Increased Myocardial Utilization of
Vitamin A in Heart Failure
Pawan K. Singal, Vince Palace, Michael Hill and Igor
Institute of Cardiovascular Sciences, University of
Manitoba, Winnipeg, Canada.
The role of vitamin A in conferring protection in cardiovascular
diseases is not fully established. Some of the controversies may arise
from the fact that plasma concentration of vitamin A may not provide an
accurate indication of myocardial utilization of vitamin A since plasma
concentration of this vitamin is maintained within a narrow physiological
range. Other tissues, including the liver, kidney and myocardium itself
may be the more appropriate vectors to reflect the overall vitamin A status.
Our studies have shown that vitamin A concentrations are relatively homogeneous
within the left and right ventricular free walls and interventricular septum.
In isolated perfused hearts, oxidative stress due to ischemia-reperfusion
caused a significant decrease in vitamin A in all regions of the myocardium.
However, following in vivo oxidative stress induced by myocardial infarction
(MI), vitamin A levels in the heart remain stable until the severe heart
failure stage. A significant reduction of vitamin A from storage organs
following MI suggested to us that there might be increased mobilization
of vitamin A from these organs to the plasma and the heart. Such an endogenous
supply of vitamin A seems to maintain its myocardial concentrations after
MI. Our experiments, using pulse chase analysis of radio labeled vitamin
A, confirmed an enhanced mobilization from the liver. This change appears
to be mediated by an increase in the activity of bile salt dependent retinyl
ester hydrolase in the liver. Thus, dietary supplementation with vitamin
A may increase resistance to cardiovascular diseases involving oxidative
stress. (Supported by the Medical Research Council of Canada).