Utilization of lactic acid and cardiovascular response in the sheep fetus receiving an infusion of lactic acid

E. Kastendieck; W. Künzel; C. S. Kurz

doi:10.1007/bf02108595

Relation of Hypoxemia and/or Hypocapnia to Lactic Acid Content of Brain and Cardiovascular Response

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1958.193.2.345 ◽

1958 ◽

Vol 193 (2) ◽

pp. 345-349 ◽

Cited By ~ 3

Author(s):

Clyde Biddulph ◽

Donald D. Van Fossan ◽

Dominic Criscuolo ◽

Robert T. Clark

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Lactic Acid ◽

Cardiovascular Response ◽

Control Level ◽

Tissue Level ◽

Chemical Analyses ◽

Lactic Acid Concentration ◽

Determining Factors ◽

Lactic Acid Content

The lactic acid concentration of brain was measured 3 hours after death in dogs which had been subject to hypocapnia, hypoxemia with hypocapnia, and hypoxemia without hypocapnia for 15 minutes. There was no elevation of brain lactic acid above the control level in those dogs subjected to hypocapnia or hypoxemia alone, however, when hypocapnia and hypoxemia were combined there was a significant increase. Cardiovascular and blood chemical analyses support the conclusion that variations in cerebral blood flow, availability of oxygen at the tissue level and interference with oxidative metabolism are important determining factors in brain lactic acid build-up. The results agree with those obtained in altitude-exposed animals, for they likewise show an elevation of brain lactic acid.

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Age-dependent metabolic effects of repeated hypoxemia in piglets

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y99-141 ◽

2000 ◽

Vol 78 (4) ◽

pp. 321-328 ◽

Cited By ~ 4

Author(s):

Aurore Côté ◽

Jill Barter ◽

Brian Meehan

Keyword(s):

Lactic Acid ◽

Body Temperature ◽

Metabolic Rate ◽

Cardiovascular Response ◽

Alveolar Ventilation ◽

Repeated Exposure ◽

Metabolic Effects ◽

Age Dependent ◽

Lactate Levels ◽

Over Time

The aim of this study was to determine whether repeated exposure to hypoxemia would modify the response to hypoxemia during maturation. We exposed piglets to three 1-h cycles of hypoxemia (PaO2 = 30 to 35 mmHg; 1 mmHg = 133.3 Pa) at 1 week (n = 9), 2-3 weeks (n = 10), and 4-5 weeks of age (n = 10). O2 consumption (VO2) and CO2 production (VCO2) were measured, and alveolar ventilation (VA) was derived from VCO2 and PaCO2. Levels of lactic acid (lactate) and serum catecholamines were also measured. With hypoxemia, time had a significant effect on VO2 and body temperature in an age-dependent fashion: that is, whereas the 1 week group and the 4-5 week group showed both variables decreasing over time, the 2-3 week group showed no drop in VO2 and a small increase in body temperature over time. Lactate levels increased with hypoxemia in all animals during the first exposure. However, with repeated exposures to hypoxemia, only the 2-3 week group continued to increase its lactate levels. Furthermore, the changes in lactate levels paralleled the changes in epinephrine levels with hypoxemia. We found, too, that although VA increased significantly with hypoxemia in all animals, this change was not modified by age or repeated exposures. No significant effects of age or repeated exposures were found in the cardiovascular response to hypoxemia. We concluded that, from a metabolic viewpoint, after repeated exposures to hypoxemia the 2-3 week animals responded differently.Key words: metabolic rate, lactic acid, maturation, catecholamines.

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Demonstration of Retinal Glycogen with Silver Methenamine

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100066875 ◽

1971 ◽

Vol 29 ◽

pp. 564-565

Author(s):

A. W. Sedar ◽

G. H. Bresnick

Keyword(s):

Lactic Acid ◽

Chromic Acid ◽

Periodic Acid ◽

Müller Cell ◽

External Limiting Membrane ◽

Electron Microscope Level ◽

Reactive Process ◽

Inner Limiting Membrane ◽

Muller Cell ◽

And Migration

After experimetnal damage to the retina with a variety of procedures Müller cell hypertrophy and migration occurs. According to Kuwabara and others the reactive process in these injuries is evidenced by a marked increase in amount of glycogen in the Müller cells. These cells were considered originally supporting elements with fiber processes extending throughout the retina from inner limiting membrane to external limiting membrane, but are known now to have high lactic acid dehydrogenase activity and the ability to synthesize glycogen. Since the periodic acid-chromic acid-silver methenamine technique was shown to demonstrate glycogen at the electron microscope level, it was selected to react with glycogen in the fine processes of the Müller cell that ramify among the neural elements in various layers of the retina and demarcate these cells cytologically. The Rhesus monkey was chosen as an example of a well vascularized retina and the rabbit as an example of a avascular retina to explore the possibilities of the technique.

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Effects of Physical Training on Stuttering

Journal of Speech and Hearing Research ◽

10.1044/jshr.1104.767 ◽

1968 ◽

Vol 11 (4) ◽

pp. 767-776 ◽

Cited By ~ 2

Author(s):

B. Don Franks ◽

Elizabeth B. Franks

Keyword(s):

College Students ◽

Group Therapy ◽

Physical Training ◽

Cardiovascular Response ◽

Training Group ◽

Physical Stress ◽

Submaximal Exercise ◽

Endurance Running ◽

Response To Exercise

Eight college students enrolled in group therapy for stuttering were divided into two equal groups for 20 weeks. The training group supplemented therapy with endurance running and calisthenics three days per week. The subjects were tested prior to and at the conclusion of the training on a battery of stuttering tests and cardiovascular measures taken at rest, after stuttering, and after submaximal exercise. There were no significant differences (0.05 level) prior to training. At the conclusion of training, the training group was significandy better in cardiovascular response to exercise and stuttering. Although physical training did not significantly aid the reduction of stuttering as measured in this study, training did cause an increased ability to adapt physiologically to physical stress and to the stress of stuttering.

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