Uncoupling mitochondrial activity maintains body VO2 during hemorrhage-induced O2 deficit in the anesthetized rat

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Abstract

During a hemorrhagic shock (HS), O2 uptake (VO2) decreases as soon as the rate of O2 delivery (DO2) drops below a " critical level" , a response accounted for by the reduction in mitochondrial O2 supply. In urethane-anesthetized rats, DO2 was decreased within 20min from 21.5 to 2.8mlmin-1 by slowly withdrawing 18mlkg-1 of blood. This led to a reduction in VO2 from 6.1 to 2.4mlmin-1 (n=5, p<0.01). Decoupling mitochondrial oxidative activity by injecting 2,4-DNP (6mgkg-1, iv) before HS elevated VO2 to 11.9±1.2mlmin-1 (n=6, p<0.01), which remained above control HS values throughout most of the hemorrhage. This was associated with higher levels of O2 extraction, cardiac output and ventilation than in control HS. DO2-VO2 relationship was shifted upward and to the left following DNP. In conclusion, cellular and systemic mechanisms, decreasing O2 demand, account for a large part of HS induced VO2 decline resulting in an additional reduction in DO2.

Original languageEnglish (US)
Pages (from-to)87-94
Number of pages8
JournalRespiratory Physiology and Neurobiology
Volume186
Issue number1
DOIs
StatePublished - Mar 1 2013

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Hemorrhagic Shock
Hemorrhage
2,4-Dinitrophenol
Urethane
Cardiac Output
Ventilation

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Physiology
  • Pulmonary and Respiratory Medicine

Cite this

@article{305c341317164cde880bc02f43623497,
title = "Uncoupling mitochondrial activity maintains body VO2 during hemorrhage-induced O2 deficit in the anesthetized rat",
abstract = "During a hemorrhagic shock (HS), O2 uptake (VO2) decreases as soon as the rate of O2 delivery (DO2) drops below a {"} critical level{"} , a response accounted for by the reduction in mitochondrial O2 supply. In urethane-anesthetized rats, DO2 was decreased within 20min from 21.5 to 2.8mlmin-1 by slowly withdrawing 18mlkg-1 of blood. This led to a reduction in VO2 from 6.1 to 2.4mlmin-1 (n=5, p<0.01). Decoupling mitochondrial oxidative activity by injecting 2,4-DNP (6mgkg-1, iv) before HS elevated VO2 to 11.9±1.2mlmin-1 (n=6, p<0.01), which remained above control HS values throughout most of the hemorrhage. This was associated with higher levels of O2 extraction, cardiac output and ventilation than in control HS. DO2-VO2 relationship was shifted upward and to the left following DNP. In conclusion, cellular and systemic mechanisms, decreasing O2 demand, account for a large part of HS induced VO2 decline resulting in an additional reduction in DO2.",
author = "Philippe Haouzi and {Van de Louw}, Andry",
year = "2013",
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language = "English (US)",
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pages = "87--94",
journal = "Respiratory Physiology and Neurobiology",
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T1 - Uncoupling mitochondrial activity maintains body VO2 during hemorrhage-induced O2 deficit in the anesthetized rat

AU - Haouzi, Philippe

AU - Van de Louw, Andry

PY - 2013/3/1

Y1 - 2013/3/1

N2 - During a hemorrhagic shock (HS), O2 uptake (VO2) decreases as soon as the rate of O2 delivery (DO2) drops below a " critical level" , a response accounted for by the reduction in mitochondrial O2 supply. In urethane-anesthetized rats, DO2 was decreased within 20min from 21.5 to 2.8mlmin-1 by slowly withdrawing 18mlkg-1 of blood. This led to a reduction in VO2 from 6.1 to 2.4mlmin-1 (n=5, p<0.01). Decoupling mitochondrial oxidative activity by injecting 2,4-DNP (6mgkg-1, iv) before HS elevated VO2 to 11.9±1.2mlmin-1 (n=6, p<0.01), which remained above control HS values throughout most of the hemorrhage. This was associated with higher levels of O2 extraction, cardiac output and ventilation than in control HS. DO2-VO2 relationship was shifted upward and to the left following DNP. In conclusion, cellular and systemic mechanisms, decreasing O2 demand, account for a large part of HS induced VO2 decline resulting in an additional reduction in DO2.

AB - During a hemorrhagic shock (HS), O2 uptake (VO2) decreases as soon as the rate of O2 delivery (DO2) drops below a " critical level" , a response accounted for by the reduction in mitochondrial O2 supply. In urethane-anesthetized rats, DO2 was decreased within 20min from 21.5 to 2.8mlmin-1 by slowly withdrawing 18mlkg-1 of blood. This led to a reduction in VO2 from 6.1 to 2.4mlmin-1 (n=5, p<0.01). Decoupling mitochondrial oxidative activity by injecting 2,4-DNP (6mgkg-1, iv) before HS elevated VO2 to 11.9±1.2mlmin-1 (n=6, p<0.01), which remained above control HS values throughout most of the hemorrhage. This was associated with higher levels of O2 extraction, cardiac output and ventilation than in control HS. DO2-VO2 relationship was shifted upward and to the left following DNP. In conclusion, cellular and systemic mechanisms, decreasing O2 demand, account for a large part of HS induced VO2 decline resulting in an additional reduction in DO2.

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