Key result
Early coronary reperfusion within 30 minutes reduces necrosis area ~54% versus permanent occlusion.
Why the study?
Collateral blood flow patterns after coronary artery occlusion and the potential for tissue salvage by reperfusion in a rat model with low collateral flow were not well characterised.
Does early coronary artery reperfusion reduce infarct size in a rat model of low collateral flow?
Does early coronary artery reperfusion reduce infarct size in a rat model of low collateral flow?
Early coronary reperfusion in a rat model of low collateral flow significantly reduces infarct size, with tissue salvage occurring mainly in the midmyocardium and subepicardium.
Answers are grounded in this paper and cite their sources.
Confirms infarct size reduction with early reperfusion in low-collateral rat model; leaves open translation to human STEMI.
To characterise collateral blood flow patterns after coronary artery occlusion in the rat and to determine whether tissue can be salvaged by reperfusion in this model, anaesthetised rats were subjected to 20, 30, 40, 60 min of coronary occlusion followed by 24 h of reperfusion or 24 h of permanent occlusion. Relative regional blood flow was measured by radioactive microspheres after 10 min of occlusion in rats undergoing 30 min of occlusion plus reperfusion and in those undergoing 24 h of permanent occlusion. The area at risk was determined by in vivo injection of fluorescent microspheres and necrosis delineated by in vitro tetrazolium staining. Tracings of heart slices were planimetered and the area of necrosis and transmural extent of the infarct measured. Blood flow in the area at risk during occlusion was similar in both the reperfused and permanent occlusion groups. In the 30 min group mean(SEM) subendocardial flow was reduced to 13(5)% of normal and subepicardial flow to 9(3)% and in the permanent occlusion group to 11(2)% and 8(3)% respectively. As delineated by fluorescent microspheres the area at risk was transmural in all rats; however, infarct size expressed as a percentage of the area at risk increased as the duration of occlusion increased. In rats reperfused up to 30 min after occlusion the area of necrosis as a percentage of the area at risk was significantly decreased compared with that in the permanent occlusion group (36.4(9.2)% in rats with 30 min occlusion plus 24 h reperfusion and 78.6(7.4)% in rats with permanent occlusion). The transmural extent of the infarct was 92(6)% in the permanent occlusion group, but in rats reperfused up to 60 min after occlusion necrosis was significantly less transmural and was located mainly in the midmyocardium and subepicardium. Thus after coronary artery occlusion in the rat ischaemia is severe, and there is no transmural gradient in collateral flow. Early reperfusion salvages tissue in this model, but the site of salvage differs from that of other models such as dog, pig, and baboon, in which salvage is mainly subepicardial.
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Hale et al. (1987) studied Coronary artery occlusion. Early coronary artery reperfusion vs. Permanent occlusion was evaluated on Area of necrosis as a percentage of the area at risk. Early coronary artery reperfusion up to 30 minutes after occlusion decreased the area of necrosis compared with permanent occlusion.
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