Lactate improves cardiac efficiency after hemorrhagic shock

This study was undertaken to examine the role of lactate on cardiac functio n and metabolism after severe acute hemorrhagic shock. Anesthetized, nonhep arinized rats were bled to a mean arterial pressure of 25-30 mm Hg for 1 h; controls were not bled. Their hearts were removed, and cardiac work and ef ficiency (work/oxygen consumption) were measured in the isolated working he art mode for 60 min. The hearts were perfused with one of five substrate co mbinations: 1) glucose (11 mM), 2) glucose + 0.4 mM palmitate, 3) glucose 0.4 mM palmitate + 8.0 mM lactate, 4) glucose + 1.2 mM palmitate, or 5) gl ucose + 1.2 mM palmitate + 8.0 mM lactate. After perfusion, hearts were fre eze-clamped, and tissue contents of free coenzyme-A (CoA), acetyl CoA, and succinyl CoA were measured, as was myocardial pyruvate dehydrogenase (PDH) activity. The addition of 8.0 mM lactate significantly improved cardiac wor k in shocked hearts perfused with 0.4 mM palmitate and increased cardiac ef ficiency in the presence of either 0.4 mM or 1.2 mM palmitate. Compared to control hearts, shocked hearts exhibited a 20-30% decrease in PDH activity. Shocked hearts perfused with lactate demonstrated no increase in acetyl Co A content but did have a significant increase in tissue succinyl CoA compar ed to control hearts perfused with lactate or shocked hearts perfused witho ut lactate. In the heart recovering from severe hemorrhagic shock, lactate improves cardiac efficiency in the presence of free fatty acids, possibly b y a anaplerosis of the tricarboxylic acid cycle.