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PubMed1992

Concentrations of D-lactate and its related metabolic intermediates in liver, blood, and muscle of diabetic and starved rats.

This is a report investigating the methylglyoxal (MG) bypass in animals, by which D-lactate is produced from triosephosphate via MG. Rats were made diabetic using streptozotocin or starved for 72 h. D-Lactate and various metabolites related to it, such as L-lactate, pyruvate, methylglyoxal, glucose, and inorganic phosphate, were measured in the blood plasma, liver, and skeletal muscle of the rats. Diabetic and starved rats had significantly higher levels of D-lactate in plasma, liver, and skeletal muscle compared with the control group. In contrast, pyruvate levels in plasma, liver, and skeletal muscle was markedly lower than normal in diabetic and starved rats. L-Lactate level lowered markedly in plasma, liver, and skeletal muscle of starved rats and elevated in liver of diabetic rats. Differences between plasma L-lactate level for diabetes and control were not significant. MG level was significantly elevated in plasma and depressed in livers and muscles of starved rats as well as livers of diabetic rats. Hepatic glycerol content was markedly increased in those states. Enzyme activities related to D- and L-lactate, such as pyruvate kinase, phosphofructokinase, aldolase, and glyoxalase I, were measured in the livers of these rats. Pyruvate kinase activity decreased in these states, but other enzyme activities showed no significant changes. D-Lactate was much more excreted than L-lactate in the urine of diabetic and fasted rats compared with normal rats.

Animals↗
PubMed1997

Rat lung phospholipid fatty acid composition in prepregnant, pregnant, and lactating rats: relationship to ozone-induced pulmonary toxicity.

Our laboratory has demonstrated recently that pulmonary inflammation induced by acute ozone exposure is much more severe in late stage pregnant and lactating rats than in postlactating rats or age-matched virgin females. It is currently widely believed that such pulmonary damage results, at least in part, from the reaction of ozone at sites of unsaturation in phospholipid fatty acid (PLFA) molecules located in the epithelial fluid layer lining the lung surfaces and/or the plasma membranes of epithelial cells underlying this fluid layer. The objective of this study was to compare the PLFA composition of lung tissue and surfactant from ozone-sensitive late stage pregnant and lactating rats with comparable tissue from relatively ozone-insensitive age-matched prepregnant (virgin female) rats to explore the possibility that changes in lung PLFA composition during pregnancy and/or lactation contribute to the enhanced sensitivity of these physiologic states to ozone. In addition, the correlation of changes in plasma PLFA composition with those in lung was investigated. There were minor differences in the composition of lung tissue and surfactant PLFAs between prepregnant rats and pregnant rats at day 17 of gestation and only slightly greater differences between prepregnant and lactating rats. Changes from the prepregnant state in the PLFA composition of lung tissue, but not surfactant, correlated with changes in the plasma only in lactating rats and not in pregnant rats. Overall, the double bond index of PLFAs in surfactant and lung tissue was decreased in pregnant and lactating rats compared with prepregnant rats. Thus, the increased sensitivity of pregnant and lactating rats to ozone-induced lung injury cannot be attributed to an increased availability of unsaturated fatty acids. In addition, the arachidonic acid composition of phospholipids did not appear to explain differences between prepregnant rats and pregnant or lactating rats in their inflammatory response to ozone. In conclusion, there is no evidence that the relatively minor changes in lung tissue PLFA composition which occur during pregnancy and lactation predispose rats in these physiologic states to ozone-induced pulmonary toxicity.

Animals↗
PubMed1993

Effect of inflation on adenosine triphosphate catabolism and lactate production during normothermic lung ischemia.

Although few biochemical data comparing adenosine triphosphate (ATP) catabolism or lactate production in isolated deflated versus inflated lung tissue are available, most transplant centers preserve their donor lungs inflated. We measured ATP level (using high-performance liquid chromatography), energy charge, and lactate level during 2 hours of normothermic ischemia in deflated lung tissue (n = 6), in lung tissue inflated with room air (n = 6), and in lung tissue inflated with 100% oxygen (n = 6). To determine the onset of anaerobic metabolism in lung tissue inflated with 100% O2, ATP and lactate levels were measured in another group (n = 6) during 8 hours of normothermic ischemia. Rabbit lungs were flushed in situ with a modified Krebs-Henseleit solution (60 mL/kg). They were isolated and immersed in 0.9% NaCl at 37 degrees C. In deflated lung tissue, ATP level (control value, 9.4 +/- 0.58 mumol/g dry wt) decreased and lactate level (control value, 5.6 +/- 1.16 mumol/g dry wt) increased after 15 minutes of ischemia (ATP, 5.2 +/- 0.86 mumol/g dry wt; lactate, 13.3 +/- 1.58 mumol/g dry wt). When the lung was stored inflated with room air, ATP breakdown and increase of lactate concentration only occurred after 90 minutes of normothermic ischemia (at 60 minutes: ATP, 8.0 +/- 0.58 mumol/g dry wt; lactate, 6.3 +/- 1.1 mumol/g dry wt). In lungs stored inflated with 100% O2, ATP breakdown and lactate accumulation only occurred after 5 hours of normothermic ischemia (at 4 hours: ATP, 8.1 +/- 0.74 mumol/g dry wt; lactate, 5.9 +/- 1.28 mumol/g dry wt).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1992

Effect of timing of administered calcium lactate on the sucrose-induced intraoral demineralization of bovine enamel.

A number of soluble calcium salts are known to reduce the demineralization of enamel in the mouth. The present study was undertaken to examine the effects of rinses containing different concentrations of calcium lactate, and the time of giving the rinses with respect to sucrose challenges. Subjects wore palatal appliances containing blocks of bovine enamel whose surfaces were covered with Streptococcus mutans IB 1600, and rinsed with 10% sucrose for 1 min. Changes in iodide penetrability of the enamel, and the pH and extracellular ion concentrations of the streptococcal plaque were determined. When added to the sucrose rinse, 100 or 150 mM calcium lactate reduced demineralization by about 35%, although the plaque pH was not affected. Plaque calcium was elevated but diffused away rapidly so that concentrations after 45 min were close to control values. Plaque inorganic phosphate and lactate were not affected. Ongoing demineralization appeared to be stopped when 100 mM calcium lactate was given 15 min after the sucrose rinse. When the lactate was given 15 min before the sucrose rinse, demineralization was reduced by only about 25%, consistent with the rapid diffusion of plaque calcium. The combination of (i) pretreatment with calcium lactate and (ii) admixture of calcium lactate with sucrose was most effective. Demineralization was reduced about 55% with 100 mM calcium lactate under these conditions, and protective effects were seen with as little as 25 mM. In summary, the findings demonstrate the enamel-protective effect of relatively low concentrations of calcium lactate, and point to the need to sustain a high plaque calcium during periods of maximum acidogenicity.

Adult↗
PubMed1991

Prolactin response to morphine in intact and adrenalectomized lactating rats.

To examine the hypothesis that the increased adrenocortical activity during lactation induced the loss of the prolactin (PRL) -releasing effect of morphine, we studied the effect of morphine in adrenalectomized (ADX) and sham-operated primiparous lactating Wistar rats. Animals were adrenalectomized 4 days after delivery. On day 11 of lactation (7 days after ADX), pups were separated from their mother 2 h before morphine or haloperidol injection. Intravenous injection of 5 mg/kg morphine did not change plasma PRL levels in the sham-operated lactating rats, but it resulted in a significant increase of plasma PRL levels in ADX lactating animals, with or without corticosterone replacement. Catalepsy following 10 mg/kg i.v. morphine was also markedly enhanced in ADX lactating animals. The PRL response to 0.5 mg/kg haloperidol was higher in ADX lactating animals than that in the controls. Morphine given 2 h after haloperidol treatment resulted in a further increase of plasma PRL in ADX, but not in the sham-operated lactating animals. These results suggest that adrenal hyperfunction may lead to a loss of sensitivity to morphine during lactation.

Adrenalectomy↗
PubMed1993

Treatment of lactating rats with PCBs induces CYP1A1 and enhances the formation of BP 7,8-dihydrodiol, the proximate carcinogen of benzo(a)pyrene.

1. Treatment of pregnant and lactating rats with a single i.p. dose of 250 mg/kg body weight produced 5-fold and 2-fold increases, respectively, in hepatic P-450 concentrations using microsomes isolated from pregnant, neonatal, lactating and foetal rats. 2. Concomitantly, 26-fold, 20-fold and 14-fold increases in neonatal, maternal and foetal ethoxyresorufin-O-deethylation (EROD), respectively were found, but only 2.5-fold increases could be determined using microsomes isolated from lactating rats. 3. The metabolism of [3H]benzo(a)pyrene was increased 9-fold and 2-fold in pregnant and foetal rats, respectively, but only 2-fold increases were measured for lactating rats. 4. Western blot analysis of microsomal proteins obtained from lactating rats showed significant CYP1A1 and CYP1A2 induction and for the same hepatic tissue 62-fold and 44-fold increases in cDNA hybridized CYP1A1 and CYP1A2 mRNA, respectively, were found. 5. Treatment of lactating rats with PCBs resulted in enhanced formation of all BP-metabolites, but the ratio of diol to total BP-metabolites was more than 3-fold greater. 6. The formation of the proximate carcinogen BP-7,8-dihydrodiol was 5-fold increased and a similar 3-fold increase in epoxide hydrolase activity was estimated for lactating rats. 7. The results of the present study indicates that lactation protects, in part, against the inductive effect of PCBs, possibly by enhanced clearance of these chemicals via lactation.

Animals↗
PubMed1983

Studies on the local immune response of the lactating ewe infected with Ostertagia circumcincta.

Changes in the flow and composition of gastric lymph were monitored in groups of lactating and non-lactating ewes which were repeatedly infected with Ostertagia circumcincta. As judged by faecal egg counts and worm burdens the lactating group was more susceptible than the non-lactating controls to the challenge infection. Increased amounts of pepsinogen as well as larger numbers of eosinophils and neutrophils entering the gastric lymph indicated considerable abomasal damage and inflammation in the lactating ewes. However, measurement of the flow of lymphocytes as well as the amount of IgA and IgA antibody in the lymph did not indicate that these aspects of the local immune response were impaired during lactation; in fact the output of IgA-containing lymphocytes as well as IgA itself was usually raised in the lactating sheep. Lymph flow was increased and lymph globulin concentrations proportionally decreased in lactating ewes, irrespectively of whether they were infected with worms. It is suggested that these changes were caused by the increase in voluntary food intake which occurs during lactation.

Animals↗
PubMed1995

Hyperpolarization of the liver cell membrane by palmitate as affected by glucose and lactate: implications for control of feeding.

Since the membrane potential of liver cells being in contact with vagal afferents has been proposed to represent a major signal in metabolic control of food intake, we investigated the effect of palmitate, glucose and lactate on the membrane potential of hepatocytes with microelectrodes using superfused mouse liver slices. The mice used for the experiments were fed a fat-enriched diet (18% fat). Palmitate (0.5 mM) hyperpolarized the membrane of hepatocytes by 3-4 mV, and this hyperpolarization was not affected by 5-10 mM glucose and 0.5-1 mM lactate. Glucose alone did not influence the potential, even when mice fed a high carbohydrate diet were employed. At lactate concentrations > or = 2 mM the palmitate induced hyperpolarization was eliminated and 5 mM lactate or pyruvate alone hyperpolarized the liver cell membrane. Similar to the palmitate induced hyperpolarization, the lactate induced hyperpolarization was prevented by the K-channel blocker TEA, suggesting that activation of K channels is involved in the hyperpolarization. The results show that physiological concentrations of glucose and lactate do not affect the hyperpolarization of the liver cell membrane due to fatty acid oxidation. The implications of these findings with regard to control of food intake by fatty acid oxidation and lactate metabolism are discussed. The observations are consistent with a signal function of the hepatic membrane potential in physiological control of food intake by fatty acid oxidation. Hepatic lactate metabolism at supraphysiological lactate concentrations may also produce a satiety signal coded by the hepatic membrane potential.

Animals↗
PubMedDate not supplied

D-lactate production in erythrocytes infected with Plasmodium falciparum.

The production of D-lactate that accompanies the metabolism of glucose to L-lactate in Plasmodium falciparum was evaluated with erythrocytes that contained either young or mature parasites. Infected cells with ring-stage parasites release L-lactate and D-lactate at rates 1340 and 81 nmol h-1 (10(8) cells)-1, respectively. These rates increase to 2050 and 136 nmol h-1 (10(8) cells)-1, respectively, in infected cells with trophozoite/schizont-stage parasites. D-Lactate represents 6-7% of the total lactate. The formation of D-lactate is by way of a methylgloxal pathway in which methylglyoxal is formed nonenzymatically from dihydroxyacetone phosphate and is then converted into D-lactate by the sequential action of parasite glycoxalase I and glyoxalase II. The kinetic properties of parasite glyoxalase I and glyoxalase II allow these enzymes to be distinguished from those in the host cell. D-Lactate production by the parasite appears to be a defense mechanism to protect the parasite from the toxic effects of methylglyoxal.

Alcohol Oxidoreductases↗
PubMed1991

Vasopressin stimulates pyruvate utilization through a Ca(2+)-dependent mechanism and lactate formation by a protein kinase C-dependent mechanism in isolated rat hepatocytes.

Vasopressin stimulates lactate production by hepatocytes from fed rats, an effect which has been attributed exclusively to Ca2+ activation of glycogenolysis. We provide evidence here for two further actions of vasopressin which affect lactate formation by rat hepatocytes. In the presence of 50 mM glucose, vasopressin inhibited lactate production by hepatocytes. The inhibition was relieved by the presence of alpha-cyano-4-hydroxycinnamate (alpha-CHC), which blocks mitochondrial pyruvate transport. This suggests that vasopressin stimulates pyruvate utilization in the presence of a high concentration of glucose. Epidermal growth factor (EGF), which also increases lactate formation by hepatocytes, did not similarly decrease lactate accumulation in the presence of high glucose, suggesting no stimulation of lactate and pyruvate utilization by this hormone. In cells depleted of Ca2+, vasopressin also stimulated lactate formation. Although vasopressin did not cause the apparent translocation of protein kinase C between cell spaces, phospholipase C treatment of hepatocytes did duplicate vasopressin stimulation of lactate formation, provided fatty acid oxidation was suppressed by the simultaneous presence of the inhibitor palmixorate. We conclude that three actions of vasopressin affect lactate and pyruvate formation: the calcium-linked activations of glycogenolysis and mitochondrial pyruvate utilization, and a stimulation of glycolysis likely mediated by protein kinase C.

Adenosine Triphosphate↗
PubMed1996

Spinal cord lactate concentration during chemical stimulation of the nucleus tractus solitarii in anesthetized rats.

This study was conducted to determine the mechanism of spinal cord blood flow (SCBF) decrease following the nucleus tractus solitarii (NTS) activation. In urethane-anesthetized, paralyzed and artificially ventilated rats, neurons in the NTS were chemically stimulated by microinjection of L-glutamate (1.7 nmol; 50 nl) and the lactate concentration, one of indicators of local neuronal metabolism, in the spinal cord was monitored in real time using an enzyme electrode. Before the chemical stimulation study, the responses of the enzyme electrode and its specificity were tested in vitro and in vivo. The electrode responded to step changes in lactate concentration and a calibration plot and regression line were obtained in vitro. The lactate concentration was significantly (P < 0.01) increased during induced apnea in vivo (n = 8). The lactate concentration in the spinal cord was not significantly changed by chemical stimulation of the NTS when arterial blood pressure (ABP) remained above the lower limit of spinal cord autoregulation (n = 21). When chemical stimulation of the NTS decreased ABP to below the lower limit of autoregulation (n = 18), the lactate concentration in the spinal cord was significantly (P < 0.01) increased. This may only be due to hypotensive effects because the lactate concentration was also significantly (P < 0.01) increased when the ABP was passively decreased below the lower limit of autoregulation by controlled hemorrhage in intact (n = 11) and sinoaortic denervated rats (n = 10). Intravenous lactate injection produced no significant increase in the current from the enzyme electrode in the spinal cord (n = 4). Using the electrode with inactivated enzyme solution, the current from the electrode did not change with the increase in lactate in the spinal cord. These findings indicate that the enzyme electrode can detect rapid changes of lactate, a product of anaerobic metabolism. These results also indicate that the spinal cord vasoconstrictor response elicited by chemical stimulation of the NTS, which was performed above the lower limit of spinal cord autoregulation in our previous study, may be due to neurogenic regulatory mechanism, but not to the secondary effects of changes in metabolism.

Anesthesia↗
PubMed1986

Tissue glycogen and lactate handling by the developing domestic fowl.

The levels of glycogen and lactate in liver, intestine, yolk sac membrane and leg and breast muscle of domestic fowl from day 10 of "in ovo" development to day 5 after hatching compared with adults have been measured and compared with the circulating concentrations in blood of glucose and lactate. Glycogen stores in most tissues increased before hatching to attain a minimum around the eclosion and then increased to adult values in muscle and liver. Lactate maintained its plasma concentrations with higher effectiveness than plasma glucose, which increased steadily up to adult levels from hatching. The study of tissue vs plasma lactate concentration ratios suggests a general activation of lactate metabolism from hatching, coinciding with the ingestion of carbohydrate-based food. Both muscles studied, as well as intestine, seem to be net lactate producers; blood cells can speculatively be considered as lactate users and liver maintains its concentration of lactate very close to that plasma, suggesting a fast utilization of this material as well as liver being the main site for control of circulating lactate.

Aging↗
PubMed1992

Lactate transport in insulin-secreting beta-cells: contrast between rat islets and HIT-T15 insulinoma cells.

The transport of L- and D-lactate into rat pancreatic islets and HIT-T15 insulinoma cells was studied by measuring uptake of 14C-labelled substrate at room temperature and by following changes in intracellular pH (pHi) in islets and HIT-T15 cells loaded with 2',7'-bis(carboxyethyl)-5'(6')-carboxyfluorescein (BCECF). Uptake of L-lactate into HIT-T15 cells was rapid, reaching equilibrium after 5 min with an apparent Km value of 4.8 mM. Transport was markedly inhibited by alpha-cyano-4-hydroxycinnamate, alpha-fluorocinnamate, quercetin and p-chloromercuribenzenesulphonate (pCMBS), and was enhanced in citrate medium. Uptake of D-lactate was less rapid, apparent equilibrium not being reached within 10 min. In contrast to HIT-T15 cells, rat pancreatic islets showed greatly reduced rates of transport of L- and D-lactate together with a correspondingly lower degree of inhibition by alpha-cyano-4-hydroxycinnamate. The addition of L- or D-lactate to HIT-T15 cells, but not dispersed islet cells, resulted in a marked and rapid intracellular acidification followed by a gradual recovery. In both HIT-T15 cells and isolated islets, the rates of transport of both L- and D-lactate in the presence of alpha-cyano-4-hydroxycinnamate were significantly greater in a depolarising K+ medium compared to the normal Na+ medium. These observations suggest that native rat islet cells have considerably reduced activity of the lactate-/H+ transport system compared to HIT-T15 insulinoma cells. There is evidence in both cell types of an additional electrogenic pathway for lactate which might play a role in coupling lactate efflux to beta-cell depolarisation.

4-Chloromercuribenzenesulfonate↗
PubMed1986

Tissue glycogen and lactate handling by the developing domestic fowl.

The levels of glycogen and lactate in liver, intestine, yolk sac membrane and leg and breast muscle of domestic fowl from day 10 of "in ovo" development to day 5 after hatching compared with adults have been measured and compared with the circulating concentrations in blood of glucose and lactate. Glycogen stores in most tissues increased before hatching to attain a minimum around the eclosion and then increased to adult values in muscle and liver. Lactate maintained its plasma concentrations with higher effectiveness than plasma glucose, which increased steadily up to adult levels from hatching. The study of tissue vs plasma lactate concentration ratios suggests a general activation of lactate metabolism from hatching, coinciding with the ingestion of carbohydrate-based food. Both muscles studied, as well as intestine, seem to be net lactate producers; blood cells can speculatively be considered as lactate users and liver maintains its concentration of lactate very close to that of plasma, suggesting a fast utilization of this material as well as liver being the main site for control of circulating lactate.

Aging↗
PubMed1991

Influence of pregnancy, lactation and environment on some clinical chemical reference values in Danish landrace dairy goats (Capra hircus) of different parity--II. Plasma urea, creatinine, bilirubin, cholesterol, glucose and total serum proteins.

1. Plasma urea, creatinine, bilirubin, glucose, cholesterol and total serum proteins were determined in Danish landrace goats from five herds in early and late gestation, during lactation and in dry goats. The purpose was to determine if there are sustained alterations in the levels of these parameters due to pregnancy and lactation and whether the changes are dependent on age, parity and environment. 2. Urea, creatinine and bilirubin were higher in young non-pregnant goats than in others. Urea decreased in goats at early and mid-lactation directly proportional to parity so that the higher the parity the more the decrease. 3. Creatinine was higher in young and adult non-pregnant goats than in others. There was an increase in late lactation that was greater in goats of higher parity than in others. 4. Bilirubin was higher in the mid-lactation stage, much more in goats of higher parity than in others. 5. Glucose concentration was lower in pregnant than in lactating goats and increased during lactation. The decrease during pregnancy was greater in higher parity goats than in others. 6. Plasma cholesterol and total serum proteins increased during lactation directly proportional to parity. 7. There were significant differences in biochemical parameters between goats from different herds (within similar physiological states). 8. Sustained alterations of these biochemical parameters occur during pregnancy and lactation in goats; the magnitude of changes depends on age and parity, and varies between herds.

Animals↗
PubMed1995

Correlation of serial blood lactate levels to organ failure and mortality after trauma.

To define the value of serial measurements of blood lactate levels after trauma, the present study investigated the correlation between blood lactate, mortality, and organ failure in 129 trauma patients, including 100 intensive care unit (ICU) survivors and 29 ICU fatalities. On admission, injury severity score (ISS) was higher and Glasgow coma score (GCS), revised trauma score (RTS), and trauma revised ISS (TRISS) were lower in the nonsurvivors than in the survivors. Serial arterial blood lactate levels were measured on admission and at least three times a day until normalization. Both initial lactate and highest lactate levels were higher in the nonsurvivors than in the survivors. Organ failure developed in 84 (65%) of the 129 patients. Patients with organ failure had significantly lower RTS and TRISS. Initial lactate and highest lactate levels were significantly higher in patients with organ failure than without organ failure (3.4 [0.7 to 12.7] versus 2.4 [0.4 to 7.6] mEq/L and 4.1 [0.7 to 12.7] versus 2.8 [0.4 to 8.9] mEq/L, respectively, both P < .01). The duration of hyperlactatemia averaged 2.2 days in the former but 1.0 day in the latter patients (P < .01). The data therefore indicate that not only the initial or the highest lactate value but also the duration of hyperlactatemia can be correlated with the development of organ failure. These observations stress the importance of the initial resuscitation in the prevention of organ failure. Serial blood lactate measurements are reliable indicators of morbidity and mortality after trauma.

Acute Kidney Injury↗
PubMed1989

Increased cancellous bone remodeling during lactation in beagles.

Changes in bone mass and cancellous bone remodeling parameters were determined during lactation in adult beagles. Bone mineral content was determined by photon absorptiometry, fraction of mineralized cancellous bone area and perimeter to area ratios by image analysis of microradiographs, and bone remodeling parameters by fluorochrome-based histomorphometry. Bone mineral content of the intact proximal humerus and fraction of mineralized tissue areas of lumbar vertebral cancellous bone were decreased during lactation when compared with controls. There were significant increases during lactation in osteoid volumes and osteoid surface, although osteoid seam thickness was not changed. There were significant increases in the fraction of fluorochrome-labeled cancellous bone surfaces in the lactating dogs when compared with controls. The mineralizing surface, bone formation rate and activation frequency were significantly increased in the lactating dogs when compared with controls. There were also significant increases in resorption parameters during lactation. These data indicate that during lactation, bone remodeling and bone turnover is increased. Increased bone remodeling during lactation in a longer-lived mammal may represent an example of a "reversible mineral deficit" which may be an important physiological mechanism in nursing mothers to ensure adequate calcium for milk production. Increased bone remodeling may also provide a physiological mechanism to enhance the capacity of the skeleton to better accommodate the greatly increased and episodic changes in mineral homeostasis during lactation.

Animals↗
PubMed2006

Lactate dehydrogenase isoform activity mapping in patients with intra-amniotic infection.

OBJECTIVE: Five distinct lactate dehydrogenase isoenzymes have been described. We sought to illustrate the specific amniotic fluid lactate dehydrogenase isoenzyme activity profiles in women with intra-amniotic infection. STUDY DESIGN: Amniotic fluid was retrieved from 82 women who were stratified in the following groups: (1) positive amniotic fluid cultures (n = 23 women; gestational age, 26 weeks [range, 21-32 weeks]); (2) negative amniotic fluid cultures (n = 22 women; gestational age, 30 weeks [range, 16-36 weeks]); (3) second trimester control (normal genetic karyotype; n = 17 women; gestational age, 18 weeks [range, 16-22 weeks]); and (4) third trimester control (fetal lung maturity testing; n = 20 women; gestational age, 36 weeks [range, 31-38 weeks]). The optical density of each isoform was determined relative to a standard with 5 known lactate dehydrogenase isoenzyme activities. Total lactate dehydrogenase activity was measured by the clinical laboratory immediately after retrieval and by a kinetic UV spectrophotometric assay at the time of the isoelectric focusing. RESULTS: Infection increased total lactate dehydrogenase activity: positive amniotic fluid cultures (median, 762.4 [range, 169.3-3374.8]) vs negative amniotic fluid cultures (median, 203.7 [range, 57.8-1939.3]; U/L; P < .001]). Lactate dehydrogenase isoform profiling identified significant and specific increases in lactate dehydrogenase isoforms 3, 4 (P < .01), and 5 (P < .05) in positive amniotic fluid cultures compared to the negative amniotic fluid cultures group. A selective up-regulation in lactate dehydrogenase isoform 5 was identified at term in healthy subjects. CONCLUSION: Intra-amniotic infection is characterized by an increase in the activities of lactate dehydrogenase isoforms 3, 4, and 5; advancing gestational age demonstrates an up-regulation of isoform 5 only.

Adult↗