Mitochondrial function in lungs of rats with different susceptibilities to hyperoxia-induced acute lung injury

Author:

Taheri Pardis1,Dave Devanshi D.1,Dash Ranjan K.12ORCID,Sharma Guru P.3,Clough Anne V.145,Jacobs Elizabeth R.46ORCID,Audi Said H.146ORCID

Affiliation:

1. Department of Biomedical Engineering, Medical College of Wisconsin, Marquette University, Milwaukee, Wisconsin, United States

2. Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States

3. Department of Radiation Oncology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States

4. Research Service, Clement J. Zablocki V.A. Medical Center, Milwaukee, Wisconsin, United States

5. Department of Mathematical and Statistical Sciences, Marquette University, Milwaukee, Wisconsin, United States

6. Division of Pulmonary and Critical Care Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin, United States

Abstract

We assessed lung tissue mitochondrial bioenergetics in rats with tolerance (H-T) or susceptibility (H-S) to hyperoxia-induced ARDS. Results from studies in isolated mitochondria, tissue homogenate, and isolated perfused lungs show that mitochondrial bioenergetics are differentially altered in H-T and H-S lungs suggesting a potential role for mitochondrial bioenergetics in hyperoxia-induced ARDS. Results are clinically relevant since hyperoxia exposure is a primary therapy for patients with ARDS, and differential sensitivity to hyperoxia surely occurs in humans.

Funder

HHS | NIH | NHLBI | Division of Intramural Research

National Science Foundation

U.S. Department of Veterans Affairs

Publisher

American Physiological Society

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