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Microcalorimetric measurement of reversible metabolic suppression induced by anoxia in isolated hepatocytes.
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Microcalorimetric measurement of reversible metabolic suppression induced by anoxia in isolated hepatocytes.

Author: LT Buck; PW Hochachka; A Schön; E Gnaiger
Edition/Format: Article Article : English
Publication:The American journal of physiology, 1993 Nov; 265(5) Pt 2: R1014-9
Database:From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Summary:
The metabolic suppression due to anoxia in hepatocytes from the anoxia-tolerant turtle Chrysemys picta bellii was measured directly using microcalorimetric techniques. The normoxic heat flux from hepatocytes in suspension (25 degrees C) was 1.08 +/- 0.08 mW/g cells and decreased by 76% to 0.26 +/- 0.03 mW/g cells in response to anoxic incubation. After an acute decrease in temperature (to 10 degrees C) anoxic heat  Read more...
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Details

Document Type: Article
All Authors / Contributors: LT Buck; PW Hochachka; A Schön; E Gnaiger
ISSN:0002-9513
OCLC Number: 121635694
Language Note: English
Awards:

Abstract:

The metabolic suppression due to anoxia in hepatocytes from the anoxia-tolerant turtle Chrysemys picta bellii was measured directly using microcalorimetric techniques. The normoxic heat flux from hepatocytes in suspension (25 degrees C) was 1.08 +/- 0.08 mW/g cells and decreased by 76% to 0.26 +/- 0.03 mW/g cells in response to anoxic incubation. After an acute decrease in temperature (to 10 degrees C) anoxic heat flux dropped by 96% relative to the normoxic control at 25 degrees C. The relative decrease in heat flux at both temperatures was similar, 76% at 25 degrees C and 68% at 10 degrees C. From the caloric equivalent of glycogen fermentation to lactate the heat flux from lactate production was calculated to be -93 microW/g cells (25 degrees C), and this accounted for 36% of the anoxic heat flux. When the enthalpy change associated with the release of free glucose (from glycogen breakdown) is considered, an additional 6% of the anoxic heat flux can be accounted for. Therefore, a portion of the anoxic heat flux is unaccounted for (58%), resulting in an "exothermic gap." This differs from the normoxically incubated hepatocytes where the indirect calorimetric measurement of heat flux (hepatocyte O2 consumption) could fully account for the calorimetrically measured heat flux. When normoxic hepatocytes were inhibited with cyanide, a rapid suppression in heat flux was observed. Because rapid reequilibration to a lower, cyanide-induced steady state occurred in < 15 min, it is also assumed that there is no short-term Pasteur effect in this tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

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