Metabolism of vitamin A in the heart increases after a myocardial infarction

The supply of vitamin A to the myocardium by storage organs during increase d oxidative stress subsequent to myocardial infarction (MI) was examined in hemodynamically assessed rats using compartment analysis of a radio-labele d vitamin A. H-3-Vitamin A was injected into two groups of rats: an MI grou p and a control group. There were no differences in the plasma or myocardia l content of total vitamin A (unlabeled + labeled) between the two groups. However, the proportion of H-3-vitamin A was greater in the myocardium as w ell as plasma of MI rats. Rats with MI also had significantly lower H-3-vit amin A levels in liver and kidney than sham controls. The greatest differen ce in vitamin A content was in the concentrations of H-3-labeled storage fo rms of vitamin A in the liver of MI animals. Activity of bile salt-dependen t retinyl ester hydrolase, an enzyme responsible for hydrolyzing vitamin A storage forms, was significantly increased in the liver of MI animals. Thes e data indicate that analysis of plasma concentrations of vitamin A to asce rtain links to cardiac conditions may be inappropriate. Specifically, durin g MI, increased amounts of vitamin A are mobilized from the liver to the he art without changing plasma concentrations. This is facilitated by an incre ase in the activity of an enzyme that hydrolyzes vitamin A storage forms. ( C) 1999 Elsevier Science Inc.