Compartmentalization of pyridoxal-5'-phosphate during the acute phase of myocardial infarction.

Vitamin B6 nutritional status is assessed by measuring the plasma concentration of one of its vitamers, pyridoxal-phosphate (PLP). Several conditions, e.g., myocardial infarction (MI), can disturb the dynamic equilibrium between the different vitamers resulting in transiently low plasma PLP levels. An important question is whether these low plasma PLP levels observed during MI represent a transient state of deficiency and what the possible clinical consequences of such a fall in plasma PLP could be. Since the main metabolic function of PLP is to act as an intracellular coenzyme, it was decided to monitor the changes not only of PLP but also of PL (transport form of vitamin B6) in both the plasma and red blood cells (RBCs) in patients with myocardial infarctions (MI): 16 patients with proven MI were investigated measuring the aforementioned parameters at regular intervals. It was found that the approximately 40% fall in plasma PLP levels was accompanied by an equivalent increase in RBC PLP levels. Subsequently plasma PLP concentrations returned to normal but RBC PLP values were maintained at the newly elevated steady state (without any vitamin supplementation). Since membranes are impermeable to PLP, the only way in which PLP could have been redistributed to the intracellular compartment was through hydrolysis to PL and rephosphorylation once inside the RBCs. This compartmentalization could be an important adaptive response since it has been shown that PLP reduces O2 affinity of deoxygenated hemoglobin, thereby facilitating O2 delivery to the tissues.(ABSTRACT TRUNCATED AT 250 WORDS)