sodium-lactate and Ischemia

Developments in infusion therapy with sodium lactate administered with its isomer, and developments in acetate utilization, both as an infusate or a dialysate, have been previously described, as have the various effects of sodium acetate on cardiovascular function, metabolism and fluid replacement. Unfavorable effects of acetate infusate or dialysate, such as cardiovascular depression, have also been reported, and although the number of studies reporting favorable effects on cardiovascular metabolism is increasing, it is still a matter of controversy. It is clear, however, that acetate can be metabolized in the liver as well as in extrahepatic organs yielding bicarbonate, which can be utilized as an alkalizing agent. Recently, the authors reported new experimental findings that sodium acetate was metabolized to ketone bodies by the kidney during hepatic inflow occlusion. Ketone bodies attract considerable attention as energy substrates in the stress phase and in the reduced redox state. Administration of sodium acetate under such conditions may therefore contribute as substrate supply.

Topics: Adenosine Triphosphate; Animals; Humans; Ischemia; Isotonic Solutions; Ketone Bodies; Kidney; Liver; Oxidation-Reduction; Resuscitation; Sodium Acetate; Sodium Lactate; Vasodilation

Reduced hepatic lactate elimination initiates blood lactate accumulation during incremental exercise. In this study, we wished to determine whether renal lactate elimination contributes to the initiation of blood lactate accumulation. The renal arterial-to-venous (a-v) lactate difference was determined in nine men during sodium lactate infusion to enhance the evaluation (0.5 mol x L(-1) at 16 ± 1 mL x min(-1); mean ± s) both at rest and during cycling exercise (heart rate 139 ± 5 beats x min(-1)). The renal release of erythropoietin was used to detect kidney tissue ischaemia. At rest, the a-v O(2) (CaO(2)-CvO(2)) and lactate concentration differences were 0.8 ± 0.2 and 0.02 ± 0.02 mmol x L(-1), respectively. During exercise, arterial lactate and CaO(2)-CvO(2) increased to 7.1 ± 1.1 and 2.6 ± 0.8 mmol x L(-1), respectively (P < 0.05), indicating a -70% reduction of renal blood flow with no significant change in the renal venous erythropoietin concentration (0.8 ± 1.4 U x L(-1)). The a-v lactate concentration difference increased to 0.5 ± 0.8 mmol x L(-1), indicating similar lactate elimination as at rest. In conclusion, a -70% reduction in renal blood flow does not provoke critical renal ischaemia, and renal lactate elimination is maintained. Thus, kidney lactate elimination is unlikely to contribute to the initial blood lactate accumulation during progressive exercise.

Topics: Adult; Arteries; Bicycling; Erythropoietin; Exercise; Humans; Ischemia; Kidney; Lactates; Male; Oxygen Consumption; Regional Blood Flow; Rest; Sodium Lactate; Young Adult