Abstract
It has already been demonstrated that ischaemic metabolites, which could diffuse frcm a myocardial infarct in vivo, can cause substantial damage to the endocardial endotheliun and this could predispose to mural thrombosis.To investigate the role of ischaemic metabolites in the pathogenesis of mural thrombosis, lactic acid (pH6.4) was passed through a two-way concentric catheter ligated into the left ventricle of isolated beating rat hearts that were perfused with oxygenated Krebs-Henseleit buffer (KHB) through an aortic cannula. After periods of 1, 2, and 4 hours, the lactic acid was followed for 10 minutes by 10 mis of whole blood from hepa-rinized donor rats. Ventricles were then flushed with KHB, fixed in 2.5% glutaraldehyde and post-fixed in 1% osmium tetrox-ide in cacodylate buffer.Scanning and transmission electron microscopy showed that platelets adhered to exposed basal lamina, microfibrils and collagen but not to intact or damaged endothelial cells. However densely aggregated thrombi only farmed on regions of exposed connective tissue and never on basal lamina. Fibrin, leukocytes and red blood cells were associated with these platelet thrombi. Thus lactic acid and other ischaemic metabolites which could possibly diffuse in vivo from an infarct can contribute to endocardial damage which predisposes to mural thrombosis.
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