Effect of site of lactate infusion on regional lactate exchange in pigs.

BACKGROUND: The rate of extra-hepatic lactate production and the route of influx of lactate to the liver may influence both hepatic and extra-hepatic lactate exchange. We assessed the dose-response of hepatic and extra-hepatic lactate exchange during portal and central venous lactate infusion. METHODS: Eighteen pigs randomly received either portal (n=5) or central venous (n=7) lactate infusion or saline (n=6). Sodium lactate was infused at 33, 66, 99, and 133 µmol kg⁻¹ min⁻¹ for 20 min each. Systemic and regional abdominal blood flows and plasma lactate were measured at 20 min intervals until 1 h post-infusion, and regional lactate exchange was calculated (area under lactate uptake-time curve). RESULTS: Total hepatic lactate uptake [median (95% confidence interval)] during the experimental protocol (140 min) was higher during portal [8198 (5487-12 798) µmol kg(-1)] than during central venous lactate infusion [4530 (3903-5514) µmol kg⁻¹, P<0.05]. At a similar hepatic lactate delivery (∼400 µmol kg⁻¹ min⁻¹), hepatic lactate uptake [mean and standard deviation (sd)] was higher during portal [118 (sd 55) µmol kg⁻¹ min⁻¹] than during central venous lactate infusion [44 (12) µmol kg⁻¹ min⁻¹, P < 0.05]. Time courses of arterial lactate concentrations and lactate uptake at other measured regions were similar in both groups. CONCLUSIONS: Higher hepatic lactate uptake during portal compared with central venous lactate infusion at a similar total hepatic lactate influx underlines the role of portal vein lactate concentration in total hepatic lactate uptake capacity. Arterial lactate concentration does not depend on the site of lactate infusion. At higher arterial lactate concentrations, all regions participated in lactate uptake.

Investigations of D-lactate metabolism and the clinical signs of D-lactataemia in calves.

Five clinically healthy calves received an intravenous injection of 25 g sodium D-lactate (223 mmol) in 100 ml sterile water and five control calves were given the same volume of 0.9 per cent sodium chloride. Two clinical examiners who were blinded to the status (test or control) of the calves observed that between eight and 40 minutes after the injections the calves that had received sodium-D-lactate could be distinguished with certainty from the control calves on the basis of their clinical signs, for example, an impaired palpebral reflex, somnolence and a staggering gait. One-compartment and two-compartment analyses of the changes in the plasma concentration of D-lactate, and its renal clearance, indicated that the calves metabolised considerable amounts of D-lactate.

No difference in net uptake or disposal of lactate by trained and untrained forearms during incremental sodium lactate infusion.

A number of training adaptations in skeletal muscle might be expected to enhance lactate extraction during hyperlactataemia. The aim of the present study was to determine whether resting endurance-trained forearms exhibit an increased net lactate removal during hyperlactataemia. Six racquet-sport players attended the laboratory for two experiments, separated by 2 weeks. In the first experiment incremental handgrip exercise to fatigue was performed to identify trained (TRFA, n = 6) and untrained (UTFA, n = 5) forearms. In the second experiment net forearm lactate exchange was compared between TRFA and UTFA during an incremental infusion of sodium lactate. TRFA performed more work than UTFA during handgrip exercise [mean (SE) TRFA, 66.1 (9.5) J.100 ml(-1); UTFA, 35.1 (2.3) J.100 ml(-1); P = 0.02] and UTFA exhibited a greater increase in net lactate output relative to work load (P = 0.003). During lactate infusion net lactate uptake across the resting forearms increased linearly with the arterial lactate concentration in both groups (TRFA, r = -0.95 (0.03); UTFA, r= -0.92 (0.04); P < 0.02], with no difference in the regression slopes [TRFA, -1.06 (0.13); UTFA, -1.07 (0.27); P = 0.97] or y-intercepts [TRFA, 0.67 (0.20); UTFA, 1.36 (0.67); P = 0.37] between groups. Almost all of the lactate taken up was disposed of by both groups of forearms [TRFA, 99.6 (0.2)%; UTFA, 98.5 (1.0)%; P = 0.37]. It was concluded that the net uptake and removal of lactate by resting skeletal muscle is a function of the concentration of lactate in the blood perfusing the muscle rather than the muscle training status.

The use of different buffers during continuous hemofiltration in critically ill patients with acute renal failure.

OBJECTIVE: To determine the impact of different hemofiltration (HF) replacement fluids on the acid-base status and cardiovascular hemodynamics in patients with acute renal failure (ARF) and continuous veno-venous hemofiltration (CVVH). DESIGN: Prospective, cohort study. SETTING: Intensive Care Unit of the Heinrich Heine University Hospital, Düsseldorf, Germany. SUBJECT AND METHODS: One hundred and thirty-two critically ill patients with acute renal failure and continuous veno-venous HF were studied. Fifty-two patients were subjected to lactate-based (group 1), and 32 to acetate-based hemofiltration (group 2) while 48 (group 3) were treated with bicarbonate-based buffer hemofiltration fluid. Fifty-seven had a septic, and 75 a cardiovascular, origin of the ARF. Creatinine, blood urea nitrogen (BUN), serum bicarbonate, arterial pH, lactate and Apache II scores were noted daily. MAIN RESULTS: The mean CVVH duration was 9.8 +/- 8.1 days, mortality was 65%. No difference was present between the groups under investigation with regard to the main clinical parameters. Lactate- and bicarbonate-based hemofiltration led to significantly higher serum bicarbonate and arterial pH values as compared to the acetate-based hemofiltration. Serum bicarbonate values at 48 h after the initiation of CVVH treatment were 25.7 +/- 3.8 mmol/l (p < 0.001) in group 1, 20.6 +/- 3.1 mmol/l in group 2 and 23.3 +/- 3.9 mmol/l (p < 0.001) in group 3. While a lack of increase in serum bicarbonate and arterial pH was correlated to poor prognosis in lactate- and bicarbonate-based hemofiltration, no such observation was made in acetate-based hemofiltration. Cardiovascular hemodynamics were superior in patients treated with lactate- and bicarbonate-based buffer solution as compared to those treated with acetate-based buffer solution. CONCLUSIONS: The degree of correction of acidosis during hemofiltration was determined by patient outcome in patients treated with lactate- and bicarbonate-based buffer solutions, but not in patients receiving acetate-buffered solution. Bicarbonate and lactate-based buffer solutions were found to be superior to acetate-based replacement fluid.