Regional Myocardial Blood Flow and Ultrastructure Following Acute Temporary Ischemia

摘要

The effect of reopening acutely occluded coronary arteries has on regional myocardial blood flow and ultrastructure was studied in open chest dogs. Temporary and permanent ischemia were produced in the same animal by ligating a branch of the left anterior descending and left circumflex coronary arteries for 30 (N=6), 60 (N=6), 90 (N=5) and 120 minutes (N=6). Release of the temporary occlusion after 30 minutes of ischemia was followed by an immediate reactive hyperemia (IRH) 150% of control flow. Sixty minutes of severe temporary ischemia was followed by an IRH 250% of control flow in 16 of 36 samples. Ultrastructural alterations (i.e., myocyte swelling, glycogen depletion, nuclear chromatin margination and mitochondrial swelling) produced with 30 minutes of ischemia were reversed with reflow. Conversely, reflow intensified lesions after 60-120 minutes of severe ischemia. Reflow was most markedly inhibited in severely ischemia myocardium after 60 minutes of ischemia; reflow was less inhibited after 90 or 120 minutes of ischemia. Peak vascular alterations occurred after 120 minutes of ischemia and thus, were not felt to be primarily responsible for the observed reflow inhibition. Vascular spasm was considered as an alternative mechanism responsible for this phenomenon, possibly as the result of a humoral agent present in ischemic myocardium acting on contractile vessels.