PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Lactation, Prolonged”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 415 records · Page 23Linked to original sources
PubMed1995

Oxygen, glucose, and lactate uptake by fetus and placenta during prolonged hypoxemia.

Our aim was to compare the effects of short (4 h) and prolonged (24 h) periods of reduced uterine blood flow (RUBF) on fetal and placental uptake of O2, glucose, and lactate. In pregnant sheep, uterine and umbilical blood flows were measured under normal conditions and after 4 and 24 h of RUBF. A 50% reduction in uterine blood flow caused a 56% reduction in fetal arterial O2 saturation (SaO2). Umbilical blood flow increased from 325 +/- 33 to 378 +/- 32 ml.min-1.kg-1 (P < 0.05) after 4 h but was not different from pre-RUBF values after 24 h. O2 uptake by the gravid uterus was not altered by RUBF, due to an increase (84%) in uterine O2 extraction. Similarly, uteroplacental and fetal O2 consumptions and fetal glucose uptake were not affected by RUBF, whereas uteroplacental glucose uptake was significantly reduced after 4 h (by 42%) and 24 h (by 58%) of RUBF. Fetal lactate uptake was greatly reduced from 78.7 +/- 15.5 to -167 +/- 57 mumol.min-1.kg-1 after 4 h and to -198 +/- 80 mumol.min-1.kg-1 after 24 h of RUBF; negative values indicate placental lactate uptake from the fetal circulation. Thus, although RUBF significantly reduced fetal SaO2, fetal and uteroplacental O2 consumptions did not change. In addition, although fetal glucose uptake was not altered by RUBF, during RUBF the placenta became a major site of lactate clearance from the fetal circulation.

Animals↗
PubMed1987

Effects of gluconeogenic precursor flux alterations on glycogen resynthesis after prolonged exercise.

The importance of gluconeogenic substrates (i.e., lactate, glycerol, and alanine) in the glycogen resynthesis observed in fasting rats after exhausting submaximal exercise [R.D. Fell et al. Am. J. Physiol. 238 (Regulatory Integrative Comp. Physiol. 7): R328-R332, 1980] was examined in muscles and liver in response to pharmacological alterations of gluconeogenic precursor flux. The minor role of lactate for glycogen resynthesis after prolonged submaximal exercise was confirmed by the insignificant accumulation of lactate neither in muscles nor in plasma. When the rate of lipolysis is reduced either by beta-blockade or by nicotinic acid injection, the replenishment of muscle glycogen persisted, suggesting that glycerol released by triglycerides hydrolysis did not play an important role in glycogen resynthesis. On the other hand, when pyruvate oxidation is enhanced by dichloroacetate (DCA), thus reducing plasma levels of lactate and alanine, glycogen resynthesis was completely blocked in liver and partly in some but not all muscles. This failure in total inhibition of glycogen resynthesis associated with the significant reduction of the plasma alanine level could be attributed to the possible stimulation of gluconeogenesis from alanine by DCA (R.A. Harris and D.W. Crabb. Arch. Biochem. Biophys. 189: 364-371, 1978). The results could point out alanine as the major gluconeogenic substrate during recovery from exhaustive exercise in fasting conditions.

Alanine↗
PubMed2001

Adenosine monophosphate-activated protein kinase mediates the protective effects of ischemic preconditioning on hepatic ischemia-reperfusion injury in the rat.

Hepatic ischemia-reperfusion (I/R) injury associated with liver transplantation and hepatic resections are an unresolved problem in the clinical practice. Preconditioning is known to preserve energy metabolism in liver during sustained ischemia, but the molecular mechanisms underlying this effect are still unclear. Different metabolic signals, including adenosine monophosphate (AMP) and nitric oxide (NO), have been implicated in preconditioning. AMP-activated protein kinase (AMPK) protects cells by acting as a low-fuel warning system, becoming switched on by adenosine triphosphate (ATP) depletion. NO synthesis is induced by AMPK in the heart during ischemia. The aim of this study was to investigate: 1) whether preconditioning induces AMPK activation; and 2) if AMPK activation leads to ATP preservation and reduced lactate accumulation during prolonged ischemia and its relationship with NO. Preconditioning activated AMPK and concomitantly reduced ATP degradation, lactate accumulation, and hepatic injury. The administration of an AMPK activator, AICAR, before ischemia simulated the benefits of preconditioning on energy metabolism and hepatic injury. The inhibition of AMPK abolished the protective effects of preconditioning. The effect of AMPK on energy metabolism was independent of NO because the inhibition of NO synthesis in the preconditioned group and the administration of the NO donor before ischemia, or to the preconditioned group with previous inhibition of AMPK, had no effect on energy metabolism. Both preconditioning and AICAR pretreatment, through AMPK activation, may be useful surgical and pharmacologic strategies aimed at reducing hepatic I/R injury.

AMP-Activated Protein Kinases↗
PubMed2004

Hematological and acid-base changes in men during prolonged exercise with and without sodium-lactate infusion.

An emerging technique used for the study of metabolic regulation is the elevation of lactate concentration with a sodium-lactate infusion, the lactate clamp (LC). However, hematological and acid-base properties affected by the infusion of hypertonic solutions containing the osmotically active strong ions sodium (Na(+)) and lactate (Lac(-)) are a concern for clinical and research applications of LC. In the present study, we characterized the hematological and plasma acid-base changes during rest and prolonged, light- to moderate-intensity (55% Vo(2 peak)) exercise with and without LC. During the control (Con) trial, subjects were administered an isotonic, isovolumetric saline infusion. During LC, plasma lactate concentration ([Lac(-)]) was elevated to 4 meq/l during rest and to 4-7 meq/l during exercise. During LC at rest, there were rapid and transient changes in plasma, erythrocyte, and blood volumes. LC resulted in decreased plasma [H(+)] (from 39.6 to 29.6 neq/l) at the end of exercise while plasma [HCO(3)(-)] increased from 26 to 32.9 meq/l. Increased plasma strong ion difference [SID], due to increased [Na(+)], was the primary contributor to decreased [H(+)] and increased [HCO(3)(-)]. A decrease in plasma total weak acid concentration also contributed to these changes, whereas Pco(2) contributed little. The infusion of hypertonic LC caused only minor volume, acid-base, and CO(2) storage responses. We conclude that an LC infusion is appropriate for studies of metabolic regulation.

Acid-Base Equilibrium↗
PubMed2006

Fluid resuscitation with hemoglobin-vesicle solution does not increase hypoxia or inflammatory responses in moderate hemorrhagic shock.

The aim of the present study was to compare the hypoxic and inflammatory effects of transfusing hemoglobin-vesicles (HbV) or lactated Ringer's (LR) solution on several organs in a hemorrhagic shock model. Hemorrhagic shock was induced in 48 anesthetized rats by withdrawing 28 mL/kg blood. The animals were resuscitated by replacing the blood with an equal volume of HbV solution or three times the volume of LR solution. The heart, lung, liver, kidney and spleen were extracted at different time points following resuscitation, and mRNA expression levels of hypoxia-induced factor 1-alpha (HIF-1alpha) and tumor necrosis factor-alpha (TNF-alpha) were determined. Blood lactate concentrations in the HbV group rapidly returned to baseline levels, whereas elevated lactate concentrations in the LR group were prolonged. There were no significant differences between the two resuscitation groups in terms of HIF-1alpha and TNF-alpha expression in the organs examined. HIF-1alpha and TNF-alpha expression in the lungs was significantly greater than in other organs. Our results suggest that resuscitation from hemorrhagic shock with HbV did not increase hypoxic or inflammatory effects in major organs, compared with resuscitation using LR solution, despite prolonged elevation of blood lactate.

Animals↗
PubMed1990

Adipocyte lactate production remains elevated during refeeding after fasting.

The metabolic state occurring with refeeding after fasting is characterized by the rapid restoration of hepatic glycogen. Recent evidence suggests that a main substrate for glycogenesis is lactate. Because adipose tissue is an active site of lactate production that increases with fasting, we examined the magnitude and duration of lactate production by isolated adipocytes from three adipose depots of rats fasted for 48 h and then refed for up to 96 h. The data show that 48 h of fasting results in a markedly elevated rate of adipocyte lactate production, which increased from 3-9% of total glucose metabolized in the fed state to 49-60% in the fasted state. During the refeeding period, lactate production remained elevated for 12-24 h and then declined. Mesenteric adipocytes had a higher rate and more prolonged elevation in lactate production than cells from the other two depots. We conclude that, with refeeding after a fast, adipocyte glucose conversion to lactate remains elevated during the time of hepatic glycogen restoration. This suggests that adipose tissue may actively produce lactate for glycogenesis during refeeding.

Adipose Tissue↗
PubMed1991

Cardiorespiratory and lactate responses to a 1-hour submaximal running at the lactate threshold.

Cardiorespiratory and blood lactate (La) responses to prolonged submaximal running at an intensity relative to lactate threshold (LT) were examined in 15 recreational runners, aged 19 to 32. In test 1 where treadmill speed was progressively incremented by 10-20m/min until exhaustion, oxygen uptake at the LT (VO2 @ LT: 2.34 +/- 0.331/min or 41.6 +/- 5.7 ml/kg/min) and VO2max (3.58 +/- 0.341/min or 63.6 +/- 5.5 ml/kg/min) were measured. In test 2, the subject was required to run on the treadmill for 1 hour at a fixed velocity (Vt) which corresponded to his Vt @ LT. As expected, mean VO2 ranged during the 1-h submaximal running from 2.31 +/- 0.411/min or 63.0 +/- 7.8% VO2max at min 10-20 to 2.52 +/- 0.351/min or 69.2 +/- 6.2% VO2max at min 50-60, both of which were close to VO2 @ LT (65.2 +/- 4.4% VO2max). The slight decrease in blood La was found from min 20 to min 60, and this was accompanied by a parallel decline in respiratory exchange ratio. Shifts in the energy substrate toward a reliance on fat oxidation may occur during the course of 1-h running at Vt @t LT. The small oxygen debt observed after the 1-h running may confirm the assumption that prolonged running at Vt at LT would be performed in an almost fully aerobic steady state. We conclude that prolonged running at Vt @ LT may possibly maximize health-related benefits in the healthy adult.

Adult↗
PubMed1982

Lactate and glucose exchange across the forearm, legs, and splanchnic bed during and after prolonged leg exercise.

The net exchange of glucose and lactate across the leg and the splanchnic bed and the arterialdeep venous (A-DV) differences for these substrates in the forearm were determined in healthy subjects during 3-3.5 h of leg exercise (bicycle ergometer) at 58% maximum O(2) uptake and during a 40-min post-exercise recovery period. Leg glucose uptake rose 16-fold during exercise and throughout the exercise period exceeded splanchnic glucose output. The latter reached a peak increment (3.5 times basal) at 90 min and fell by 60% during the third hour. As a result, blood glucose declined 40%, reaching frank hypoglycemia (blood glucose, <45 mg/dl) in 50% of subjects at 3.5 h. Splanchnic lactate uptake rose progressively during exercise to values four times the basal rate at 3 h in association with a rise in arterial lactate to 1.5 mM. There was, however, no significant net output of lactate from the legs beyond 90 min of exercise. In contrast, the A-DV lactate difference in the forearm became progressively more negative throughout exercise, reaching values three times the basal level at 3.5 h. The rise in arterial lactate during exercise was proportional to the elevation in plasma epinephrine, which rose ninefold. During recovery, splanchnic lactate uptake rose further to values six times the basal rate, whereas lactate output by the legs was no greater than in the basal state. The A-DV lactate difference in the forearm became even more negative than during exercise, reaching values four times basal. During exercise as well as recovery, forearm uptake of blood glucose could account for no more than 25-67% of forearm lactate release. Leg glucose uptake during recovery was threefold to fivefold higher than in the basal state in the face of plasma insulin concentrations that were 60% below basal and in association with a respiratory exchange ratio of 0.7. We conclude that (a) during prolonged leg exercise at 58% maximum O(2) uptake an imbalance between splanchnic glucose production and leg glucose utilization results in a fall in blood glucose that may reach hypoglycemic levels in healthy subjects; (b) there is a marked increase in the uptake of lactate by the splanchnic bed that cannot be attributed to increased output of lactate from the exercising legs; (c) lactate is released by forearm muscle and, together with other relatively inactive muscle, may be an important source of the increased lactate turnover during and after prolonged leg exercise; (d) the increasingly negative A-DV lactate difference in the forearm cannot be accounted for by uptake of blood glucose, suggesting the breakdown of glycogen in forearm muscle during and after leg exercise; (e) increased glucose uptake by the legs in association with hypoinsulinemia during recovery suggests an increase in insulin sensitivity that permits glycogen repletion in previously exercising muscle in the absence of food ingestion; and (f) the evidence for increased lactate output in the forearm and augmented glucose uptake in the legs during recovery raises the possibility that after leg exercise glycogen stores are decreasing in muscle that was relatively inactive (e.g., that of the forearm) while increasing in the previously exercising leg muscles.

Adult↗
PubMed1994

Breastmilk can mediate chemical imprinting. Benzpyrene exposure during lactation reduces the thymic glucocorticoid receptor density of the offspring.

1. Prolonged benzpyrene treatment during lactation reduced the number of glucocorticoid receptors of offspring in adulthood significantly without altering the receptor affinity. 2. Dexamethasone treatment identical to benzpyrene exposure had no effect either on receptor number or affinity. 3. The results of the present investigations draw attention to the possible way of receptor alteration via breastmilk.

Animals↗
PubMedDate not supplied

Lactation suppression. Nonpharmaceutical versus pharmaceutical method.

Mothers bottle feeding their infants need an adequate method of lactation suppression to prevent/lessen discomfort related to breast engorgement. This study compared the effectiveness of a non- pharmaceutical method (ice and tight bra) of suppressing lactation to a pharmaceutical therapy (bromocriptine mesylate). The sample consisted of 36 subjects who used the pharmaceutical therapy (drug group) and 17 subjects who used the non-pharmaceutical method (protocol group). The data showed that the drug group had significantly less engorgement, milk production, and discomfort on the fourth postpartum day, but the lactation process was prolonged until postpartum day nine or 16. The protocol group had more engorgement, milk leakage, and discomfort on postpartum day four, but the lactation process was completed before postpartum day 16.

Adult↗
PubMed1992

Primiparous rhesus monkey mothers are more sensitive to the nursing-induced inhibition of LH and ovarian steroid secretion.

The duration of lactational infertility is prolonged significantly in adolescent, primiparous rhesus monkey (Macaca mulatta) mothers compared with adult, multiparous mothers. The present study examined the hypothesis that this parity/age difference in lactational infertility is due to a difference in the physiological responsiveness to nursing behaviour between adolescent and fully adult mothers and is not a consequence of differences in nursing behaviour, per se. At 22 weeks postpartum, mother-infant pairs were randomly assigned to one of four conditions: primiparous, nursing restricted (PR; n = 9); primiparous, nursing unrestricted (PU; n = 11); multiparous, nursing restricted (MR; n = 12); and multiparous, nursing unrestricted (MU; n = 8). Nursing was restricted for a 2-week period by mothers wearing a primate vest which prevented suckling behaviour but allowed infants to interact with their mothers. Nursing restriction resulted in a significant increase in serum oestradiol concentrations in both PR and MR mothers. Although nursing bout frequencies and durations were similar between PU and MU mothers, serum oestradiol also rose in MU mothers but remained suppressed in PU mothers. Once the nursing manipulation period ended and all mothers were allowed to nurse ad libitum, serum oestradiol concentrations continued to rise in all but the PU mothers. This brief interruption of nursing at 22 weeks postpartum advanced the subsequent timing of the first postpartum ovulation in MR and PR mothers relative to that of PU mothers. Again, despite similarities in nursing behaviour, the occurrence of first ovulation was also advanced in MU mothers compared with PU mothers. Just prior to the first postpartum ovulation, females were randomly assigned to one of four treatment groups to determine the effects of nursing behaviour on the hormonal parameters of the luteal phase: primiparous, nursing restricted (PRL; n = 9); primiparous, nursing unrestricted (PUL; n = 11); multiparous, nursing restricted (MRL; n = 10); and multiparous, nursing unrestricted (MUL; n = 10). Nursing restriction significantly elevated serum progesterone concentrations in PRL females compared with other mothers. Serum concentrations of oestradiol were higher in PRL, MRL and MUL mothers relative to PUL females. Again, this difference in oestradiol between PUL and MUL mothers occurred despite similarities in nursing behaviour. These data suggest that parity/age differences in the period of lactational infertility are not due to differences in nursing behaviour but rather to an increased sensitivity to the inhibitory aspects of the suckling stimulus in adolescent primiparous mothers.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1998

Prolonged pneumoperitoneum at 15 mmHg causes lactic acidosis.

BACKGROUND: Acute increases in intraabdominal pressure (IAP) induce systemic and regional circulatory changes. Besides, mechanical compression on the capillary beds may decrease oxygen availability to the tissues. The purpose of this clinical study was to analyze the effects of increased IAP on acid-base disturbances and plasma lactate levels during prolonged carbon dioxide pneumoperitoneum. METHODS: Twenty-eight patients undergoing laparoscopic sigmoidectomy were included in this study. Fourteen of them (group A) had IAP of 15 +/- 1 mmHg while the remaining 14 (group B) had IAP of 10 +/- 1 mmHg. The control group included six patients undergoing conventional sigmoidectomy. RESULTS: A progressive significant increase in PaCO2 was observed in the laparoscopic groups (p < 0.01). Plasma lactate levels in group A significantly increased 90 min after insufflation (p < 0.05) and reached the highest value 1 h after deflation (9.9 +/- 1 vs 31.9 +/- 2.5 mg/dl, p < 0.005). Simultaneously, arterial pH decreased in all groups; however, at 1 h after surgery, it was significantly lower (p = 0.02) in group A. There was a significant correlation between acid concentration due to lactate and lactate concentration (GA: R2 = 0.717, p = 0.03; GB: R2 = 0.879, p = 0.006 and GC: R2 = 0.853, p = 0.008). CONCLUSION: High IAP causes lactic acidic accumulation in patients undergoing prolonged laparoscopic procedures.

Acidosis, Lactic↗
PubMed1994

Effect of concurrent exercise and physostigmine on lactate and pyruvate in plasma, muscle, and brain tissue of rats.

The purpose of this investigation was to determine the effect of physostigmine (Phy) and/or concurrent exercise on lactate, pyruvate, and L/P ratio in plasma, skeletal muscle, and brain tissue in male Sprague-Dawley rats. The Phy-dosed (Phy-D) and Phy-dosed + concurrent acute exercise (Phy-D + CAE) groups elicited significantly higher L/P ratios in plasma compared to the acutely exercised (AE) group at 30 min postexercise. Physostigmine dosing, with or without exercise, resulted in significantly lower muscle pyruvate levels, from 30 to 50 min postdrug administration, in Phy-D and Phy-D + CAE groups compared to the AE group. In the brain, lactate values were significantly elevated in the acutely exercised groups at 5 min postexercise with or without Phy dosing. However, at 15 to 30 min postexercise, lactate values were significantly elevated in the Phy-D + CAE compared to the AE group. These data suggest that when Phy is administered prior to a 20-min moderately intensive exercise bout, there is an accumulation of lactate for a prolonged period of time in recovery.

Animals↗
PubMedDate not supplied

[Pathophysiological aspects of the development of circulatory hypoxia in artificial circulation].

Metabolic status of 650 patients operated on under artificial circulation for various cardiac diseases was studied. Circulatory hypoxia was found to underlie all metabolic disorders in artificial circulation which manifest by loss of buffer bases and lactate accumulation. Development of circulatory hypoxia in artificial circulation is caused by inadequate oxygen supply to tissues due to initially present disorders of the peripheral bloodstream which augment during perfusion by circulation centralization and due to changes of blood rheology, particularly so in increase of hypothermia and prolongation of perfusion. Lactate concentration during artificial circulation is an objective criterion of tissue hypoxia which sufficiently well correlates with development of heart failure in the early postperfusion period. When correcting circulatory hypoxia during artificial circulation the anesthesiologist and perfusiologist should aim at changing the vascular tone towards an increase of the peripheral bloodflow. This is particularly important during prolonged hypothermic perfusions in patients with initially low reserve potential of the myocardium.

Cardiac Surgical Procedures↗
PubMed1997

Changes in neuropeptide Y immunoreactivity in the arcuate nucleus during and after food restriction in lactating rats.

Previous studies have demonstrated that food restriction during lactation extends the length of lactational infertility in rats. In order to determine whether Neuropeptide Y (NPY) plays a role in the increased length of lactational infertility seen in food-restricted rats, NPY immunoreactivity in the arcuate nucleus of lactating rats that were ad lib fed or food restricted from Day 8 to 14 postpartum was compared. Food-restricted rats showed higher numbers of NPY-stained cells at the end of the food-restriction period (Day 15 postpartum) than did ad lib-fed rats at the same stage of lactation. This difference persisted until Day 25 postpartum although all animals were fed ad libitum from Day 15 onwards. Switching litters between ad lib-fed and food-restricted females from Day 15 until Day 20 postpartum did not eliminate the difference in NPY immunoreactivity between the two diet conditions. Given that food restriction during lactation leads to a prolonged suppression of LH release that also persists after refeeding and is not affected by the nutritional status of the litter, these data are consistent with a role for NPY in the prolonged suppression of reproductive function seen in food restricted lactating rats.

Animals↗
PubMed1990

A scanning electron microscopic and photon absorptiometric study of the development, prolongation, and pattern of recovery from lactation-induced osteopenia in rats.

Measurements by scanning electron microscopy (SEM) of femoral hemisections confirmed and amplified results by single-photon absorptiometry that had shown a marked increase in lactation osteopenia in rats fed a low-calcium diet (LCD, 0.04% Ca) as compared with a medium-(adequate) calcium diet (ACD, 0.4% Ca). SEM of bones from rats at the end of lactation on either diet showed a large loss of trabecular bone, increased porosity of endosteal surfaces, and cortical thinning. These changes were much more striking in LCD rats than in ACD rats. Backscattered electron imaging of cross sections of the femora revealed marked cortical thinning at midshaft after lactation, especially in rats on the LCD; this method also showed a marked increase in newly formed, less dense diaphyseal bone on the endosteal surface when dietary calcium had been made available to the LCD rats after lactation ceased. Unlike the rats fed the ACD after lactation, the rats continued on the LCD for the first 3 weeks postlactation failed to recover bone mineral, even though there was a marked decrease in resorbing surfaces of the femora as revealed by morphologic examination. When the diet was changed from the LCD to the ACD for the second 3 weeks postlactation (week 4-6), the bone mineral increased substantially. Overall, these results demonstrate the marked loss of bone during lactation, especially severe in rats fed a low-calcium diet, and the rapid postlactational recovery of bone when adequate dietary calcium was made available, even if the recovery had been delayed for the first 3 weeks by feeding a diet very low in calcium.

Absorptiometry, Photon↗
PubMed1989

Prolongation of the half-life of lactate after maximal exercise in patients with hepatic dysfunction.

Decreased hepatic clearance of exogenous sodium lactate has previously been demonstrated in patients with hepatic dysfunction. The purpose of this study was to obtain a more precise understanding of the rate of metabolic normalization or decrease of endogenously produced lactate in patients with hepatic cirrhosis. The differential kinetics of lactate metabolism are of clinical interest. Male volunteer patients with hepatic cirrhosis (n = 7), who had survived acute hospitalization, were compared to healthy age-matched males with normal liver function (n = 7). After arterial cannulation, bicycle ergometry was performed at a workload of 25 watts (W); the load was increased by increments of 25 W at 2-min intervals to maximum aerobic capacity. Lactate was measured in arterial blood before, at 4-min intervals during, and on a minimum of 11 occasions in the 30 to 70 min after exercise. The time interval during which lactate declined linearly to half its maximal concentration (Lt50) was graphically computed. The Lt50 was 34.8 +/- 4.5 min (mean +/- SEM) in the experimental group and 14.1 +/- 1.3 min in the control subjects (p less than .005). Lactate disappears from the bloodstream almost three times more slowly in patients with hepatic cirrhosis. The implication for interpretation of changes in lactate during circulatory shock in the presence of liver dysfunction is addressed.

Half-Life↗