Critical flow: A parameter to observe the evolution of infarct size over 24 HRS in a closed chest canine model M. Gottwik, P. Zimmer, B. Winkler, W. Schaper, Max-Planck-Institute, Bad Nauheim, West Germany

1981 ◽  
Vol 13 ◽  
pp. 33
Keyword(s):  
Infarct Size ◽  
Canine Model ◽  
West Germany ◽  
Critical Flow ◽  
Max Planck ◽  
Closed Chest ◽  
Bad Nauheim

scholarly journals The xanthine oxidase inhibitor oxypurinol does not limit infarct size in a canine model of 40 minutes of ischemia with reperfusion

1988 ◽  
Vol 12 (1) ◽  
pp. 209-217 ◽  
Author(s):  
James M Kinsman ◽  
Charles E Murry ◽  
Vincent J Richard ◽  
Robert B Jennings ◽  
Keith A Reimer
Keyword(s):  
Infarct Size ◽  
Xanthine Oxidase ◽  
Canine Model ◽  
Oxidase Inhibitor ◽  
Xanthine Oxidase Inhibitor

Progression of myocardial injury during coronary occlusion in the collateral-deficient heart: a non-wavefront phenomenon

2007 ◽  
Vol 293 (3) ◽  
pp. H1799-H1804 ◽  
Author(s):  
Bradley G. Leshnower ◽  
Hiroaki Sakamoto ◽  
Hirotsugu Hamamoto ◽  
Ahmad Zeeshan ◽  
Joseph H. Gorman ◽  
...  
Keyword(s):  
Infarct Size ◽  
Functional Capacity ◽  
Collateral Circulation ◽  
Coronary Occlusion ◽  
Regional Blood Flow ◽  
Microvascular Dysfunction ◽  
Canine Model ◽  
Ischemic Time ◽  
Coronary Collaterals ◽  
Wide Range

It is widely accepted that, during acute coronary occlusion, ischemic cell death progresses from the subendocardium to the subepicardium in a wavefront fashion. This concept, which implies that the subendocardium is the most susceptible myocardial region to ischemic injury, was established using a canine model with an extensive system of subepicardial coronary collaterals. In humans, particularly in those with coronary artery disease, there is a wide range in the distribution and functional capacity of the collateral circulation, which may affect the pattern of infarct evolution. Using an ovine model with a limited system of preformed subendocardial coronary collaterals, we characterized the effect of increasing lengths of ischemia on regional blood flow and infarct size in three regions of the ventricular wall: subendocardium, midmyocardium, and subepicardium. Our results demonstrate that the myocardium and microvasculature in these three regions are equally susceptible to injury after 45 min of ischemia. When ischemic time is increased to 1 h, infarct size in the midmyocardium (90 ± 2%) is greater than in the subendocardium (76 ± 4%, P = 0.004) and subepicardium (84 ± 3%, P = 0.13). Microvascular dysfunction as assessed as a percentage of baseline flow is also greater in the midmyocardium (14 ± 5%) compared with the subendocardium (20 ± 3%, P = 0.23) and subepicardium (51 ± 9%, P = 0.007). These findings suggest that, in subjects with a limited system of coronary collateral circulation, the midmyocardium is the most susceptible myocardial region to ischemia and the subendocardium is the most resistant. Myocardial viability during coronary occlusion appears to be primarily determined by the distribution and functional capacity of the collateral circulation.

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