Blood lactate kinetics in normal and stress-susceptible pigs.

In vitro rates of lactate metabolism were determined in stress-susceptible (SS) and stress-resistant (SR) pigs. Three SR and three SS pigs were given 20 muCi of [U-14C] L-lactate by a single injection method and resting blood lactate kinetics were measured. Seventeen blood samples were taken during the 60 min after injection. Lactate was separated from the deproteinized plasma by silicic acid column chromatography, and specific radioactivity was determined. Kinetic characteristics were calculated from plots of specific activity versus time. Pigs met steady-state requirements during the sampling period. There were no differences in kinetic characteristics of resting SS and SR pigs. Later, a second isotope injection was given after 5 min of electrical stress. Lactate pool sizes increased similarly in both types of pigs after stress; however, SS pigs had greater plasma lactate concentrations after stress. It is concluded that SS and SR pigs respond differently to stress but have similar capacities to metabolize lactate while resting.

Conversion of alanine, aspartate and lactate to glucose and CO2 in liver from stress-susceptible and stress-resistant pigs.

Rates of conversion of lactate, alanine and aspartate to glucose and oxidation of each to CO2 were determined in incubated liver slices from nine stress-susceptible (SS) and seven stress-resistant (SR) Yorkshire pigs ranging in body weight from 24 to 54 kg. Pigs were screened for stress susceptibility by exposure to halothane at 7 weeks of age. Stress was minimized before slaughter, and liver samples were obtained immediately after death. Rates of lactate and aspartate conversion to glucose were not significantly different between pig types. Mean rates of lactate conversion to glucose in livers of SS and SR pigs were 637 and 413 nmoles/(100 mg X 2 hours), respectively. Mean rates of aspartate conversion to glucose were 441 and 540 nmoles/(100 mg X 2 hours) in SS and SR pigs, respectively. Alanine conversion to glucose in livers of SS pigs was slower than that in SR pigs [527 and 813 nmoles/(100 mg X 2 hours), respectively]. Rates of hepatic gluconeogenesis from lactate probably do not predispose SS pigs to the lactic acidosis observed during the porcine stress syndrome. Rates of lactate, alanine and aspartate oxidation to CO2 in livers of SS pigs were 61, 59 and 76%, respectively, of the rates observed in SR pigs. Decreased rates of substrate oxidation to CO2 may contribute to the development of the syndrome in SS pigs.