Formation and release of @entity10043 catabolites during hypoperfusion, XXXX , and @entity63 .

@entity2353 @entity859 @entity3625 @entity63 @entity10043 @entity95 @entity14572 @entity519
To answer some of the as yet unresolved questions about the formation, metabolism, and release of @entity10043 catabolites in @entity519 myocardium, we compared their release from isolated @entity95 hearts during hypoperfusion, @entity519 , and after @entity63 , with and without @entity2353 -transport inhibition. Results provide evidence to suggest the following. Besides the supply-to-demand ratio for O2, other factors may affect the formation of @entity859 . The myocyte is the major source of @entity10043 catabolites. @entity859 is not produced within the myocyte. Once in the interstitium, @entity859 is (largely) taken up in the endothelial cells, where it is catabolized to @entity14572 and @entity3625 and released that way into the lumen. Some of the @entity859 can reach the lumen unchanged through clefts. @entity2353 transport inhibition prevents the escape through the endothelial cells and thus the formation and release of @entity14572 and @entity3625 . As a consequence, more @entity859 will accumulate in the interstitium and more will reach the lumen through the clefts. The pathway, as proposed, explains the long known paradox of increased extracellular levels of @entity859 after inhibition of @entity2353 transport.
