; Medical sciences; Myocardial Ischemia - diagnosis; Myocardial Reperfusion Injury - diagnosis; Platelet Aggregation; platelets; Swine; thrombosis; Troponin T - biosynthesis; Animal model; Infarct; Biological marker; Cardiovascular disease; Coronary heart disease; Myocardial disease; Thrombosis; Pig; Vertebrata; Platelet; Troponin; Mammalia; Reperfusion; Ischemia; Animal; Myocardium; Artiodactyla; Biological accumulation; Ungulata
• ISSN: 0903-4641; 1600-0463
• DOI: 10.1034/j.1600-0463.2000.d01-71.x

Background: The purpose of the present study was to describe infarct size and platelet accumulation when reperfusion injury was combined with a thrombogenic lesion in the coronary artery. The left anterior descending artery was damaged in 11 pigs and subsequently occluded proximal to the lesion for 50 min, followed by 4 h of reperfusion. Results: The infarct size/area at risk was 40 (35–63)%. Infarct size correlated with troponin‐T‐3 h (p=0.85, p<0.002), but not with creatine kinase‐3 h. Platelet aggregation decreased by 34% (p<0.01) at 15 min of reperfusion, but returned to baseline. Platelet accumulation in the left ventricle was significantly higher in the area at risk (194 (157–206)%) compared to the right ventricle (137 (120–142)%); p<0.05). Conclusion: A decreased platelet reactivity and increased accumulation of platelets in the area at risk indicates that activated platelets become entrapped in the myocardium. Troponin‐T was a better marker of myocardial damage than creatine kinase in this in vivo model with pigs.