Increased Myocardial Utilization of Vitamin A in Heart Failure

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).

  
 
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