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Both sodium 6(+) and D(-) lactate stimulate insulin secretion from the isolated perfused rat pancreas; however the insulin secretory effect of the L(+) form is much superior to that of the D(-) form. Glucagon secretion is not modified by the two isomers.
INTRODUCTION: Bicarbonate-buffered crystalloids avoid exogenous lactate and have physicochemical properties distinct from compound sodium lactate (CSL), but direct comparative evidence during major abdominal surgery remains limited. METHODS: This single-center, open-label, randomized non-inferiority trial enrolled high-risk adults undergoing elective major abdominal surgery. Participants received bicarbonate-buffered solution or CSL as the allocated intraoperative crystalloid. The primary estimand was the arithmetic mean difference in standard base excess (SBE) at skin closure (bicarbonate-buffered solution minus CSL). The non-inferiority margin was -1.5 mEq/L. The trial was prospectively registered with the Australian New Zealand Clinical Trials Registry (ACTRN12619001228178). RESULTS: Fifty participants were randomized (25 per group) and received their allocated intervention. End-of-surgery arterial blood gas data were missing for two CSL participants. In the intention-to-treat analysis using multiple imputation, the estimated mean difference in end-of-surgery SBE was -0.42 mEq/L (95% confidence interval [CI], -1.92 to 1.09 mEq/L). The complete-case per-protocol estimate was -0.48 mEq/L (95% CI, -2.02 to 1.06 mEq/L). In both analyses, the lower CI bound was below the prespecified non-inferiority margin; non-inferiority was not established. Secondary outcomes were exploratory; observed end-of-surgery lactate was lower with bicarbonate-buffered solution (median 0.9 vs 1.2 mmol/L; unadjusted P = 0.031), without a corresponding difference in SBE or pH. CONCLUSIONS: In this small trial of hemodynamically stable adults undergoing elective major abdominal surgery, the primary non-inferiority result was inconclusive. The data did not establish interchangeability, equivalence, superiority, or inferiority of the two fluids. As the trial was powered for a physiologic endpoint, no comparative inference can be made about organ dysfunction, postoperative complications, recovery, or mortality. Larger trials with standardized co-interventions and patient-important outcomes are required before routine substitution for CSL can be recommended.
1. The effects of sodium DL-lactate and sodium chloride (2.5 mg/kg as 865 mmol/l solutions given by intravenous infusion over 20 min) on the renal tubular reabsorption of phosphate have been compared in five normal adults. 2. Sodium lactate produced a marked but transient increase in urinary phosphate excretion due to a reduction in net renal tubular reabsorption of phosphate; the mean value of the maximum rate of renal tubular reabsorption of phosphate/unit of glomerular filtration rate (TmP/GFR) decreased from 1.14 to 0.82 mmol/l. 3. This effect was not due simply to expansion of the volume of the extracellular fluid, since the reduction in TmP/GFR after sodium chloride infusion was less marked, nor did it seem to be due entirely to alkalinization of the urine since the maximum increase in urinary pH occurred 20--40 min after the maximum decrease in TmP/GFR.
In 15 dogs who had been given propranolol and 5 humans who had been given Pindolol, an infusion of sodium lactate produced: 1) an increased in blood lactate levels and pH; 2) an increase in the cardiac index; 3) a state in which an infusion of isoproterenol (inactive on its own) could act as it would have done had the betaadrenergic receptors not been blocked. A perfusion of lactic acid which was sufficient to cause the variations in pH and blood lactate levels that are seen with exercise had no action on the heart rate nor on the cardiac index of 10 dogs treated with propranolol and could not re-establish the betastimulating properties of isoproterenol. Finally, alkalosis produced by an infusion of THAM in 13 dogs or sodium bicarbonate in 2 humans, changed neither the cardiac index nor the heart rate, nor the response to isoproterenol after a betaadrenergic blockade. Infusion of sodium lactate associated with isoproterenol could be used to combat the depressent effects of betablockers in patients with cardiac disorders.
In samples of brain tissue obtained during operations from 40 neurosurgical patients the concentrations of lactate, sodium and potassium were determined. A statistically significant fall of potassium concentration and increased sodium concentration was found in patients with lactate concentration exceeding 0.9 mg/g of fresh tissue. All patients with raised lactate level in the cerebrospinal fluid before the operation tolerated poorly the neurosurgical intervention. Examination of brain tissue in these cases showed changes compatible with advanced brain oedema.
A chemostat curve has been constructed for changes in the Propionibacterium shermanii population density with an increase in the flow rate of the medium from 0.04 to 0.55 h-1 upon limitation of the growth with sodium lactate deficiency. The curve differs from the classic chemostat curve described with the Monod equation, thus indicating changes in metabolism at different growth rates. Fermentation of lactate to acetic and propionic acids by the culture is most complete at low flow rates of the medium (D = 0.04 h-1). The rates of oxidation processes increase at average flow rates (D = 0.1--0.33 h-1). Lactate is both fermented to yield volatile acids, and oxidized. The growth rate D = mu = 0.55 h-1 approaches the maximal one. The rate of fermentation by the culture at this growth rate decreases while the rate of oxidation increases. The ratio between the rates of these two processes shifts towards oxidation. The cells display now a very high synthetic activity: constructive metabolism of the cells is realized practically only at the account of the nitrogen from ammonium rather than the nitrogen of amino acids. The chemical composition of the cells along the chemostat curve is relatively constant. The content of protein and DNA does not change; the content of RNA slightly rises with an increase in the growth rate, and the protein synthesizing activity of RNA is directly proportional to D = mu.
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In acute cerebrovascular accidents the uptake of lactate by the brain tissue is enhanced, possibly in an attempt to buffer the increased local lactic acidosis. In this paper the results obtained by the administration of the lactate in 78 cases of hyperventilatory syndromes secondary to acute brain injuries, and the biochemistry of the cerebrospinal fluid and blood, are reported.
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Goats were injected intraruminally during spontaneous meals with ammonium chloride, urea, ammonium lactate, or sodium lactate arranged in a Latin square experimental design randomized for order of treatments. Urea and ammonium injections shortened meal length by 20 to 30%. Rate of eating and meal frequency were reduced. Sodium lactate injections reduced meal size. In cows, meal length and meal size also were measured. Grain concentrate, corn silage, and chopped hay were fed as complete mixed rations. In the concentrates 58+ of the nitrogen was either from soybean meal or urea. Length of the first meal after feeding was reduced from 24.3 min with soybean meal to 12.4 with urea. Meal size was reduced from 3.2 kg to 1.8 kg when urea was fed. Total feed intake was similar, 12.0 kg/day (soybean meal) and 11.6 kg/day (urea) since spontaneous meal number and size were 17 and .30 kg for soybean meal but increased to 23 and .36 kg for urea. The physiological basis for the limit on meal length with urea rations is unknown but is an important factor in successful feeding of urea when eating time is limited for cows.
A growth medium with a specific oxidation-reduction potential containing peptone, dextrose, sodium succinate, sodium lactate, gelatin, sodium bicarbonate and blue tetrazolium, an indicator dye, in a tris(hydroxymethyl)aminomethane buffer was used to detect the presence of microorganisms in blood. The procedure involved the introduction of blood (and bacteria) into the growth medium with the dye in its colorless state. As the bacteria grew, they converted the dye to a visible blue color (formazan) with their reductases. The growth medium served as its own contamination control, since microbial growth and be detected by a color change before it was used for blood culture. The experiments described herein demonstrate that the composition of this medium (with the dye) provides a unique system that is able to make a reliable and rapid detection of both gram-positive and gram-negative microorganisms and yeasts (Candida albicans) commonly associated with bacteremia.
Effect of lactate on FFA--release and cyclic 3', 5-AMP accumulation in fat cells at different pH. Acta Physiol. Pol., 1977, 28 (6): 505--510. The effect of sodium lactate on noradrenaline (NA), theophyline (Th), and dibutyryl cyclic 3', 5'AMP stimulated free fatty acid (FFA) release as well as on NA--stimulated cyclic 3', 5'AMP (cAMP) accumulation in isolated fat cells at different pH was studied. It was shown that at each of examined pH (6.8, 7.1, 7.4, 7.7) sodium lactate inhibits NA and Th-induced FFA release and NA-stimulated cAMP accumulation. It did not significantly change FFA release induced by dibutryl cyclic 3', 5'AMP. The inhibitory effect of sodium lactate both on FFA release and cAMP accumulation was markedly augmented at pH 7.1 and especially at pH 6.8 as compared to pH 7.4, while at pH 7.7 it remained essentially the same as at pH 7.4. The obtained results showed that lactate exerts its antilipolytic effect through the inhibitory action on cAMP accumulation and subsequently on the activity of the hormone-sensitive triglyceride lipase. An effect of lactate on FFA reesterification cannot be however excluded. It seems that the potentiation of the antilipolytic effect of lactate at pH below 7.4 has an important physiological significance. The mechanism protects effectively against an excessive, undesirable FFA-outflow from adipose tissue in situations in which FFA cannot be utilized.
Intrarenal arterial infusions of sodium and potassium salts with anions other than chloride were given to evaluate the role of the chloride ion in influencing renin secretion (RS). The studies were conducted in dogs with thoracic caval constriction. Sodium lactate increased renal venous plasma sodium concentration (RVPNa) from 142 to 166 meq/liter (n, 6); RS decreased from 3,070 to 1,510 ng angiotensin/min (P less than 0.005). Arterial blood pressure and renal blood flow were not changed appreciably. Sodium excretion (ENa) increased, whereas chloride excretion (EC1) fell during the first three 15-min infusion periods. Potassium lactate increased renal venous plasma potassium concentration from 4.1 to 6.2 meq/liter (N, b). RS decreased during the first three 15-min periods of infusion (from 3,470 to 2,180 ng angiotensin/min, P less than 0.01). ENa and EC1 increased during the infusion. Potassium sulfate also decreased RS, and EC1 was usually increased. The results with sodium lactate favor a role for sodium compared with chloride in mediating the decreased renin release, but there are other possible interpretations which have been discussed. Additional studies are needed to resolve the role of chloride during potassium infusion.
Rapidly induced systemic alkalinization due to either sodium-lactate or sodium-bicarbonate infusion in prolonged-fasted subjects with steady-state ketoacidosis was associated with a decrease in urine pH. This decrease in urine pH from 5.50 to 5.20 was the result of a significant decrease in urinary ammonium excretion from 8.40 to 6.35 mEg/hr and was not accompanied by an increase in net acid excretion (11.3 vs. 10.6 mEg/hr). The decreased ammonium excretion is attributed to the raised pH of the proximal tubular fluid resulting in a less favorable pH gradient for gaseous ammonia entry. This would decrease gaseous ammonia generated in the loop of Henle for collecting duct buffering of secreted hydrogen ions.
Treatment of chronic uremia by hemodiafiltration requires replacement of the filtrate. Using Ringer's solution alone, there is a depression of pH because of bicarbonate loss. To bring the acid base status back to normal, sodium lactate in increasing concentrations (283 mg% = 32 mM/1, 361 mg% = 40 mM/1; 462 mg% = 51 mM/1; 508 mg% = 57 mM/1) was added to the replacement fluid. The optimal concentration is 450 mg% (=50 mM/1) sodium lactate, provided the following conditions are fulfilled: (a) substitution after the filter; (b) mixing ratio of blood and substitution fluid 1:2. Using 12-15 liters of substitution fluid during a 5 hr treatment, the added lactate amounts to 60 g (=0.54 M). With continuous addition of lactate, the serum concentration of lactate is 3.5 times normal and the concentration of serum pyruvate 4 times normal. An excess lactate concentration, according to Huckabee [1,2], was thus not observed. The sieving coefficients were the following: sodium, potassium, urea, lactate, pyruvate, and phosphate 1; chloride greater then 1; calcium and protein less than 1. Serum osmolality fell, on the average, 9 mOsmol/1 during diafiltration.
The diaphragm muscle (the red muscle) and m. obliquus externus abdominis (the white muscle) were incubated in phosphate buffer at pH 7.4 and 6.8 in the presence of different concentrations of sodium lactate (0, 5, 10 and 30 mM). None of the used lactate concentrations changed significantly glucose uptake by the both muscles at pH 7.4. At pH 6.8 lactate in a concentration of 30 mM decreased significantly glucose uptake by the white muscle. At pH 7.4 glucose uptake by the white muscle was significantly lower than that by the red one in the presence of 10 and 30 mM of sodium lactate while at pH 6.8 in the absence of lactate and in the presence of 5 and 30 mM of lactate. Acidosis affected in smaller degree glucose uptake by the red muscle than by the white one. It may be supposed that the impairement of glucose uptake by acidosis and lactic acid in strenously working skeletal muscles can limit the amount of energy sources available for the muscles. Subsequently, it may be one of the factors limiting the ability of the muscles to continue the exhausting exercise.