Functional role of aerobic glycolysis in rat portal vein.

The functional role of aerobic lactate production in the rat portal vein was investigated. Changing substrate from glucose (11.5 mM) to pyruvate (11.5 mM) or beta-hydroxybutyrate (3 mM) had virtually no effect on spontaneous mechanical activity. Lactate production (FLA) was smaller with pyruvate than with glucose (0.05 +/- 0.01 vs. 0.14 +/- 0.03 mumol g-1 min-1, n = 4). Addition of 0.5 mM iodoacetate to inhibit glycolysis abolished mechanical activity in 15-20 min with glucose as substrate, whereas with pyruvate the mechanical activity was only moderately reduced over this time period. With beta-hydroxybutyrate (3 mM) as substrate no aerobic lactate production was detected during normal spontaneous activity. Inhibition of cellular respiration with increasing concentrations of cyanide in beta-hydroxybutyrate medium led to a graded decrease in mechanical activity and FO2, but only a marginal increase in lactate production. With glucose as substrate, repeated stimulation with a combination of isoproterenol (10(-5) M) and papaverine (10(-4) M) gave similar increases in lactate production at each exposure. With beta-hydroxybutyrate some lactate production was found at the first stimulation, but decreased to be abolished at the third stimulation. The mechanical inhibition caused by the stimulation was however similar at the three exposures for both substrates. Lactate production induced by cAMP-raising stimulation in beta-hydroxybutyrate could be accounted for by glycogenolysis. These results show that aerobic glycolysis leading to net lactate production is not necessary for normal spontaneous mechanical activity or the relaxing effect of hypoxia or cAMP raising stimuli in rat portal vein.