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


CONCLUSIONS
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.
Institute of Experimental & Clinical Research, Aarhus University Hospital, Denmark.
H B
HB
Ravn
U
U
Møldrup
L B
LB
Ilkjaer
M
M
Chew
L
L
Jensen
S
S
Johnsen
L
L
Birk-Sørensen
E
E
Tønnesen
V E
VE
Hjortdal
D000818:Animals; D001792:Blood Platelets / Q000502:physiology; D003328:Coronary Thrombosis / Q000175:diagnosis*; D003402:Creatine Kinase / Q000096:biosynthesis; D017202:Myocardial Ischemia / Q000175:diagnosis*; D015428:Myocardial Reperfusion Injury / Q000175:diagnosis*; D010974:Platelet Aggregation; D013552:Swine; D020107:Troponin T / Q000096:biosynthesis
D020107:Troponin T; D003402:Creatine Kinase