• Philippe Haouzi and Andry Van de Louw.
• Pennsylvania State University, College of Medicine, Division of Pulmonary and Critical Care Medicine, Penn State Hershey Medical Center, Hershey, PA, United States. phaouzi@hmc.psu.edu
• Respir Physiol Neurobiol. 2013 Mar 1;186(1):87-94.

AbstractDuring a hemorrhagic shock (HS), O2 uptake ( [Formula: see text] ) decreases as soon as the rate of O2 delivery ( [Formula: see text] ) drops below a "critical level", a response accounted for by the reduction in mitochondrial O2supply. In urethane-anesthetized rats, [Formula: see text] was decreased within 20min from 21.5 to 2.8mlmin(-1) by slowly withdrawing 18mlkg(-1) of blood. This led to a reduction in [Formula: see text] 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 [Formula: see text] 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. [Formula: see text] relationship was shifted upward and to the left following DNP. In conclusion, cellular and systemic mechanisms, decreasing O2demand, account for a large part of HS induced [Formula: see text] decline resulting in an additional reduction in [Formula: see text] .Copyright © 2013 Elsevier B.V. All rights reserved.

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