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PubMed1995

Insulin sensitivity accounts for glucose and lactate kinetics after intravenous glucose injection.

Mathematical modeling was used to explore the interaction between glucose, insulin, and lactate during the frequently sampled intravenous glucose tolerance test (FSIGTT). Insulin-modified FSIGTs were performed in 25 lean volunteers, and an additional 5 volunteers underwent FSIGTs with glucose injection alone to illustrate the effect of insulin on both glucose and lactate kinetics. The model chosen as the best representation of the system extended the minimal model of glucose kinetics (MM) by including a two-compartment model of lactate kinetics. The model accounted for both glucose and lactate kinetics, provided traditional MM parameters of insulin sensitivity and glucose effectiveness, and descriptive parameters of lactate kinetics. Modeling suggested that lactate production was limited by the rate of glucose disappearance, with no indication of direct effects of insulin on lactate. Inclusion of lactate kinetics had no adverse effect on MM parameters (SG: 0.023 +/- 0.009 vs. 0.023 +/- 0.010 min-1, SI: 1.01 +/- 0.70 vs. 1.03 +/- 0.71 x 10(4).min-1.pmol-1.1; P > 0.50, lactate model vs. MM), and indicated that approximately 1.2% min-1 of total glucose disappearance during the FSIGT is converted to lactate. An additional benefit of including lactate kinetics was the significant improvement in precision in MM parameter estimates as reflected by the fractional standard deviations (FSDs). This effect was most prominent for SG, in which a threefold improvement in parameter precision was observed (FSD: 13.5 +/- 3.1 vs. 42.5 +/- 48.5; means +/- SD).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Effects of metformin on lactate uptake and gluconeogenesis in the perfused rat liver.

To directly assess the effects of the biguanide, metformin, on hepatic gluconeogenesis, it was added at high therapeutic levels (90 microg/ml) to the medium perfusing an isolated rat liver. Lactate (1 mg/min) was infused simultaneously along with [14C]lactate with or without [3H]lactate. [6-(3)H]glucose was added at the beginning of the perfusion in studies where [3H]lactate was not infused. Glucose levels decreased relative to control studies (metformin dose = 0) and lactate concentrations increased in this closed system. Quantitative analysis of the relationship between labeled glucose and lactate indicated that the flux of carbon from lactate to glucose and CO2 was halved, whereas reflux from glucose to lactate increased by approximately 80%. This was corroborated by measurement of labeled lactate extraction as well as glucose, CO2, and lactate production across the liver. Glycogen content of the liver fell by 60% relative to control and was greater for the gluconeogenic pathway. These data are consistent with an inhibitory action of metformin on gluconeogenesis, which is due to a primary inhibition of hepatic lactate uptake.

Animals↗
PubMed1991

Effect of a Saccharomyces cerevisiae culture on lactate utilization by the ruminal bacterium Selenomonas ruminantium.

The objective of this study was to examine the effects of a Saccharomyces cerevisiae culture (YEA-SACC) on lactate utilization by the predominant ruminal bacterium Selenomonas ruminantium. Lactate uptake was stimulated by YEA-SACC concentrations between 2.5 and 10 g/liter, and the 5-g/liter level increased uptake 3.8-fold. When YEA-SACC concentrations were increased above the 5-g/liter level lactate uptake was decreased, but 10 g/liter still stimulated uptake more than threefold. A filter-sterilized YEA-SACC filtrate also increased lactate uptake more than fourfold at all concentrations tested (10 to 100 microliters/ml), and the 25-microliters/ml level increased uptake ninefold. Growth of S. ruminantium in medium that contained 2 g/liter of DL-lactate was stimulated more than twofold by either 2 or 5% (vol/vol) YEA-SACC filtrate after 24 h. The YEA-SACC filtrate also increased the production of acetate, propionate, total VFA, and YLACTATE (grams of cells/mole of lactate) from lactate-grown cells. Because the increase in propionate production was greater relative to acetate, a decrease in the acetate:propionate ratio was observed. Growth on lactate and uptake of radiolabeled lactate by S. ruminantium was stimulated by a filter-sterilized YEA-SACC filtrate. The concentration of L-malic acid in the YEA-SACC filtrate was 4.9 mM, and it seemed that L-malic acid played a role in the stimulation of growth on lactate as well as lactate uptake by S. ruminantium treated with YEA-SACC.

Animals↗
PubMed1992

Recombinant porcine somatotropin for sows during late gestation and throughout lactation.

Two experiments were conducted to evaluate whether administration of recombinant porcine somatotropin (pST) to sows (Hampshire-Yorkshire) enhanced lactational performance. In Exp. 1, sows (n = 84) were fed a corn-soybean meal diet (17.8% CP), or a similar diet with 8% added fat, from d 108 of gestation to d 28 of lactation. Half of the sows fed each diet were injected with 6 mg/d of pST from d 108 of gestation to d 24 of lactation. Diets were fed at 2.27 kg/d from d 108 of gestation until farrowing and then were self-fed during lactation. By d 3 of lactation, litter size was standardized at 8 to 10 pigs per litter. Treating sows with pST resulted in a 10-fold increase (P less than .001) in serum somatotropin at 4 h postinjection. Serum glucose was increased (P less than .01) and serum triglycerides, creatinine, and urea N were decreased (P less than .01) by pST. During the summer, apparent heat stress occurred in pST-treated sows, resulting in 14 deaths. Most (10) of the deaths occurred just before, during, or shortly after farrowing. Fewer (P less than .08) deaths occurred when pST-treated sows were fed the diet with added fat. Sows treated with pST consumed less feed (P less than .10) and lost more backfat (P less than .10) during lactation than controls. Increasing the dietary fat did not prevent these changes. Weaning weights of pigs and milk yield of sows (estimated by deuterium oxide dilution) were not affected by pST treatment. In Exp. 2, sows (n = 42) were injected weekly with 0 or 70 mg of pST on d 3, 10, 17, and 24 of lactation. Litters were standardized by d 3 at 8 to 10 pigs, and sows were fed the same control (low fat) diet as in Exp. 1. Sows treated with pST consumed less feed and lost more weight and backfat during lactation than untreated sows. Litter size, average pig weaning weights, and milk yield were not influenced by pST treatment. These data indicate that a 6-mg daily injection of pST from 6 d prepartum to d 24 of lactation or a 70-mg weekly injection of pST from 3 d postpartum to d 24 of lactation does not increase milk production in lactating sows.

Animals↗
PubMed2001

The influence of gestation feeding strategy on body composition of gilts at farrowing and response to dietary protein in a modified lactation.

Previous experiments have indicated that reproductive function in lean, modern genotypes may be more dependent on body protein mass than, as previously believed, on body lipid reserves. This was investigated in a 3 x 2 factorial arrangement of treatments, involving 60 first-parity sows, comparing three pregnancy feeding strategies and two lactation diets. During pregnancy, sows were fed either a basal diet (5 g lysine/kg, 13 MJ of DE/kg [C]) or the same quantity of basal diet + energy source [E], or additional basal diet supplying both protein and energy [A]. The level of supplement for E and A was adjusted weekly to achieve a backfat thickness measurement (P2 position) of 28 mm at farrowing. Isoenergetic lactation diets were fed to appetite and provided either high (180 g CP/kg, 9 g lysine/kg [H]) or low lysine (120 g CP/kg, 6 g lysine/kg [L]). From d 21 of lactation, sows were separated from their litters and housed next to a boar for 8 h each day; final weaning occurred on d 31. Pregnancy treatment differences in backfat and weight were achieved, with C sows having less backfat on d 1 of lactation than E and A sows (E = 28.1, A = 28.0, C = 22.7 kg, P < 0.001). Sows fed additional basal diet were heavier than E sows, which were heavier than C sows (E = 190, A = 201, C = 178 kg, P < 0.001). Average feed intake over lactation showed a pregnancy feeding effect, with E sows eating less than A or C sows (E = 4.9, A = 5.2, C = 5.4 kg/d, P < 0.005). Total lactation weight loss was affected by pregnancy feeding (E = 18.0, A = 19.0, C = 8.4 kg, P < 0.05) and by lactation diet (L = 19.0, H = 11.3 kg, P < 0.05), whereas total lactation backfat loss was affected only by pregnancy treatment (E = 6.9, A = 6.5, C = 4.6 mm, P < 0.05). No pregnancy treatment or lactation diet effects were observed for litter performance. Lactation diet affected weaning-to-estrus interval, with more sows on the H diet coming into estrus within 6 d of partial weaning (P < 0.05), but there was no pregnancy treatment effect. Therefore, voluntary feed intake during lactation was suppressed by increased fat reserves at a limited body protein mass but not when body protein mass was also increased. Partial weaning-to-estrus interval was increased by reduced dietary protein.

Animals↗
PubMed2003

Performance of sows fed high levels of nonstarch polysaccharides during gestation and lactation over three parities.

The effect of feeding sows a starch diet or a diet with a high level of nonstarch polysaccharides (NSP) during gestation, lactation, or both gestation and lactation during the first three parities on reproductive performance, body weight, and backfat was studied. Four-hundred and forty-four postpuberal gilts were allotted to a 2 x 2 x 2 factorial experiment. Treatments were diet composition during gestation (including the weaning-to-estrus interval; G-Starch: 274 g/kg of starch and 123 g/kg of fermentable NSP or G-NSP: 86 g/kg of starch and 300 g/kg of fermentable NSP), diet composition during lactation (L-Starch: 293 g/kg of starch and 113 g/kg of fermentable NSP or L-NSP: 189 g/kg of starch and 216 g/kg of fermentable NSP) and group-housing system during gestation (free access stalls or electronic feeding). Both gestation diets were formulated to be isoenergetic. During lactation, sows were given free access to the lactation diets from d 6 after parturition onwards. Body weight and backfat gains during gestation were lower in sows fed the G-NSP diet than in those fed the G-starch diet (P < 0.001). The effects were more pronounced in the electronic feeding system than in the free access stalls. These results indicate an overestimation of the energy value of fermentable NSP. Body weight and backfat losses during lactation were less in sows fed the G-NSP diet during gestation than in those fed the G-starch diet (P < 0.05),which can be explained by a 0.4 kg/d higher (P < 0.001) feed intake during lactation of the sows fed the G-NSP diet. Sows fed the L-NSP diet lost more backfat during lactation than sows fed the L-starch diet (P < 0.05). The number of total piglets born and live-born piglets was 0.5 piglet higher in sows fed the G-NSP diet than in those fed the G-starch diet (P < 0.05). Lactation diet did not affect the number of total piglets born or live-born piglets. This study shows that, although high NSP diets negatively influence body weight and backfat thickness of the sows, it is possible to feed sows a diet with a high level of fermentable NSP diet during both gestation and lactation without negative effects on reproductive performance. Under the conditions of this study, feeding sows a diet with a high level of fermentable NSP during gestation and a high level of starch during lactation seems the most favorable feeding strategy.

Adipose Tissue↗
PubMed2003

Lactation persistency: insights from mammary cell proliferation studies.

A persistent lactation is dependent on maintaining the number and activity of milk secreting cells with advancing lactation. When dairy cows are milked twice daily, the increase in milk yield from parturition to peak lactation is due to increased secretory activity per cell rather than to accretion of additional epithelial cells. After peak lactation, declining milk yield is due to loss of mammary epithelial cells by apoptosis. During lactation, only 0.3% of mammary cells proliferate in a 24-h period. Yet this proliferative rate is sufficient to replace most mammary epithelial cells by the end of lactation. Management practices can influence lactation persistency. Administration of bovine somatotropin may enhance persistency by increasing cell proliferation and turnover, or by reducing the rate of apoptosis. Increased photoperiod may also increase persistency of lactation by mechanisms that are as yet undefined. Increased milking frequency during the first weeks of lactation increases milk yield, even after return to less frequent milking, with increases of approximately 8% over the entire lactation. A mammary cell proliferation response to frequent milking during early lactation appears to be involved. Conversely, advanced pregnancy, infrequent milking, and mastitis increase death of epithelial cells by apoptosis. Regulation of mammary cell renewal provides a key to increasing persistency. Investigations to characterize epithelial cells that serve as the proliferative population in the bovine mammary gland have been initiated. Epithelial cells that stain lightly in histological sections are evident through all phases of mammary development and secretion and account for nearly all proliferation in the prepubertal gland. Characterization of these cells may provide a means to regulate mammary cell proliferation and thus to enhance persistency, reduce the effects of mastitis, and decrease the necessity for a dry period.

Animals↗
PubMed2006

Effects of postpartum dietary fat and body condition score at parturition on plasma, adipose tissue, and milk fatty acid composition of lactating beef cows.

Two experiments were conducted with lactating Angus x Gelbvieh beef cows to determine the effects of postpartum lipid supplementation, BCS at parturition, and day of lactation on fatty acid profiles in plasma, adipose tissue, and milk. In Exp. 1, 36 pri-miparous cows (488 +/- 10 kg of initial BW; 5.5 +/- 0.02 initial BCS) were given ad libitum access to hay and assigned randomly to a low-fat (control) supplement or supplements with cracked, high-linoleate safflower seeds (linoleate) or cracked, high-oleate safflower seeds (oleate) from d 3 to 90 of lactation. Diets were formulated to be isonitrogenous and isocaloric; safflower seed diets provided 5% of DMI as fat. Plasma and milk samples were collected on d 30, 60, and 90 of lactation. Adipose tissue biopsies were collected near the tail-head region of cows on d 45 and 90 of lactation. In Exp. 2, 3-yr-old cows achieving a BCS of 4 +/- 0.07 (479 +/- 36 kg of BW) or 6 +/- 0.07 (580 +/- 53 kg of BW) at parturition were used in a 2-yr experiment (n = 36/yr). Beginning 3 d postpartum through d 61 of lactation, cows were fed diets similar to those of Exp. 1. Adipose tissue and milk samples were collected on d 30 and 60, and plasma was collected on d 31 and 61 of lactation. Responses to postpartum dietary treatment were comparable in both experiments. Cows fed linoleate and oleate had greater (P < 0.001) total fatty acid concentrations in plasma than cows fed control. Except for 15:1, milk fatty acids with <18 carbons were greatest (P < or = 0.01) for cows fed control, whereas milk from cows fed linoleate had the greatest (P < or = 0.02) 18:1trans-11, 18:2n-6, and cis-9, trans-11 CLA. Milk from cows fed oleate had the greatest (P < 0.001) 18:1cis-9. In Exp. 1, total fatty acid concentrations in adipose tissue samples decreased at d 90 compared with d 45 of lactation, but the fatty acid profile of cow adipose tissue was not affected (P = 0.14 to 0.80) by dietary treatment. In Exp. 2, the percentage of cis-9, trans-11 CLA in adipose tissue of cows with a BCS of 6 decreased (P = 0.001) from d 30 to 60 of lactation. Plasma and milk fatty acid composition reflected alterations in postpartum diet. Less medium-chain fatty acids and more 18-carbon fatty acids in milk were indicative of reduced de novo fatty acid synthesis in the mammary gland of beef cows fed lipid supplements; however, the metabolic demands of lactation prevented the deposition of exogenously derived fatty acids in adipose tissue through d 90 of lactation.

Adipose Tissue↗
PubMed1995

Selection of a mathematical model to generate lactation curves using daily milk yields of Holstein cows.

Mathematical descriptions of early stages of lactation were investigated using daily milk yields of 117 first, 78 second, 57 third, and 36 fourth lactations of 120 Holstein cows fitted by 10 models. The measure of fit was the error mean squares, which were replaced by ranks to perform an analysis of variance with lactation number, model, and period as factors and with cows as replicates. The interaction of model and lactation number was significant for the fit of the entire lactation. A significant interaction of model and period was obtained for the fit of three 30-d intervals. For the entire lactation, the best fit for all four lactations occurred from the diphasic logistic function, y = d1(1-tanh2(b1(nk-c1))) + d2(1-tanh2(b2(n-c2))). For the first 30 d, a modified gamma function gave the best fit for the first lactation, the inverse polynomial function for the second lactation, and the quadratic log function for the third lactation. The diphasic logistic function gave the best fit for the remaining two periods and was not significantly different from the best fitting models for the first 30-d period. Hence, this function may be useful to describe the lactation curve of Holstein cows for dairy herds in which the daily milk yield of individual cows is constantly monitored with a computer.

Animals↗
PubMed1999

Anti-idiotypic responses of lactating cows immunized with monoclonal antibodies against bovine somatotropin.

The objective of this study was to produce anti-idiotypic antibodies with bovine somatotropin (bST)-like activity by active immunization of lactating cows and to determine their effects on milk yield. Several monoclonal antibodies against bST were evaluated for their interaction with bST in a rat growth bioassay. Two bST-agonist monoclonal antibodies (1 and 2), and two bST-antagonist monoclonal antibodies (3 and 4) were selected. Cows were immunized with immunoglobulin G as a control (n = 12) or with one of the four anti-bST monoclonal antibodies (1, 2, 3, 4; n = 12) on d 3, 24, 45, 66, 87, 108, 129, and 150 of lactation. From wk 3 of lactation, all cows immunized with each of the four anti-bST monoclonal antibodies developed anti-idiotypes until wk 30 of lactation. Total lactation yields were not different among monoclonal antibodies 2, 3, and 4 and control cows (9299, 9321, 9733, and 9415 kg, respectively). However, cows immunized with anti-bST monoclonal antibody 1 had reduced lactation yield compared with cows on other treatments (8136 kg). Daily milk yield of cows immunized with monoclonal antibody 1 was decreased from wk 9 of lactation [36.2 vs. 40.9 kg/d (control)] until the end of lactation, concomitantly with decreased bST concentration from wk 9 of lactation. Cows immunized with anti-bST monoclonal antibody 4 had increased milk yield compared with that of controls during wk 3 to 6 and wk 18 to 21 of lactation. Therefore, anti-idiotypes directed against anti-bST 1 had bST-antagonistic effects on lactation performance; anti-idiotypes against anti-bST 4 transiently increased milk yield.

Animals↗
PubMed1991

Lactational [correction of Lacational] anovulation in rats and its dependency on progesterone.

The relationship between prolactin (PRL) secretion and anovulation in lactating rats was studied. Normal lactating rats and lactating rats treated with antiserum against luteinizing hormone-releasing hormone at the time of postpartal ovulation were used. Normal lactating rats were treated with either a dopamine agonist (CB-154, 150 micrograms/rat) on Day 10 or 13, or pups removal on Day 7 or 10, and thereafter luteolysis and inhibition on PRL secretion were assessed. With the CB-154 treatment, the incidence of luteolysis increased as the lactational period advanced (42% vs 72%), whereas it decreased (73% vs 14%) with the pups removal. Thus, dopamine effectively inhibited PRL secretion during the later lactational stage, but could not do so during the earlier stage when there were mechanisms other than dopamine stimulating PRL secretion. Following luteal regression induced by CB-154, ovulation did not occur if the rats were treated with CB-154 on Day 10, whereas 50% of the rats ovulated within 4 days if treated on Day 13. Furthermore, in the lactating rats treated with anti-luteinizing hormone-releasing hormone serum during late pregnancy, ovulation was not observed until Day 10 of lactation. Since the serum progesterone levels were low in these rats due to the absence of ovulation and lactational corpora lutea, the blockade of ovulation was not due to elevated circulating progesterone during the early lactational period. The mechanism of ovulation blockade during lactation thus seems to shift from being progesterone independent to progesterone dependent at a similar period when the neuroendocrine control of PRL secretion shifts from dopamine independent to dependent.

Animals↗
PubMed2002

Inhibition of Listeria monocytogenes by sodium diacetate and sodium lactate on wieners and cooked bratwurst.

The inhibition of Listeria monocytogenes by sodium lactate and sodium diacetate was evaluated for wieners containing pork, turkey, and beef and for cooked bratwurst containing beef and pork. Both products were supplied by commercial manufacturers. Treated products were surface-inoculated with 10(5) CFU of L. monocytogenes per package and vacuum-packed in gas-impermeable pouches. Wieners were stored for 60 days at 4.5 degrees C, and bratwurst were stored for 84 days at 3 and 7degrees C. A surface treatment that consisted of dipping wieners into solutions containing < or = 6% lactate and < or = 3% diacetate for 5 s did not delay pathogen growth compared with that for untreated wieners. In additional trials, the antilisterial activity of lactate and diacetate in wiener and bratwurst formulations was evaluated. Lactate levels ranged from 1.32 to 3.4%, and diacetate was evaluated at 0.1 and 0.25%. The growth of L. monocytogenes was delayed for 4 and 12 weeks at 7 and 3 degrees C, respectively, on uncured, unsmoked bratwurst formulated with 3.4% lactate/0.1% diacetate, compared with 1 and 2 weeks, respectively, for the formulation containing 2% lactate. L. monocytogenes grew by > or = 1 log unit after 4 weeks' storage at 3 or 7 degrees C on cured, smoked bratwurst without lactate or diacetate, but growth was inhibited for 12 weeks on cured, smoked bratwurst formulated with 3.4% lactate and 0.1% diacetate. Sodium lactate levels of > or = 3% and combinations of > or = 1% lactate plus > or = 0.1% diacetate prevented listerial growth on wieners stored for 60 days at 4.5 degrees C. These results indicate that dipping wieners in lactate-diacetate solutions is not an efficient way to apply these antimicrobial agents to wieners. However, the inclusion of combinations of sodium lactate and sodium diacetate in wiener or bratwurst formulations inhibits the growth of L monocytogenes at < or = 7 degrees C, and an additional margin of safety was observed for products that are cured and smoked.

Acetates↗
PubMed1994

Lower anion gap increases sensitivity in predicting elevated lactate.

OBJECTIVE: The normal reference range for the anion gap (AG) has recently been questioned by several authors. Lowering the upper limit of normal of the AG has been found to be more sensitive in predicting elevated lactate in critically ill adults. The objectives of this study are i) to define a new upper limit of normal of the AG in a study population of healthy adult volunteers, ii) to determine the sensitivity, specificity, the positive predictive value and the negative predictive value of the new upper limit for AG in detecting elevated lactate in critically ill children and to compare these results to the old upper limit of normal of AG (16 mmol/l), iii) to construct a receiver-operating-characteristic (ROC) curve for anion gap as a predictor of elevated lactate, iv) to determine the relationship between anion gap and serum lactate levels in critically ill patients. DESIGN: A prospective, cohort study. SETTING: Paediatric Intensive Care Unit of a University Hospital. SUBJECTS: Part I: Convenience sample of healthy adult volunteers to provide a reference range for anion gap calculation. Part II: Consecutive children admitted to the Paediatric Intensive Care Unit who had lactate levels measured for clinical reasons. MEASUREMENTS: Part I: Electrolytes and blood gases were measured from blood samples drawn from 25 adult volunteers. The reference range for AG was calculated using the equation, AG = Na - (Cl + HCO3). The upper limit of normal was calculated as mean + 2 SD. Part II: Eligible ICU patients were included in this study if they had lactate, electrolytes and blood gases obtained simultaneously. The AG was calculated as above. The new upper limit of normal AG was compared to an AG of 16 for diagnosing an elevated plasma lactate. RESULTS: The mean anion gap in the normal population was 9.4 +/- 1 mmol/l with 11 mmol/l being used as the new upper limit of normal. Thirty-six ICU patients had 189 arterial blood samples from which lactate, electrolytes and blood gas were measured simultaneously. The sensitivity, specificity, positive predictive value and negative predictive value of using an AG of 11 mmol/l as the upper limit of normal were 86%, 40%, 65% and 69% respectively, compared to 49%, 84%, 80% and 55% respectively using the upper limit of normal of AG of 16 mmol/l. The ROC curve supported lowering the upper limit of normal for the anion gap to predict an elevated lactate. There was a linear relationship between anion gap and serum lactate levels. CONCLUSIONS: An AG of 11 mmol/l as the upper limit of normal has a higher sensitivity and higher negative predictive value but lower specificity and lower positive predictive value for detecting elevated lactate in critically ill children.

Acid-Base Equilibrium↗
PubMed2003

[Lactate measurements and acid-base balance in cord blood].

OBJECTIVE: To compare two techniques of lactate measurements in cord blood: either by electrochemical strip method with Lactate Pro of KDK in the umbilical artery alone (series 1) or by enzymatic method with Rapid lab Analyzer of Bayer in the two vessels (series 2) with acid base balance being also determined. SUBJECTS AND METHODS: Series 1 included 353 neonates with a mean gestational age of 37 (+/- 3.6) weeks and series 2 included 410 newborns with a mean gestational age of 38 (+/- 3.1) weeks. RESULTS: Data was presented as mean and SD. In the first series mean umbilical artery lactate concentration was 3.71 (+/- 1.81) mmol/l. In the second series mean umbilical artery blood gas and lactate levels were as follows: pH = 7.25 (+/- 0.9), pCO2 = 6.55 (+/- 1.39) kPa; BD = 6.61 (+/- 3.33) mmol/l, lactate 3.92 (+/- 1.81) mmol/l. The 3rd percentile of pH was 7.05 whereas the 97th percentile of lactate was 7.54 mmol/l. There was a close correlation between lactate and pH, and lactate and BD. Lactate concentration was higher in case of instrumental delivery compared to spontaneous one: 4.65 versus 3.76 mmol/l (p = 0.0001, Student test). No perfect correlation was found between lactate level and neonatal outcome but there was not a significant number of neonates with immediate complication. CONCLUSION: Lactate measurements obtained with single use strip method are valuable and easy to perform.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Cabergoline for inhibition of lactation].

INTRODUCTION: Despite advances in prevention inhibition of lactation, only administration of estrogens or these combined with androgens show variable effectiveness and are indirectly associated with high percentage for lactation rebound, thrombosis, or pulmonary embolism or both of the later during puerperium; in addition, bromocriptine, also used indirectly for inhibition of lactation, is associated with lactation, rebound in 18-40%. Cabergolin is a new ergoline with efficient and durable prolactin reducer effect with fewer adverse effects. PROBLEM: Which will the smallest cabergolin dosage be to inhibit lactation? OBJECTIVE: To demonstrate clinical effectiveness with smallest cabergolina dosage in lactation inhibition. MATERIAL AND METHODS: We carried on a the Service Clinical test on patients hospitalization with an indication to inhibit lactation as the Hospital of Gynecology and Obstetrics, Infantil Maternal Institute of the State of Mexico (IMIEM). The study was done 80 patients to who we administered oral 0.5 mg cabergoline to 40 patients and another group of 40 whom we administered 1.0 mg of cabergoline orally at random and blinded by means of out-patient consultation. We studied correlation between dose and inhibition of lactation as well as presence of adverse effects. RESULTS: In the group of patients to whom administered 0.5 mg, we found 65% (n = 26) with lactation inhibition; adverse effects in this group appeared in 32.5% (n = 13) the second group with a dose of 1.0 mg; 95% with adverse effects in 25% P < 0.001. CONCLUSIONS: Inhibition of lactation with unique dose of 1.0 has satisfactory clinical effectiveness, this being the smaller dose to inhibit lactation at a suitable percentage.

Adult↗
PubMed2004

Reciprocal relationships between blood lactate and hemorheology in athletes: another hemorheologic paradox?

Blood lactate increases during exercise. Although this increase was classically interpreted as a "Pasteur-like effect" resulting from anaerobiosis, it is now clear that it mostly results from a shift in the balance of oxidation of substrates in the muscle, with carbohydrate becoming the predominant fuel. However, we have repeatedly observed that the rise in blood lactate during exercise is correlated to blood viscosity and red cell aggregation. More recently we investigated this issue with the modelling of postexercise lactate kinetics, that allows a fair evaluation of lactate production by muscles (gamma1) and lactate disappearance (gamma2). Postexercise red cell aggregation (Myrenne M1) appears to be correlated to gamma2. Thus microcirculatory adaptations influenced by red cell aggregation may influence lactate disposal, adding its effect to that of the balance between carbohydrates and fat. On the other hand, the rise in blood lactate seems to induce some alterations in erythrocyte rheology at exercise. Correlations between its concentrations during exercise and erythrocyte rigidity support the concept that lactate, at least when it rises above the 4 mmol.l(-1) threshold impairs red cell deformability. Moreover, it seems that endurance training influences erythrocyte response to lactate. While lactate did not in vitro affect erythrocyte aggregation, it impaired (as expected) erythrocyte deformability in sedentary subjects but it (unexpectedly) improved it in trained subjects. This difference may be due to training-induced adaptations in erythrocyte metabolism, including transmembrane transfer via monocarboxylate transporters which show marked alterations in this context. This specific training-induced pattern of response to lactate may provide an alternative explanation to the exercise-induced arterial hypoxemia that occurs in such athletes.

Blood Viscosity↗
PubMed1991

Lysine and protein metabolism in the young lactating woman.

Five lactating and five postpartum non-lactating women of similar ages, times postpartum, body weight and height consumed a liquid formula diet that supplied 1.3 g protein and 32 kcal/kg per day (lactating subjects) and 1.1 g protein and 26 kcal/kg per day (non-lactating subjects). Their last meal supplied 25% of the daily intake and was consumed 4 h before they received L-[13C1]lysine (27 mumol/kg) by a single intravenous injection and L-[15N2]lysine (27 mumol/kg) orally. Frequent plasma and breath samples were collected for 6 h during which time they consumed no food. On a separate day, subjects received NaH13CO3 (10 mumol/kg) as a single intravenous dose and breath samples were collected for 6 h. Plasma tracer lysine levels were determined by gas chromatography-mass spectrometry isotope ratiometry, and breath 13CO2 levels were measured by gas-isotope-ratio mass spectrometry. Averaged tracer data for the two groups were fitted to a multicompartmental model of lysine and protein metabolism that partitioned lysine kinetics between a central and two tissue compartments. The tissue compartments had characteristically fast and slow rates of lysine turnover. The results were compared with those previously obtained in nulliparous women. The postpartum state was associated with a reduction in protein turnover in a compartment with a rapid rate of protein turnover and postpartum women catabolized significantly less lysine than nulliparous controls. Lactating women catabolized slightly more lysine than the non-lactating postpartum subjects, especially when lysine catabolism was expressed as a proportion of lysine flux. Lactation was associated with smaller splanchnic and extracellular pools of free lysine and with an increase in the rate constant for absorption of orally administered lysine. Lysine flux was significantly lower in the lactating subjects and this was associated with a decrease in the rate of lysine turnover in the slowly turning over lysine compartment. The results suggest that lactation is associated with a slower rate of protein turnover in a peripheral tissue compartment. We conclude that an intake of 1.3 g protein/kg per day may be inadequate to support the protein needs of lactation and body protein metabolism and may result in metabolic adaptations that maintain lactation at the potential expense of other aspects of maternal protein turnover.

Adult↗
PubMed1986

Can lactate be used as a fuel by wounded tissue?

The role of lactate in the metabolism of the healing wound is poorly understood. The purpose of the present studies was to determine if despite a net lactate production, wounded (Wx) tissue could metabolize lactate and use it as an oxidative fuel. The extensor digitorum longus muscles (EDL) of weanling, male, Fischer rats were injured with lambda-carrageenan or injured thermally, and 5 and 3 days later, respectively, were incubated in a standard incubate that contained varying amounts of lactate (0 to 6 mmol/L added). Lactate uptake and oxidation, occurred in lambda-carrageenan Wx EDL, thermally injured EDL and non-Wx EDL in a dose-dependent manner. At lactate concentrations of less than 3 mmol/L in the incubate, there was net lactate production, but at lactate concentrations of 6 mmol/L there was no net lactate production by both Wx and non-Wx EDL. The increase in lactate oxidation was not associated with an alteration in the tissue content of adenosine triphosphate or creatine phosphate. It was associated with a reduction in glucose oxidation in Wx and non-Wx EDL and by a decrease in glucose uptake by Wx EDL. These data suggest that lactate may be used as an oxidative fuel by wounded tissue and in this regard may substitute for glucose.

Adenosine Triphosphate↗