Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LACTATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,657 records · Page 92Linked to original sources
PubMed2006

Luminal concentrations of L- and D-lactate in the rectum may relate to severity of disease and outcome in septic patients.

INTRODUCTION: Little is known about the condition of the large bowel in patients with sepsis. We have previously demonstrated increased concentrations of L-lactate in the rectal lumen in patients with abdominal septic shock. The present study was undertaken to assess the concentrations of L- and D-lactate in rectal lumen and plasma in septic patients including the possible relation to site of infection, severity of disease, and outcome. METHODS: An intensive care unit observational study was conducted at two university hospitals, and 23 septic patients and 11 healthy subjects were enrolled. Participants were subjected to rectal equilibrium dialysis, and concentrations of L- and D-lactate in dialysates and plasma were analysed by spectrophotometry. RESULTS: Luminal concentrations of L-lactate in rectum were related to the sequential organ failure assessment scores (R2 = 0.27, P = 0.01) and were higher in non-survivors compared to survivors and healthy subjects (mean [range] 5.0 [0.9 to 11.8] versus 2.2 [0.4 to 4.9] and 0.5 [0 to 1.6] mmol/l, respectively, P < 0.0001), with a positive linear trend (R2 = 0.53, P < 0.0001). Also, luminal concentrations of D-lactate were increased in non-survivors compared to survivors and healthy subjects (1.1 [0.3 to 2.5] versus 0.3 [0 to 1.2] and 0.1 [0 to 0.8] mmol/l, respectively, P = 0.01), with a positive linear trend (R2 = 0.14, P = 0.04). Luminal concentrations of L- and D-lactate were unaffected by the site of infection. Plasma concentrations of L-lactate were also increased in non-survivors compared to survivors (3.8 [1.7 to 7.0] versus 1.5 [0 to 3.6] mmol/l, P < 0.01). In contrast, plasma concentrations of D-lactate were equally raised in non-survivors (0.4 [0.1 to 0.7] mmol/l) and survivors (0.3 [0.1 to 0.6] mmol/l) compared with healthy subjects (0.03 [0 to 0.13] mmol/l). CONCLUSION: In patients with severe sepsis and septic shock, luminal concentrations of L- and D-lactate in the rectum were related to severity of disease and outcome.

Adult↗
PubMed1996

Effects of hyperinsulinemia and hyperglycemia on lactate release and local blood flow in subcutaneous adipose tissue of healthy humans.

To determine the effects of hyperglycemia and hyperinsulinemia on lactate production by adipocytes, healthy volunteers were studied during three experimental protocols. In protocol 1, the changes in interstitial lactate concentrations were measured by microdialysis (sc tissue) after oral glucose administration. The plasma lactate concentration increased by 39.4 +/- 6.0%, and the dialysate lactate concentration increased by 117.9 +/- 16.3%. In protocol 2, a 2.5-h hyperinsulinemic euglycemic clamp and somatostatin infusion were performed. The plasma and dialysate lactate concentrations increased by 27.1 +/- 5.5% and 146.8 +/- 44.5%, respectively. In addition, [U-13C]glucose was infused through the probe, and dialysate lactate was enriched in 13C at 2.5 +/- 0.3 molar percent excess basally and at 3.4 +/- 0.3 molar percent excess during the clamp (P < 0.05 vs. basal). [13C]Urea was also infused through the probe, and the outflow to inflow ratio of [13C]urea was used as an index of local blood flow. It decreased by 10.2 +/- 3.6% (P < 0.001) at the end of the hyperinsulinemic euglycemic clamp, indicating an increase in blood flow. In protocol 3, a hyperglycemic clamp (10.0 mmol/L) at the basal insulin concentration was performed. It increased the dialysate lactate concentration by 43.5 +/- 15.9% and did not alter the plasma lactate concentration or local blood flow. It is concluded that hyperinsulinemia and, to a lesser extent, hyperglycemia stimulate glucose conversion into lactate in adipocytes. Hyperinsulinemia, but not hyperglycemia, also increases adipose tissue blood flow.

Adipose Tissue↗
PubMedDate not supplied

Prognostic value of blood lactate, blood glucose, and hematocrit in canine babesiosis.

Canine babesiosis typically causes hemolytic anemia but also can result in multiple organ dysfunction. Human patients with severe disease often have persistent hyperlactatemia, and blood lactate concentration is correlated with survival rate. In dogs, blood lactate concentration has been shown to be of prognostic value in patients with gastric dilatation-volvulus and in dogs admitted to intensive care units. Serial blood lactate and glucose concentrations and hematocrit on admission were determined in 90 dogs with naturally occurring, severe or complicated canine babesiosis. Forty-five dogs (50%) had hyperlactatemia (blood lactate concentration >22.5 mg/dL) and 20 (22.2%) had hypoglycemia (blood glucose concentration <59.4 mg/dL) at presentation. Measurements significantly associated with mortality were hypoglycemia on admission, blood lactate concentration >45 mg/dL on admission, blood lactate concentration >22.5 mg/dL at 8, 16, and 24 hours after admission, and increase or <50% decrease in blood lactate concentration within 8 and 16 hours after admission. Blood lactate concentration persistently >40 mg/dL indicated a very poor prognosis. We conclude that serial blood lactate measurements are useful in predicting survival in dogs with severe and complicated canine babesiosis.

Animals↗
PubMedDate not supplied

D-lactate production and excretion in diarrheic calves.

The origin of D-lactate, the most important acid contributing to metabolic acidosis in the diarrheic calf, is unknown. We hypothesized that because D-lactate is produced only by microbes, gastrointestinal fermentation is the source. The objective of this study was to determine whether D-lactate production occurs in the rumen, colon, or both, and to measure D- and L-lactate concentrations in urine. Fecal, rumen, blood, and urine samples were obtained from 16 diarrheic and 11 healthy calves. Serum electrolyte concentrations were measured in both groups, and blood gas analyses were performed for diarrheic calves. All samples were analyzed for D- and L-lactate by high performance liquid chromatography (HPLC). Diarrheic calves were generally hyperkalemic with high serum anion gap, depressed serum bicarbonate, and low blood pH. L-lactate was markedly higher in rumen contents (22.7 mmol/ L [median]) and feces (8.6 mmol/L) of diarrheic calves than healthy calves (0.5 mmol/L and 5.1 mmol/L, respectively), but not different in serum or urine. Rumen, fecal, serum, and urine D-lactate concentrations were all significantly higher (P < .05) in diarrheic calves (17.0, 25.4, 13.9, and 19.2 mmol/L, respectively) than in healthy calves (0.5, 9.1, 1.4, and 0.5 mmol/L, respectively). Higher D-lactate concentrations in the rumen and feces of diarrheic calves suggests these sites as the source of D-lactate in blood and urine.

Acetic Acid↗
PubMed1997

The maximal lactate steady state in elite endurance athletes.

The upper limit of blood lactate resulting in a lactate steady state during prolonged exercise is called the maximal lactate steady state (MLSS). The purpose of this study was to investigate the lactate response to steady-state exercise during a field test in elite endurance athletes. Plasma lactate levels were assessed in 13 elite triathletes and 13 elite cyclists (mean +/- SD; age 23.7 +/- 5.1 yr; HT 180.2 +/- 6.3 cm; WT 70.3 +/- 5.9 kg; VO2 max 68 +/- 3.7 ml/min/kg) during a 40 km-long time trial on a bicycle (4 km course x 10 laps). The steady state was demonstrated by monitoring the heart rate and timing every course run. The lactate levels were expected to correspond to MLSS. The mean level of lactate during the time trial was 7.4 +/- 2.5 mmol/l. Five athletes maintained plasma lactate levels which exceeded 10 mmol/l or more for almost 1 h. The large value of individual variability was conspicuous (range 3.2-12.2 mmol/l). These values exceeded all previous reported levels for MLSS from other investigators. Our observations are important in sport medical practice since the different lactate responses to exercise are used as parameters in training management.

Adolescent↗
PubMed2001

Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats.

AIM: To explore the kinetic changes in plasma D(-)-lactate and lipopolysaccharide (LPS) levels, and investigate whether D(-)-lactate could be used as a marker of intestinal injury in rats following gut ischemia/reperfusion, burn, and acute necrotizing pancreatitis (ANP). METHODS: Three models were developed in rats: (1)gut ischemia/reperfusion obtained by one hour of superior mesenteric artery occlusion followed by reperfusion; (2)severe burn injury created by 30% of total body surface area (TBSA) full-thickness scald burn; and (3)ANP induced by continuous inverse infusion of sodium taurocholate and trypsin into main pancreatic duct. Plasma levels of D(-)-lactate in systemic circulation and LPS in portal circulation were measured by enzymatic-spectrophotometric method and limulus amebocyte lysate (LAL) test kit, respectively. Tissue samples of intestine were taken for histological analysis. RESULTS: One hour gut ischemia followed by reperfusion injuries resulted in a significant elevation in plasma D(-)-lactate and LPS levels, and there was a significant correlation between the plasma D(-)-lactate and LPS (r = 0.719, P<0.05). The plasma concentrations of D(-)-lactate and LPS increased significantly at 6h postburn, and there was also a remarkable correlation between them (r=0.877 P<0.01). D(-)-lactate and LPS levels elevated significantly at 2h after ANP, with a similar significant correlation between the two levels (r = 0.798, P < 0.01). The desquamation of intestine villi and infiltration of inflammatory cells in the lamina propria were observed in all groups. CONCLUSION: The changes of plasma D(-)-lactate levels in systemic blood paralleled with LPS levels in the portal vein blood. The measurement of plasma D(-)-lactate level may be a useful marker to assess the intestinal injury and to monitor an increase of intestinal permeability and endotoxemia following severe injuries in early stage.

Animals↗
PubMed1999

Effect of sampling site, repeated sampling, pH, and PCO2 on plasma lactate concentration in healthy dogs.

OBJECTIVE: To characterize the variation in plasma lactate concentration among samples from commonly used blood sampling sites in conscious, healthy dogs. ANIMALS: 60 healthy dogs. PROCEDURE: Cross-sectional study using a replicated Latin square design. Each dog was assigned to 1 of 6 groups (n = 10) representing all possible orders for 3 sites (cephalic vein, jugular vein, and femoral artery) used to obtain blood. Samples were analyzed immediately, by use of direct amperometry for pH, PO2, Pco2, glucose, and lactate concentration. RESULTS: Significant differences in plasma lactate concentrations were detected among blood samples from the cephalic vein (highest), femoral artery, and jugular vein (lowest). Mean plasma lactate concentration in the first sample obtained, irrespective of sampling site, was lower than in subsequent samples. Covariation was identified among plasma lactate concentration, pH, and PCO2, but correlation coefficients were low. CONCLUSIONS AND CLINICAL RELEVANCE: Plasma lactate concentrations differed among blood samples from various sites. A reference range for plasma lactate concentration was 0.3 to 2.5 mmol/L. Differences in plasma lactate concentrations among samples from various sites and with repeated sampling, in healthy dogs, are small. Use of the reference range may facilitate the clinical use of plasma lactate concentration in dogs.

Animals↗
PubMed1999

Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with gastric dilatation-volvulus: 102 cases (1995-1998).

OBJECTIVE: To determine relationships between plasma lactate concentration and gastric necrosis and between plasma lactate concentration and outcome for dogs with gastric dilatation-volvulus. DESIGN: Retrospective study. ANIMALS: 102 dogs. PROCEDURE: Information on signalment, history, plasma lactate concentration, medical and surgical treatment, cost of hospitalization, and outcome was retrieved from medical records. RESULTS: 69 of 70 (99%) dogs with plasma lactate concentration < 6.0 mmol/L survived, compared with 18 of 31 (58%) dogs with plasma lactate concentration > 6.0 mmol/L (1 dog euthanatized for economic reasons was not included). Gastric necrosis was identified in 38 (37%) dogs. Median plasma lactate concentration in dogs with gastric necrosis (6.6 mmol/L) was significantly higher than concentration in dogs without gastric necrosis (3.3 mmol/L). Specificity and sensitivity of using plasma lactate concentration (with a cutoff of 6.0 mmol/L) to predict which dogs had gastric necrosis were 88 and 61%, respectively. Sixty-two of 63 (98%) dogs without gastric necrosis survived, compared with 25 of 38 (66%) dogs with gastric necrosis. CONCLUSIONS AND CLINICAL RELEVANCE: Preoperative plasma lactate concentration was a good predictor of gastric necrosis and outcome for dogs with GDV. Preoperative measurement of plasma lactate concentration may assist in determining prognosis of dogs with GDV.

Animals↗
PubMed2001

Serum lactates are not predictive of heart failure severity in status I cardiac transplant candidates.

BACKGROUND: Blood lactate is an accurate predictor of outcome in clinical shock syndrome patients. However, its usefulness in status I heart transplant candidates with failing myocardium is largely unknown. The purpose of this study was to determine whether serum lactate levels are predictive of congestive heart failure severity in cardiomyopathic status I cardiac transplant candidates. METHODS: Over a 6-month period, serial arterial serum lactate levels in 30 status I heart transplant candidates were measured. Measured serum lactate values (mmol/L) included the initial lactate level upon admission to the intensive care unit and the lactate level at 6-week intervals up to 24-weeks. Surveillance right heart catheterizations were also performed at 6-week intervals to determine pulmonary artery pressures and cardiac index. Baseline measurements were compared with the values obtained at time intervals of 6-, 12-, 18-, and 24-weeks. RESULTS: All status I heart transplant candidates were admitted to the intensive care unit for treatment of worsening heart failure with intravenous inotropic therapy. All patients had severe pulmonary hypertension (greater than two-thirds of systemic arterial pressure, mmHg) and/or severe low cardiac output state (cardiac index less than 2.0 L/min/M(2)). Admission lactate level was normal in all candidates. Intravenous inotropic therapy improved patients' symptoms and cardiopulmonary hemodynamic derangements although lactate levels remained within the normal range until the time of heart transplant operation or up to 24-weeks (p=NS). CONCLUSIONS: Blood lactate remains unaffected by worsening congestive heart failure of cardiomyopathy patients and is not predictive of heart failure severity in status I cardiac transplant candidates.

Biomarkers↗
PubMed2002

[Prognostic value of the pediatric index of mortality (PIM) score and lactate values in critically-ill children].

OBJECTIVE: To analyze and compare the prognostic value of the pediatric index of mortality (PIM) score and lactate values on admission to a pediatric intensive care unit (PICU). PATIENTS AND METHODS: We performed a prospective study of 500 consecutive children: 237 girls (47.4 %) and 263 boys (52.6 %) with a mean age of 51.5 59.7 (range: 3 days-18 years) admitted to our PICU. PIM scores and blood lactate concentrations were determined on admission. The predictive ability of PIM and lactate concentrations in relation to mortality and length of stay in the PICU were analyzed. RESULTS: Thirty-six patients (7.2 %) died. According to the PIM score, the mean probability of death in children who died was 23.6 % 28.9, which was significantly higher than that in surviving children (3.4 % 7.3; p < 0.001). The area under the ROC curve for PIM was 0.81 0.03 (95 % CI: 0.74-0.89). Lactate level in nonsurvivors was 4.9 % 3.5 mmol/L, which was significantly higher than that in survivors (1.9 % 1.5 mmol/L; p < 0.001). The area under the ROC curve for blood lactate was 0.76 0.04 (95 % CI: 0.67-0.85). No statistically significant differences were found between either ROC curves. In survivors, a significant relationship was found between PIM score and length of stay in the PICU while in nonsurvivors an inverse relationship was found between blood lactate concentrations and length of stay. CONCLUSIONS: Both PIM score and blood lactate concentrations on admission to the PICU have a moderate prognostic value in critically-ill children. The prognostic value of the PIM score is greater than that of blood lactate concentration but is more difficult to obtain, whereas blood lactate determination is fast and easy.

Adolescent↗
PubMed2000

Oxygen consumption and lactate release by the lung after cardiopulmonary bypass and during septic shock.

OBJECTIVE: We sought to determine whether a correlation exists between lung lactate release and lung oxygen consumption by studying adult intensive care patients, either after cardiopulmonary bypass (CPB) or with septic shock. METHODS: A prospective observational study of six post cardiopulmonary bypass patients and seven patients with septic shock was performed in an intensive care unit of a major teaching hospital. Pulmonary oxygen consumption was estimated by subtracting oxygen consumption calculated using the reverse Fick equation (V O2Fick) from that measured by indirect calorimetry (V O2meas). Pulmonary lactate release was derived from the difference between arterial and mixed-venous lactate, multiplied by cardiac output. RESULTS: Pulmonary oxygen consumption comprised a substantial component of total oxygen consumption (CPB-median: 20.6%; interquartile range (IQR): 15.4 - 27.3%; septic shock-median: 32.3%; IQR: -4.0 - 35.4%). Lung lactate release occurred both after CPB (median: 27.5 mmol/hr; IQR: 24.8-64.1 mmol/hr) and with septic shock (median: 55.4 mmol/hr; IQR: 24.3 - 217.6 mmol/hr). Although no correlation was found between lung lactate release and pulmonary oxygen consumption, lactate release correlated with V O2meas and V O2Fick in septic patients (p < 0.005). CONCLUSIONS: We conclude that lung oxygen consumption and lactate release are substantial in conditions associated with lung inflammation. Lactate release and lung oxygen consumption may not share a common pathogenesis, however there is an association between lung lactate release and systemic oxygen consumption in sepsis.

Journal Article↗
PubMed1997

Measurement of lactate in cerebrospinal fluid in investigation of inherited metabolic disease.

Measurement of lactate concentrations in cerebrospinal fluid (CSF) has been suggested as part of the investigation of inborn errors of the electron transport chain, but little information exists regarding the reference range in children or the relationship between CSF and plasma concentrations. In 39 children without bacterial meningitis, diabetes, or recent seizures, we determined that the median (range) lactate concentrations in CSF and plasma collected concurrently were 1.4 (0.8-2.2) and 1.5 (0.6-2.3) mmol/L; the regression equation was CSF lactate = (0.38+/-0.06) plasma lactate + 0.83 (r2 = 0.14). In 8 of 11 (73%) children with electron transport chain defects, CSF lactate was > or =3.0 mmol/L; however, 2 of these 8 had a normal plasma lactate concentration. CSF lactate was also increased in 2 children with nonketotic hyperglycinemia. The finding that CSF lactate concentrations may be increased despite a normal plasma lactate value in children with electron transport chain defects is an important clue to the diagnosis of these disorders.

Adolescent↗
PubMed1998

Lactate turnover in rat glioma measured by in vivo nuclear magnetic resonance spectroscopy.

Elevated tissue lactate concentrations typically found in tumors can be measured by in vivo nuclear magnetic resonance (NMR) spectroscopy. In this study, lactate turnover in rat C6 glioma was determined from in vivo 1H NMR measurements of [3-13C]lactate buildup during steady-state hyperglycemia with [1-13C]glucose. With this tumor model, a narrow range of values was observed for the first-order rate constant that describes lactate efflux, k2 = 0.043 +/- 0.007 (n = 12) SD min-1. For individual animals, the standard error in k2 was small (< 18%), which indicated that the NMR data fit the kinetic model well. Lactate measurements before and after infusing [1-13C]glucose showed that the majority of the tumor lactate pool was metabolically active. Signals from 13C-labeled glutamate in tumors were at least 10-fold smaller than the [3-13C]lactate signal, whereas spectra of the contralateral hemispheres revealed the expected labeling of [4-13C]glutamate, as well as [2-13C] and [3-13C]glutamate, which indicates that label cycled through the tricarboxylic acid cycle in the brain tissue. Lack of significant 13C labeling of glutamate was consistent with low respiratory metabolism in this glioma. It is concluded that lactate in rat C6 glioma is actively turning over and that the kinetics of lactate efflux can be quantified noninvasively by 1H NMR detection of 13C label. This noninvasive NMR approach may offer a valuable tool to help evaluate tumor growth and metabolic responsiveness to therapies.

Animals↗
PubMed1977

The effect of temperature on the kinetic constants of human lactate dehydrogenase 1 and 5.

The kinetic constants of human lactate dehydrogenase 1 and 5 (L-lactate: NAD+ oxidoreductase, EC 1.1.1.27), assayed lactate-to-pyruvate increase with temperature. The reaction mechanism is ordered sequential as has been found with lactate dehydrogenase from other sources. The KM values for each substrate are larger for isoenzyme 5 than for 1. For lactate dehydrogenase 1 the KM(lactate) increases from 1.07 mM at 25 degrees C to 3.95 mM at 37 degrees C and for lactate dehydrogenase 5 it increases from 5.37 mM at 25 degrees C to 6.88 mM at 37 degrees C. The KM(NAD+) for lactate dehydrogenase 5 is 0.14 mM at 25 degrees C and 0.29 mM at 37 degrees C. The increase in the KM for each substrate with increasing temperature confirms that additional substrate is required for optimal reaction conditions at higher temperatures.

Humans↗
PubMed1994

Glucose and amino acid transport and metabolism in flat duodenal sheets of dairy cattle at three stages of lactation.

The apparent duodenal transport and metabolism of amino acids and glucose in early-, mid-, late- and non-lactating dairy cows was investigated. Km values for glucose were not affected by stage of lactation. The capacity (Iscmax) of duodenal sheets to transport glucose was greater in lactating than in non-lactating cows. Lactating cows had a greater transport capability for amino acids than non-lactating cows. Duodenal sheets of early-lactation cows metabolized a greater percentage of absorbed glucose carbon to carbon dioxide than cows in mid-, late- and non-lactating cows.

3-O-Methylglucose↗
PubMed2003

Alteration of lactate production and transport in the adult rat testis exposed in utero to flutamide.

Although it is established that in utero exposure to the antiandrogen flutamide induces alteration of spermatogenesis in the adult rat testis offspring, the cellular and molecular mechanisms involved in such an effect remain to be investigated. In the present paper, by using as model adult rats exposed in utero to flutamide (0, 2, 10 mg/kg per day), we have investigated the hypothesis that germ cell alterations could be related to defects of energy metabolism and particularly to defects of the production and transport of lactate. Lactate is a preferential energy substrate produced by Sertoli cells and transported to germ cells by monocarboxylate transporters (MCT). A significant decrease (60%, P<0.001) in lactate production was observed in cultured Sertoli cells from rat testes exposed in utero to flutamide from the dose of 2 mg/kg per day. Such a decrease is concurrent to a decrease in lactate dehydrogenase A (LDHA) mRNA levels (evaluated through semiquantitative RT-PCR) and LDHA4 activity. The decrease in LDHA mRNA levels (to 64 +/- 9% of the control, P<0.05) was observed with the lowest dose (2 mg/kg per day) of flutamide tested. The decrease in LDHA mRNA levels was observed in both the whole testis and in isolated Sertoli cells, suggesting that such a decrease in LDHA expression occurred also in the (Sertoli) cells producing lactate. Lactate is transported from Sertoli cells to germ cells via MCT1 and MCT2. We immunolocalized MCT1 to all the different germ cell types and MCT2 exclusively to elongated spermatids. In the adult testis exposed in utero to flutamide, MCT1 (53 +/- 8%, P<0.02) and MCT2 (52 +/- 9%, P<0.02) mRNA levels were significantly reduced indicating that lactate transport to germ cells could be also altered. Together, these data support (i) the existence of a relationship between the antiandrogen activity and the energy metabolism in the testis and (ii) the concept of an androgen-dependent programming, occurring early in the fetal life in relation to the expression of some of the key genes involved in the production and transport of lactate in the seminiferous tubules.

Androgen Antagonists↗
PubMedDate not supplied

Exacerbation of hyperlactatemia by infusion of lactated Ringer's solution in dogs with lymphoma.

Blood lactate concentrations and acid-base status of six dogs with lymphoma were compared statistically with those from six healthy control dogs before, during, and after a 6-hour infusion of lactated Ringer's solution (LRS). Blood lactate concentrations in dogs with lymphoma were significantly (P less than 0.05) higher immediately before, and at the 1-, 2-, 4-, and 6-hour time periods after infusion when compared with controls. Blood lactate concentrations increased significantly (P = 0.016) after the first hour of infusion in dogs with lymphoma but did not increase in the control dogs. The increase in blood lactate concentrations over baseline values after 1 hour of LRS infusion was significantly (P = 0.008) greater in dogs with lymphoma when compared with controls. Blood lactate concentrations returned to baseline levels after 2 hours of infusion in dogs with lymphoma, suggesting that dogs with lymphoma have a transient inability to handle increased lactate loads when compared with controls. However, the potential to augment lactate use, clearance, or both is present and does occur over time. Blood gas values were not significantly altered within the lymphoma or control dog groups after 6 hours of LRS infusion. Blood bicarbonate concentrations in dogs with lymphoma were significantly decreased before and after LRS infusion when compared with controls.

Acid-Base Equilibrium↗
PubMedDate not supplied

Effect of lactate on the recovery of CHO-KI cells from gamma radiation damage.

The effect of pre-exposure of CHO-KI cells to lactate on their capacity to recover from or repair radiation damage was examined. Prolonged pre-exposure to lactate and a number of inhibitors of glycolysis has previously been shown to reduce the cell survival after irradiation. Following a split dose of irradiation, cells pre-treated with lactate for 18 hours had a higher relative recovery factor than controls even though survival following a single dose was reduced. Where lactate was added just before irradiation it had a radiation protective effect on the single dose survival curve and no effect on recovery. To investigate a possible involvement of NADH generation via lactate dehydrogenase in the mechanism, oxamate, a non-metabolisable analogue of lactate, was investigated. It reduced the survival of irradiated CHO-KI cells following prolonged and short pre-exposure and did not significantly affect the recovery factor. It is suggested that since lactate and oxamate both inhibit glucose breakdown, their radiobiologic effects may be due to depletion of cellular energy substrates necessary for repair. In contrast, the increased recovery and short term radiation protective effect seen with lactate only may involve LDH activity.

Animals↗