Metabolism of vitamin A in the heart increases after a myocardial infarction.
The supply of vitamin A to the myocardium by storage organs during increased oxidative stress subsequent to myocardial infarction (MI) was examined in hemodynamically assessed rats using compartment analysis of a radio-labeled vitamin A. 3H-Vitamin A was injected into two groups of rats: an MI group and a control group. There were no differences in the plasma or myocardial content of total vitamin A (unlabeled + labeled) between the two groups. However, the proportion of 3H-vitamin A was greater in the myocardium as well as plasma of MI rats. Rats with MI also had significantly lower 3H-vitamin A levels in liver and kidney than sham controls. The greatest difference in vitamin A content was in the concentrations of 3H-labeled storage forms of vitamin A in the liver of MI animals. Activity of bile salt-dependent retinyl ester hydrolase, an enzyme responsible for hydrolyzing vitamin A storage forms, was significantly increased in the liver of MI animals. These data indicate that analysis of plasma concentrations of vitamin A to ascertain links to cardiac conditions may be inappropriate. Specifically, during MI, increased amounts of vitamin A are mobilized from the liver to the heart without changing plasma concentrations. This is facilitated by an increase in the activity of an enzyme that hydrolyzes vitamin A storage forms.
Palace
V P
VP
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Center, Winnipeg, Canada.
Hill
M F
MF
Khaper
N
N
Singal
P K
PK
D000818:Animals; D002265:Carboxylic Ester Hydrolases / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014801:Vitamin A / Q000378:metabolism*
D014801:Vitamin A; D002265:Carboxylic Ester Hydrolases; C022523:retinyl esterase