Lactic acid infusion in dogs: effects of varying infusate pH

1983 ◽  
Vol 54 (5) ◽  
pp. 1254-1260 ◽  
Author(s):  
L. B. Gladden ◽  
J. W. Yates

This study had two purposes: 1) to determine the effects of varying the pH of lactic acid infusion solutions on the acid-base status of anesthetized dogs, and 2) to determine the effect of elevated blood lactate concentration on muscle lactate concentration. The experiments were performed on the in situ gastro cnemius-plantaris muscle group in 14 mongrel dogs. The infusions increased the arterial blood lactate concentration to 11.0 +/- 0.5 (SE) mM after 20 min. Above an infusate pH of 4.4, the arterial pH increased by 0.118–0.167 during infusion; the arterial pH was unchanged when the infusate pH was between 3.4 and 4.0; and the arterial pH decreased as infusate pH decreased below 3.0. The effect of lactic acid infusion on blood pH appears to be the result of two opposing effects: 1) an acidifying effect due to its weak acid properties, and 2) an alkalinizing effect due to the metabolism of sodium lactate. The estimated ratio between intracellular muscle lactate and venous plasma water lactate averaged 0.647 +/- 0.038, indicative of a substantial gradient between blood and muscle. The infusion produced a significant change from lactate output to lactate uptake by the muscles. The infusion also transiently increased muscle blood flow and oxygen uptake.

1993 ◽  
Vol 75 (3) ◽  
pp. 1070-1074 ◽  
Author(s):  
B. Kayser ◽  
G. Ferretti ◽  
B. Grassi ◽  
T. Binzoni ◽  
P. Cerretelli

The aim of the present study was to test the hypothesis that the net maximal blood lactate accumulation ([La]max) during heavy exercise in lowlanders acclimatized to chronic hypoxia may be limited by the reduced bicarbonate stores. Six men [age 32 +/- 4 (SD) yr] performed supramaximal exercise until voluntary exhaustion at sea level (204 +/- 54 W) and after sojourning for 1 mo at 5,050 m (175 +/- 23 W), without (C) and with (B) oral sodium-bicarbonate loading (0.3 g/kg body wt). Exhaustion time, arterial blood lactate concentration, arterial pH (pHa), arterial PCO2, and intramuscular pH were measured at rest and after exercise. At sea level, exhaustion time increased from 6.5 +/- 2.8 min in C to 7.5 +/- 2.7 min in B (P < 0.05). At altitude, exhaustion times were similar to the sea level C values and the same in C and B. At sea level, resting pHa increased from 7.41 +/- 0.02 in C to 7.46 +/- 0.03 in B (P < 0.001); the corresponding values at altitude were 7.46 +/- 0.04 and 7.55 +/- 0.03 (P < 0.001). Postexercise pHa at sea level was 7.22 +/- 0.02 in C and 7.25 +/- 0.08 in B (NS). After exercise at altitude, pHa was 7.32 +/- 0.04 and 7.44 +/- 0.03 in C and B, respectively (P < 0.001). [La]max increased from 12.86 +/- 1.45 mM in C to 16.63 +/- 1.76 mM in B (P < 0.01) at sea level and from 6.85 +/- 1.40 mM in C to 7.95 +/- 1.74 mM in B (NS) at altitude.(ABSTRACT TRUNCATED AT 250 WORDS)


1985 ◽  
Vol 63 (12) ◽  
pp. 1570-1576
Author(s):  
Mitchell L. Halperin ◽  
Ching B. Chen ◽  
Surinder Cheema-Dhadli

It appears that glutamine and lactate are the principal substrates for the kidney in dogs with chronic metabolic acidosis. Accordingly, the purpose of this study was to determine if a higher or lower rate of renal lactate extraction would influence the rate of glutamine extraction at a constant rate of renal ATP turnover. The blood lactate concentration was 0.9 ± 0.01 mM in 15 acidotic dogs. However, eight dogs with chronic metabolic acidosis had a spontaneous blood lactate concentration of 0.5 mM or lower. The kidneys of these dogs extracted considerably less lactate from the arterial blood (19 vs. 62 μmol/100 mL glomerular filtration rate (GFR)). Nevertheless, glutamine, alanine, citrate, and ammonium metabolism were not significantly different in these two groups of dogs. Renal ATP balance in acidotic dogs with a low blood lactate could only be achieved if a substrate other than additional glutamine were oxidized in that segment of the nephron which normally oxidized lactate; presumably a fat-derived substrate and (or) lactate derived from glucose was now the metabolic fuel at these more distal sites. When the blood lactate concentration was greater than 1.9 mM, lactate extraction rose to 219 μmol/100 mL GFR. Glutamine, alanine, citrate, and ammonium metabolism were again unchanged; in this case, ATP balance required substrate flux to products other than carbon dioxide, presumably, gluconeogenesis. It appears that renal ammoniagenesis is a proximal event and is independent of the rate of renal lactate extraction.


1994 ◽  
Vol 76 (2) ◽  
pp. 846-852 ◽  
Author(s):  
C. Duan ◽  
W. W. Winder

Endurance training attenuates exercise-induced increases in blood lactate at the same submaximal work rate. Three intramuscular compounds that influence muscle lactate production were measured in fasted non-trained (NT) and endurance-trained (T) rats. The T rats were subjected to a progressive endurance-training program. At the end of the program (11 wk), they were running 2 h/day at 31 m/min up a 15% grade 5 days/wk. NT and T rats were fasted for 24 h and then anesthetized (pentobarbital, iv) at rest or after running for 30 min at 21 m/min (15% grade). Blood lactate levels were significantly lower in the T rats than in the NT rats after 30 min of running (2.3 +/- 0.2 vs. 3.9 +/- 0.2 mM). The lower blood lactate concentration was accompanied by lower plasma epinephrine (2.8 +/- 0.4 vs. 6.0 +/- 0.8 nM), adenosine 3′, 3′,5′-cyclic monophosphate (0.36 +/- 0.02 vs. 0.50 +/- 0.03 pmol/mg), mg), glucose 1,6-diphosphate (26 +/- 2 vs. 40 +/- 5 pmol/mg), and fructose 2,6-diphosphate (3.2 +/- 0.2 vs. 4.3 +/- 0.3 pmol/mg) in white quadriceps muscle in T than in NT rats. Red quadriceps muscle glucose 1,6-diphosphate and adenosine 3′,5′-cyclic monophosphate were also lower in T than in NT rats. These adaptations may be responsible in part for the lower exercise-induced blood lactate in fasted rats as a consequence of endurance training.


1991 ◽  
Vol 71 (2) ◽  
pp. 514-520 ◽  
Author(s):  
L. B. Gladden

The purpose of this study was to determine the changes in net lactate uptake (L) by skeletal muscle with a constant elevated blood lactate concentration during steady-level contractions of increasing intensity. The gastrocnemius-plantaris muscle group was isolated in situ in 11 anesthetized dogs. An infusion of lactate/lactic acid at a pH of 3.5–3.7 established a blood lactate concentration of approximately 9 mM while maintaining normal blood gas/pH status. L was measured during three consecutive 30-min periods during which the muscles 1) rested, 2) contracted at 1 Hz, and 3) contracted at 4 Hz. L was always positive, indicating net uptake throughout the lactate/lactic acid infusion. Steady-level O2 uptake averaged 10.9 +/- 2.2 ml.kg-1.min-1 (0.49 +/- 0.10 mmol.kg-1.min-1) at rest, 39.3 +/- 2.1 (1.75 +/- 0.09) at 1 Hz, and 127.8 +/- 9.2 (5.70 +/- 0.41) at 4 Hz. Steady-level L increased with the metabolic rate from 0.113 +/- 0.058 mmol.kg-1.min-1 at rest to 0.329 +/- 0.026 at 1 Hz and 0.715 +/- 0.108 at 4 Hz. The increase in L from rest to 1 Hz was accomplished mainly by an increase in arteriovenous lactate difference, whereas the increase from 1 to 4 Hz was entirely due to a large increase in blood flow. These results support the idea that skeletal muscle is not simply a producer of lactate but can be a significant consumer of lactate even during contractions with a large elevation in metabolic rate.


1976 ◽  
Vol 160 (1) ◽  
pp. 125-128 ◽  
Author(s):  
E J Squires ◽  
D E Hall ◽  
J T Brosnan

1. Arteriovenous differences fro amino acids across kidneys of normal and chronically acidotic rats were measured. Glutamine was the only amino acid extracted in increased amounts in acidosis. There was a considerable production of serine by kidneys from both normal and acidotic rats. 2. The arterial blood concentration of glutamine was significantly decreased in acidotic animals. 3. The glutamine extracted by kidneys of acidotic rats was largely and probably exclusively derived from the plasma. 4. The blood lactate concentration was unchanged in acidosis, as was the uptake of lactate by the kidney.


1998 ◽  
Vol 26 (2) ◽  
pp. 184-188 ◽  
Author(s):  
J. V. Divatia ◽  
T. Jacques ◽  
P. Day ◽  
D. J. Bihari

In critically ill patients, serial measurements of blood lactate may indicate adequacy of therapy and predict development of multi-organ failure. We studied the accuracy, precision, and repeatability of the newly developed 800 Series Lactate Sensor (Ciba Corning Diagnostic Corp., Medfield, U.S.A.). Lactate levels determined with the sensor were compared with the standard laboratory method (Abbott TDX) in 75 paired arterial blood samples from 20 patients. Agreement between methods was determined and the mean coefficient of variation calculated for repeated measurements. The bias of the sensor was -0.38 mmol/l (CI -0.23 to -0.53), and the precision ±0.67. The coefficient of variation for repeated measurements was 1.95% with the sensor, and 11.5% with the TDX (P=0.007). The new sensor offers a more reproducible, rapid method of measuring lactate, vital for serial measurements. The relatively wide limits of agreement between the methods reflect the greater variability of the TDX assay.


2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Giuseppe Nardi ◽  
Gianfranco Sanson ◽  
Lucia Tassinari ◽  
Giovanna Guiotto ◽  
Antonella Potalivo ◽  
...  

Objective. In physiological conditions, arterial blood lactate concentration is equal to or lower than central venous blood lactate concentration. A reversal in this rate (i.e., higher lactate concentration in central venous blood), which could reflect a derangement in the mitochondrial metabolism of lung cells induced by inflammation, has been previously reported in patients with ARDS but has been never explored in COVID-19 patients. The aim of this study was to explore if the COVID-19-induced lung cell damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of anti-inflammatory therapy (i.e., canakinumab 300 mg subcutaneous) could normalize such abnormal lactate a-cv difference. Methods. A prospective cohort study was conducted, started on March 25, 2020, for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy. Arterial and central venous blood samples were contemporarily collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentrations within 24 h from tracheal intubation (T0) and 24 hours after canakinumab administration (T1). Results. At T0, 19 of 21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.15 mmol/L; IQR 0.07–0.25). In the 13 patients undergoing canakinumab administration, at T1, Delta a-cv lactate decreased in 92.3% of cases, the decrease being statistically significant (T0: median 0.24, IQR 0.09–0.31 mmol/L; T1: median −0.01, IQR −0.08–0.04 mmol/L; p=0.002). Conclusion. A reversed Delta a-cv lactate might be interpreted as one of the effects of COVID-19-related cytokine storm, which could reflect a derangement in the mitochondrial metabolism of lung cells induced by severe inflammation or other uncoupling mediators. In addition, Delta a-cv lactate decrease might also reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies.


1970 ◽  
Vol 39 (1) ◽  
pp. 51-60 ◽  
Author(s):  
S. R. Dixon ◽  
W. I. McKean ◽  
J. E. Pryor ◽  
R. O. H. Irvine

1. Twenty-three peritoneal dialyses with fluid containing 45 mEq lactate per litre were carried out on six patients with acute or chronic renal failure. During dialysis arterial blood pH and base excess rose. 2. The lactate ions were rapidly and almost completely absorbed from the fluid in the peritoneal cavity. Blood lactate concentration rose, but in patients with adequate liver function it did not exceed the normal range. One patient with poor hepatic function and renal failure showed abnormally high blood lactate levels after peritoneal dialysis, but metabolic acidosis was still corrected. 3. The concentration of bicarbonate ions in the fluid drained from the peritoneal cavity rose as the dialysis progressed. A significant positive correlation was found between the arterial blood bicarbonate concentration and the bicarbonate concentration in the fluid drained from the peritoneal cavity. 4. If the lactate ions absorbed from the peritoneal cavity had not been metabolized the loss of bicarbonate ions in the fluid drained from the peritoneal cavity would have increased the metabolic acidosis.


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