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lactic acid/hypoxia

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Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition.

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The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios -delta[La].delta pH-1 (where delta[La] is change in lactic acid concentration and delta pH is change in pH) and delta[HCO3-].delta pH-1 (where delta[HCO3-] is change in bicarbonate

The role of mineralized tissue in the buffering of lactic acid during anoxia and exercise in the leopard frog Rana pipiens.

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To evaluate the role of mineralized tissues of the leopard frog in buffering acid, we analyzed the composition of femur and auditory capsule, the latter of which encloses a portion of the endolymphatic lime sacs, and investigated the extent to which these tissues are involved in buffering lactic

[Effects of acute hypoxia on plasma lactic acid and lactic dehydrogenase content in pilots].

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Objective. To study the effect of acute moderate hypoxia on plasma lactic acid (LA) and lactic dehydrogenase (LDH) content in pilots. Method. Concentrations of plasma LA and LDH were measured by colorimetry in 16 healthy male pilots in the early morning (6:00 a.m.), following acute moderate hypoxic

Effects of ischemic and hypoxic hypoxia on VO2 and lactic acid output during tetanic contractions.

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We measured O2 uptake (VO2), CO2 output (VCO2), and net lactic acid output (L) during a 30-min period of repetitive 1/s isotonic tetanic contractions of the dog gastrocnemius-plantaris muscle group. The conditions were modest ischemic hypoxia (ischemia), hypoxia hypoxia (hypoxia), and free-flow

[Effect of short-term hypoxia on body temperature and lactic acid in the blood of the mouse].

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In mice, changes of body temperature and concentration of lactic acid in the blood were studied after three modes of barochamber hypoxia (altitude 8000 m) at the temperatures +10, +20 and +36 degrees C. The greatest drop of body temperature occurred at +10 degrees C, the least one at +36 degrees C.

[Concentration of lactic acid in the blood and erythropoiesis during exposure to hypoxia].

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The data obtained with the aid of additional hypoxic load (blood loss, ascending in a barochamber) reveal a considerable lactacidemia occurring prior to erythropoiesis activation which corroborates the theory of activation of the erythropoietin formation with lactic acid. The degree of lactacidemia

Vascular lactic acid infusions do not alter the incidence of fetal breathing movements or their inhibition by acute hypoxemia.

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Hypoxemia transiently inhibits the incidence of fetal breathing movements (FBM), but their incidence returns to normal after several hours despite maintained hypoxemia. We hypothesized that the lactic acidosis associated with prolonged systemic hypoxemia might mediate the adaptation of the hypoxemic

Lactic acid accumulation as a cause of hypoxia-induced malformations in the chick embryo.

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Most hypoxia-induced malformations are caused by a syndrome involving tremendous edema followed by formation of clear blisters and hematomas. These, in turn, mechanically interfere with development. Studies of blood pH and lactic acid indicate that lactate accumulation initiates this syndrome. The

The effects of lactic acid production on contraction and intracellular pH during hypoxia in cardiac muscle.

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During hypoxia cardiac contraction declines and there is an intracellular acidosis. We find that, if this acidosis is abolished by decreasing pCO2 there is little restoration of force. Therefore the acidosis is not the major cause of the decline of force. The acidosis may partly result from the

Lactic Acid efflux as a mechanism of hypoxic acclimation of maize root tips to anoxia.

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Hypoxic pretreatment (3 kPa oxygen) of maize (Zea mays L.) root tips improved their survival time in a subsequent anoxic incubation from 10 h to more than 3 d, provided that glucose was added to the medium to sustain metabolism. The glycolytic flux (lactate + ethanol) was the same in both pretreated

Targeting Melanoma Hypoxia with the Food-Grade Lactic Acid Bacterium Lactococcus Lactis.

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Melanoma is the most aggressive form of skin cancer. Hypoxia is a feature of the tumor microenvironment that reduces efficacy of immuno- and chemotherapies, resulting in poor clinical outcomes. Lactococcus lactis is a facultative anaerobic gram-positive lactic acid bacterium (LAB) that is

Lactic Acid Suppresses IL-33-Mediated Mast Cell Inflammatory Responses via Hypoxia-Inducible Factor-1α-Dependent miR-155 Suppression.

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Lactic acid (LA) is present in tumors, asthma, and wound healing, environments with elevated IL-33 and mast cell infiltration. Although IL-33 is a potent mast cell activator, how LA affects IL-33-mediated mast cell function is unknown. To investigate this, mouse bone marrow-derived mast cells were

[Effects of muscular exertion in a hypoxic and hypoxic-hypercapnic respiratory environment on acid-base equilibrium and blood lactic acid in the albino rat raised in hypoxic hypoxia from birth].

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Albino rats of the Wistar family were raised from the time of birth in the normobaric hypoxic environment. They were subjected at two subsequent equal trials of muscular work: the first in hypoxic normobaric conditions; the second in hypoxic hypercapnic conditions (CO2 = 2%). The modifications of

Effect of stagnant hypoxia of the brain on the blood glucose and lactic acid level and on serum lactic dehydrogenase activity during ontogenesis in the rat.

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[Acid-base equilibrium, blood lactic acid and pyruvic acid in albino rats after muscular exertion under conditions of normal oxygen, hypoxia and hypoxia-hypercapnia].

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Albino rats of the Wistar family were subjected at three subsequent equal trials of muscular work: the first in normoxyc conditions; the second in hypoxic normobaric conditions; the third in hypoxic-hypercapnic normobaric conditions. The modifications of the lactacidemia, pyruvicemia and acid-base
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