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PubMed1995

Dietary cation-anion difference, acid-base status, mineral metabolism, renal function, and milk production of lactating cows.

Three switchback experiments were conducted with 12 cows in early lactation, 12 cows in midlactation, and 12 cows in late lactation. Each experiment compared two dietary cation-anion differences. Increasing dietary cation-anion difference increased DMI and milk production in early and midlactation. These effects were not observed in late lactation. Production of milk protein and lactose and concentration of lactose were increased by the higher dietary cation-anion difference in early lactation. Higher dietary cation-anion difference reduced milk fat concentration in midlactation because of the higher milk production. In late lactation, none of the milk components were affected by dietary cation-anion difference. In early and midlactation, apparent absorption of water and urine volume were increased by a higher dietary cation-anion difference; these effects were not caused by higher intake of Na or by higher glomerular filtration rate. Intake, balance, and concentration of S in plasma were increased by the lower cation-anion difference at all stages of lactation. Excretion of HCO3- in urine was reduced by a lower dietary cation-anion difference at all stages of lactation, but secretion of protons in milk was reduced in late lactation only. Increasing dietary cation-anion difference does affect acid-base parameters in urine at all stages of lactation, but DMI and milk production of cows were affected in early and midlactation only.

Acid-Base Equilibrium↗
PubMed1984

D- and L-lactate catabolism to CO2 in rat tissues.

The current study was initiated in order to compare the rates of oxidative catabolism of D- and L-lactate in various rat tissues. Uniformly labeled D- or L-[14C]lactate was incubated at 37 degrees C in a closed system with tissue homogenates in Krebs-Ringer phosphate buffer. Evolved 14CO2 was trapped in a center well containing a fluted filter paper saturated with strong base and the radioactivity determined. The ratio of L-lactate to D-lactate oxidation was greatest in brain, followed by kidney, heart, and liver. In liver the rate of oxidation of D-lactate exceeded that of L-lactate, in heart the rates were not significantly different and in the other two tissues L-lactate was oxidized more rapidly than D-lactate. These results indicate that the rate of D-lactate catabolism is considerable and is relatively greater than had been reported previously.

Animals↗
PubMed1987

The role of food intake on gastric mucosal growth and gastrin receptors during pregnancy and lactation.

We examined the effects of pregnancy and lactation on mucosal growth and the numbers and affinity of gastrin receptors in the oxyntic gland mucosa in rats and compared these with changes in serum gastrin levels and food consumption. Gastric mucosal DNA, RNA, and protein contents were significantly increased during lactation. These changes were not observed in either pregnant or nonlactating rats which had given birth at the same time as the lactating animals. The gastrin-binding capacity of a membrane fraction of the oxyntic mucosa was also increased at the corresponding periods in lactating rats (Days 7, 15, 20). Scatchard plot analysis revealed that the number of gastrin receptors was significantly increased without any change in affinity. Food consumption and levels of serum gastrin remained unaltered in pregnant and non-lactating rats compared to virgin controls, but were significantly increased in lactating rats. Increased serum gastrin levels and gastrin binding capacities in lactating rats (Day 15) were abolished by preventing increased food consumption by means of pair feeding. The results demonstrate that the number of gastrin receptors in the oxyntic mucosa increases during lactation in rats. This increase is probably due to hypergastrinemia caused by increased food intake. The increased number of gastrin receptors may be involved in the mechanism of hypertrophic responses of the gastric mucosa in lactating rats.

Animals↗
PubMed1999

Lactate- or bicarbonate-buffered solutions in continuous extracorporeal renal replacement therapies.

BACKGROUND: Continuous renal replacement therapies (CRRTs) are well accepted for critically ill patients with acute renal failure (ARF). Today, daily fluid exchange in CRRT reaches 30 to 40 liter and more. Therefore, the composition of the substitution/dialysate fluid, often primarily developed either for intermittent treatment or for peritoneal dialysis, becomes more relevant. Lactate (30 to 45 mmol/liter) is frequently used as the buffer because of the high stability of this substance. However, lactate is thought to have negative effects on metabolic and hemodynamic parameters. METHODS: Published data for different substitution fluids are presented with respect to acidosis and lactate concentration, uremia, and hemodynamic and metabolic alterations. RESULTS: Only a few studies compare substitution fluids with different buffers. Uremia and acidosis (pH, base excess) were sufficiently controlled during CRRT with an exchange volume of in average 30 liters using either buffer. If patients with severe liver failure and lactic acidosis were excluded, no difference in hemodynamic and metabolic parameters between the solutions occurred. The plasma lactate concentration was elevated during lactate use in some cases, but lactate levels remained within normal limits in patients without liver impairment. The bicarbonate concentration in the solutions should exceed 35 to 40 mmol/liter, as in some cases the buffer capacity of the solutions was inadequate. In patients with severe liver failure or lactic acidosis, solutions with lactate buffer were shown not to be indicated. CONCLUSION: In patients with reduced lactate metabolism, for example, concomitant severe liver failure, after liver transplantation or in lactic acidosis, bicarbonate-buffered solutions should be used. In nearly all other cases of critically ill patients with ARF, lactate-buffered solutions may be used as well as bicarbonate solutions.

Acute Kidney Injury↗
PubMed2002

[Recovery of bone mineral density following pregnancy and lactation a longitudinal study].

OBJECTIVE: The purpose of the study was to examine the recovery of maternal bone mineral density (BMD) following pregnancy and lactation, including the effects of subsequent pregnancy and lactation. SUBJECTS AND METHODS: Twenty-eight pregnant women were followed longitudinally from early pregnancy (baseline) to five years postpartum (maximum). BMD was measured by ultrasonic bone densitometry at early pregnancy, one week postpartum and at a six-month intervals thereafter. Stiffness calculated from the combined value of speed of sound and broadband ultrasound attenuation was used as an index of BMD. Changes in BMD were examined in 19 women without subsequent pregnancy, divided by the period of lactation, 0-1 month (control), 2-6 months and 8 months or longer. Then, the relationship of recovery of BMD to the interval before a subsequent pregnancy was examined. RESULTS AND CONCLUSIONS: 1. BMD in women with 0-1 and 2-6 months lactation duration returned to baseline levels within 1 and 1.5 years postpartum, respectively. That in women with a lactation duration of 8-12 months returned to the baseline within 4 years postlivery after an interval of more than 1 year following weaning showed recovery at subsequent delivery. In some, increase was observed after the period of lactation. 3. BMD in women with subsequent delivery within 1 year after weaning showed an overall decrease at subsequent delivery. These results show that BMD lost during pregnancy and lactation returns to the baseline within four years postpartum, depending on the lactation period, and the length of time from weaning to the next delivery, rather than the lactation period, affect BMD recovery.

Adult↗
PubMed1991

Changes in calcium homeostasis over the first year postpartum: effect of lactation and weaning.

There is little information on the effect of lactation on maternal mineral and calcitropic hormone status. Therefore, we prospectively compared 26 lactating women with 32 nonlactating postpartum controls over the first year postpartum. Nineteen of the 26 women breast-fed their infants for fewer than 12 months and seven breast-fed for at least 12 months. During the first 6 months postpartum, serum phosphorus and parathyroid hormone (PTH) concentrations decreased with increasing time (P = .04 and P = .003, respectively) and were higher in lactating compared with nonlactating women (P less than .001 and P = .06, respectively). Mean serum phosphorus concentrations at 1, 3, and 6 months postpartum were 4.45, 4.75, and 4.34 mg/dL, respectively, in lactating women, versus 4.01, 3.64, and 3.44 mg/dL in controls. Mean PTH concentrations were 1.58, 1.48, and 1.36 ng/mL in lactating women, compared with 1.45, 1.20, and 1.16 ng/mL, respectively, in controls. At 12 months, women who were weaning had significantly higher mean serum calcium (10.11 mg/dL) and magnesium (2.36 mg/dL) concentrations than those who had weaned (8.79 and 2.03 mg/dL, respectively) or who had never lactated (8.90 and 1.95 mg/dL, respectively). Serum phosphorus, PTH, and 1,25-dihydroxyvitamin D were similar among women who were weaning (4.02 mg/dL, 1.46 ng/mL, and 54 pg/mL, respectively) and those who had weaned (3.94 mg/dL, 1.68 ng/mL, and 55 pg/mL), and were significantly higher than concentrations in women who had never lactated (3.25 mg/dL, 0.92 ng/mL, and 39 pg/mL). Our findings during lactation and the persistent differences observed during and after weaning are consistent with bone mobilization during lactation and a recovery of bone mass during and after weaning.

Calcium↗
PubMed1990

Lactate generation following glucose ingestion: relation to obesity, carbohydrate tolerance and insulin sensitivity.

To examine early metabolic abnormalities in obesity prior to the development of carbohydrate intolerance, we studied 14 lean and 37 obese subjects with normal glucose tolerance. All subjects underwent a standard 75 g oral glucose tolerance test (OGTT) with the addition of lactate measurement. As expected, there was a positive relationship between basal insulin and body mass index (BMI kg/m2;r=0.64, P less than 0.0001). In addition, even though the subjects had normal glucose tolerance, both basal glucose and sum of glucose during OGTT showed significant positive associations with obesity. Basal lactate correlated significantly and positively with obesity (r = 0.29, P = 0.04). When incremental areas during OGTT were examined, glucose area during OGTT was positively associated with BMI and insulin area was positively associated with both BMI and sum of glucose. Conversely, the incremental area of lactate decreased as BMI increased (r = -0.41, P = 0.003), despite the increasing glucose area. The results indicate that even prior to frank carbohydrate intolerance, progressive changes in basal levels of glucose, insulin, and lactate, as well as sum of glucose, accompany the expansion of adipose mass in obesity. Two different aspects of lactate metabolism have been examined in obesity. First, the association of increased basal lactate levels with increased obesity may reflect increased lactate production from enlarged adipocytes and an increased fat mass. Secondly, the inverse association between acute lactate generation following glucose ingestion and obesity, despite the increased sum of glucose in obese subjects, may reflect a decreased ability of adipose and/or extra-adipose tissues to convert glucose to lactate due to insulin resistance.

Adult↗
PubMedDate not supplied

The effect of lactate infusion on myocardial metabolism and ventricular function following ischemia and cardioplegia.

Impaired myocardial fatty acid and glucose metabolism following ischemia and cardioplegia may limit the recovery of myocardial oxidative metabolism and ventricular function. Lactate, a simple three carbon compound, can be readily metabolized to pyruvate and is possibly the preferred substrate for aerobic metabolism. Therefore, increasing arterial lactate concentrations may improve myocardial metabolic recovery after ischemia and cardioplegia. Myocardial lactate metabolism and ventricular function were assessed in a canine model of 45 mins of global normothermic ischemia followed by 60 mins of cold potassium cardioplegic arrest. Thirteen dogs received a perioperative infusion of sodium lactate to elevate arterial concentrations (from 6 to 12 mmol/L) and 12 dogs received an equivalent amount of saline. The high arterial lactate concentrations were associated with an increased myocardial lactate consumption and oxidation (as assessed by 14C-labelled lactate) during reperfusion. Myocardial ATP concentrations fell during reperfusion despite improved myocardial oxidation. The recovery of ventricular function (as assessed by a compliant intraventricular balloon) was incomplete and only marginally better with the high arterial lactate concentrations. An infusion of lactate improved myocardial oxidative metabolism following ischemia and cardioplegia. However, the recovery of ventricular function was incomplete perhaps because of inadequate preservation of myocardial ATP.

Adenosine Triphosphate↗
PubMed1987

Receptor-mediated endocytosis of lactate dehydrogenase M4 by liver macrophages: a mechanism for elimination of enzymes from plasma. Evidence for competition by creatine kinase MM, adenylate kinase, malate, and alcohol dehydrogenase.

We have previously shown that the rapid clearance of intravenously injected lactate dehydrogenase M4 from plasma is mainly due to endocytosis by macrophages in liver, spleen, and bone marrow. We have now studied endocytosis of lactate dehydrogenase M4 in detail, using freshly isolated rat liver macrophages (Kupffer cells) in vitro. 125I-lactate dehydrogenase M4 rapidly accumulated in the cells and was subsequently degraded to trichloroacetic acid-soluble material. Degradation was inhibited by leupeptin, an inhibitor of lysosomal proteases. Breakdown of the protein was also greatly diminished by treatment of the cells with chloroquine, a weak base which inhibits proteolysis by raising the pH in endosomes and lysosomes. High concentrations of chloroquine inhibited uptake. Lactate dehydrogenase M4 was not endocytosed by liver endothelial cells, although, under the same conditions, these cells were shown to accumulate horse radish peroxidase via a mannose-specific receptor. Uptake of lactate dehydrogenase M4 by Kupffer cells was strongly reduced after pretreatment of the cells with low concentrations of proteases. Endocytosis of lactate dehydrogenase M4 exhibited saturation kinetics (Km = 0.8 microM) and was competitively inhibited by mitochondrial and cytosolic malate dehydrogenase, alcohol dehydrogenase, adenylate kinase, and creatine kinase MM, enzymes which are rapidly cleared in vivo. Enzymes with long half-lives in plasma, namely lactate dehydrogenase H4, alanine aminotransferase, and cytosolic aspartate aminotransferase did not compete at concentrations up to 10 microM. Our results indicate that Kupffer cells contain a receptor that is involved in the clearance of lactate dehydrogenase M4 and a number of other tissue-derived enzymes from plasma. Uptake of lactate dehydrogenase M4 does not occur via a receptor that recognizes carbohydrate residues, for the enzyme is not a glycoprotein.

Adenylate Kinase↗
PubMed1988

Striated muscle tissue oxygenation and lactate levels during normo-, hyper- and hypocapnia. A study in the rabbit.

The relationship between striated muscle tissue oxygenation during hyper- and hypocapnia, and lactate levels and venous pO2 (pvO2) was studied in a rabbit model. Seven rabbits were ventilated with constant volume during ether anesthesia, and arterial pCO2 (paCO2) was varied by addition of CO2. Muscle tissue oxygenation was measured with a multichannel electrode on the striated muscle surface, the results presented as oxygen pressure distributions (OPD:s). The principal result during hypercapnia (paCO2 9.9 kPa) was a tendency toward increased mean oxygen pressure (ptxO2) of the OPD; OPD shape was normal in 5/7 runs. Arterial lactates (aLa) decreased. During duplicate hypocapnia to paCO2 2.9 and 2.8 kPa ptxO2 decreased, but only in 4/14 runs were tissue oxygen pressures (ptO2) below 0.6 kPa found. OPD shape was scattered in 6/14 runs indicating disturbance in regulation of tissue oxygenation (but without signs of hypoxia). An increase in aLa was found, as well as a decrease in arterio-venous lactate difference (avDLa). Lacking direct blood flow measurements, these two results could not be interpreted as increased lactate efflux per se. Muscle lactates (mLa) were high but, on average, not higher than a control group. A decrease in pvO2 was seen during hypocapnia. Subgrouping OPD:s according to shape and presence of low ptO2 values did, however, suggest that lactate was released in cases with low ptO2 values: a covariation was seen in runs with low oxygen pressures between high arterial and muscle lactates, decreased avDLa and pvO2; runs with scattered OPD:s had only intermediately high lactates and low avDLa and pvO2 when compared to normally shaped OPD:s. In this study, hypercapnia influenced striated muscle tissue oxygenation only to a minor degree while hypocapnia influenced it more but not as much as expected. Only when low oxygen pressures were present in the OPD:s were there indications of peripheral lactate release.

Animals↗
PubMed1988

'Lactate washout' following circulatory arrest.

The measurement of arterial blood lactate concentration for the purpose of estimating the severity and prognosis of acute perfusion failure is suspect because of theoretical errors due to systemic "lactate washout" immediately following restoration of perfusion. If arterial lactate concentrations continue to increase following resuscitation, the assumption that increasing lactate concentrations indicate progression of anaerobiosis due to perfusion failure would be invalidated. Lactate washout was therefore investigated in a porcine model of cardiac arrest due to electromechanical dissociation. Cardiopulmonary resuscitation was initiated and maintained for intervals of 30 minutes or until spontaneous circulation was restored. In 25 trials on 14 successfully resuscitated animals, the arterial blood lactate concentration decreased within four minutes after resuscitation from cardiac arrest. In 24 animals in whom resuscitation efforts failed, arterial lactate concentrations increased throughout the observation period. Lactate washout occurred during an interval of only 2.6 +/- 0.3 minutes (mean +/- SEM). These results indicate that lactate measurements are not invalidated because of a washout phenomenon under the extreme conditions of cardiac arrest.

Animals↗
PubMed1985

[Cell concentration of individual cow's milk: effect of the status of mammary infection, parity, lactation stage and milk production].

The relative effect of the intramammary infections and of different factors related to the cow (parity, stage of lactation, milk yield) on the individual cell counts, were studied for 30 months on the 62 black-and-white Holstein cows of an experimental herd. During this period, the cows were regularly submitted to bacteriological tests for intramammary infections, individual cell counts and controls of the milk yield. The infection status of the cows at the time of counting was the main factor affecting the cell concentrations in the milk: the values ranged from around 5 X 10(4) cells/ml in the absence of infection in the four quarters, to values that were on average twice as high in the case of infection by a minor pathogen and ten times as high in the case of infection by a major pathogen. The mean cell concentrations in the milk of uninfected cows were significantly lower during the first lactation; they varied during the lactation according to a curve which had the form of an inverted lactation curve. The mean cell count during a lactation was independent of the mean milk yield per day of lactation. In cows infected by a major pathogen, the effect of the number and stage of lactation was different. Only the variation apparently associated with the stage of lactation had a sufficient amplitude to bring the mean cell concentrations of uninfected cows close to the values recorded in cows infected by a minor pathogen. The average results from cows infected by a major pathogen were, however, much higher at all stages of lactation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

In vivo lactate production and utilization by Jensen sarcoma and Morris hepatoma 7288CTC.

These experiments were designed to determine the characteristics of lactic acid utilization and production in vivo in Jensen sarcoma and Morris hepatoma 7288CTC. Arteriovenous differences for lactic and pyruvic acids, glucose, and the ketone bodies were measured across "tissue-isolated" tumors growing in fed and fasted rats. Lactic acid was utilized (n = 18), produced (n = 24), or neither utilized nor produced (n = 1) by the tumors. Net tumor lactate production or utilization did not depend on the mean rate of glucose utilization which was the same in the lactate-utilizing and -producing tumors. For the lactic acid-utilizing tumors, the mean arterial whole blood lactate concentration entering the tumor was 3.47 +/- 0.39 mM, and the concentration in the tumor venous blood was 2.31 +/- 0.25 mM. For the lactic acid-producing tumors, the mean arterial lactic acid concentration was 1.29 +/- 0.10 mM, and the tumor venous blood concentration was 2.19 +/- 0.19 mM. Thus, both lactate-producing and lactate-utilizing tumors showed identical rates of glucose utilization and identical lactic acid concentrations in the venous blood leaving the tumors. Metabolite levels were also measured in tumors that were freeze clamped in situ immediately following collection of the arterial and tumor venous blood samples. The lactic acid content in the tumor mass (corrected for total tumor water) and the concentration in the tumor venous blood plasma were nearly identical, suggesting that the lactate concentrations in the tumor cells and tumor venous blood are at equilibrium. Transport of lactic acid between arterial plasma and tumor or between tumor and venous plasma was always down a concentration gradient; net lactate uptake and release in these tumors followed the law of mass action. High lactate concentrations were not observed in the Jensen sarcomas or in the venous blood leaving these tumors, and we were unable to confirm earlier studies indicating that Jensen sarcomas are consistently high net lactate producers in vivo.

Animals↗
PubMed1984

L(+)-Lactate binding to preparations of rat hepatocyte plasma membranes.

Incubation of rat hepatocyte plasma membranes with L-[14C]lactate resulted in the labeling of protein(s) of apparent molecular weight 40,000 when examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The binding was saturable, irreversible, and inhibited by pyruvate, 2-oxoglutarate, and alpha-cyano-3-hydroxycinnamate, but not by D-lactate. It was markedly enhanced by L-alanine, but not D-alanine or beta-alanine. The binding protein(s) could be solubilized in cholic acid giving a single peak on gel filtration corresponding to a molecular weight of 26,000 and an isoelectric point of 5.1. This peak, when subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, ran in a position corresponding to an apparent molecular weight of 40,000. When membranes were treated with Triton X-100, lactate binding was retained by the Triton-insoluble fraction. The binding of L-[14C]lactate increased with incubation time, due apparently to the appearance of new binding sites and not to sequestration into vesicles. As many of the characteristics of lactate binding to rat hepatocyte plasma membranes were found to be similar to those of lactate entry into isolated hepatocytes, we speculate that the lactate-binding protein could represent part or whole of a plasma-membrane lactate transporter. Lactate-binding proteins of the same molecular weight were identified in the plasma membranes from rat erythrocytes, cardiac muscle, skeletal muscle, lung, and brain.

Animals↗
PubMed1983

Renal oxygenation and lactate metabolism in hemorrhagic shock in dogs.

Renal tissue oxygen tension and lactate metabolism were studied in hemorrhagic shock in dogs. The renal tissue PO2 and oxygen consumption declined in proportion to blood loss and decreasing blood flow. The decrease of tissue PO2 was greater in the cortex than in the medulla. Renal lactate uptake remained constant at the control level until 30% blood loss through an increase of renal arteriovenous lactate difference in direct proportion to arterial lactate concentration. During hemorrhagic shock after 40% blood loss lactate uptake decreased sharply and ceased almost totally. Before shock renal lactate uptake correlated highly significantly with arterial pH whereas after shock the correlation between these parameters was less significant. After reinfusions of shed blood the renal tissue PO2 returned to the prehemorrhage level in both tissue layers despite the reduced renal blood flow. At this phase renal oxygen consumption and lactate uptake failed to reach the control levels. These findings indicate that in moderate hypotension renal lactate uptake is not restricted by the local oxygen supply. During established shock tissue hypoperfusion and hypoxia seem to be responsible for deterioration of renal lactate metabolism.

Animals↗
PubMed1978

The anatomic and metabolic source of lactate in shock.

The size of the lactate pool in canine shock was measured directly by determining the lactate concentration of various organs. All organs tested, except skeletal muscle, had lactate concentrations similar to those of arterial blood. Skeletal muscles had much higher concentrations of lactate than did arterial blood. When 14C-labeled glucose was infused intravenously, it was concluded from the relative specific activities of glucose and lactate in blood that about one-third of lactic acid originates from blood glucose in shock. Only skeletal muscle had lower lactate specific activity than did blood. This is a possible indication that skeletal muscle is the site of production of lactate. Low glucose specific activity in muscle indicates massive glycogen breakdown, which probably serves as a metabolic precursor of lactate. Lactate production from amino acids produced by proteolysis could also play a role.

Amino Acids↗
PubMed1981

Stimulation of protein synthesis in round spermatids from rat testes by lactate.

Lactate markedly increased the rate of [3H]leucine incorporation into the protein of isolated round spermatids (steps 1-8) from rat testes. Four kinds of hexoses, glucose, fructose, galactose, and monnose, also stimulated [3H]leucine incorporation, but to much lesser extents than lactate. Ribose had no effect. The glucose-induced stimulation of protein synthesis was entirely suppressed by iodoacetate and NaF, whereas iodoacetate and NaF were without effect on the lactate-induced increase in protein synthesis. Lactate stimulated both protein synthesis and ATP production in the spermatids. However, both of these stimulatory effects of lactate were completely blocked by DNP and rotenone. Rotenone entirely blocked oxygen consumption, as expected, whilst DNP enhanced it additively with lactate. Moreover, lactate was without influence on either transport of alpha-[3H]AIB into spermatids or incorporation of [3H]leucine into protein of a cell-free system of spermatids. These findings suggest that lactate may increase the protein synthesis of spermatids in the same fashion as glucose, and that the effect of lactate in increasing the level of ATP during incubation in vitro may be a major factor in the mechanism of stimulation of protein synthesis in the spermatids.

Adenosine Triphosphate↗
PubMed1995

Elevated serum lactate correlates with intracranial hemorrhage in neonates treated with extracorporeal life support.

OBJECTIVES: To correlate the initial and maximal lactate levels with the occurrence of intracranial hemorrhage (ICH) and survival in patients treated with extracorporeal life support (ECLS). DESIGN: Retrospective chart review. SETTING: Pediatric intensive care unit. PATIENTS: Eighty-two neonatal patients placed on ECLS for respiratory failure due to sepsis, meconium aspiration, or persistent pulmonary hypertension of the newborn. MEASUREMENTS: The initial lactate level measured within 6 hours of initiating ECLS and the maximal lactate level measured throughout the ECLS course were collected. Lactate levels were described as mean lactate +/- SE (mM). Head ultrasound reports and survival were reviewed. Platelet counts and activated clotting times (ACTs) were examined. RESULTS: The mean initial and maximal lactate levels were higher in ECLS patients who developed ICH (initial: 10 +/- 1.7 mM vs 6.4 +/- 0.8 mM, p = .05 and maximal: 12.4 +/- 2.5 mM vs 7.9 +/- 0.8 mM, p = .04). Initial and maximal lactate levels were also elevated in nonsurvivors (initial: 11.7 +/- 3 mM vs 6.4 +/- 0.7 mM, p = .01 and maximal: 14.8 +/- 3.3 mM vs 7.8 +/- 0.8 mM, P < .01). Platelet counts and ACT did not differ in patients with and without ICH. CONCLUSIONS: Lactate is a useful marker for the development of ICH in ECLS patients. In addition, elevated lactates during ECLS identify a subgroup of patients with poor outcome. Prospective studies are needed to determine whether the incorporation of this information into pre-ECLS and ECLS management will decrease the occurrence of ICH and improve survival.

Cerebral Hemorrhage↗