• Katsumi Shimoda, Kazunori Murakami, Perenlei Enkhbaatar, Lillian D Traber, Robert A Cox, Hal K Hawkins, Frank C Schmalstieg, Katalin Komjati, Jon G Mabley, Csaba Szabo, Andrew L Salzman, and Daniel L Traber.
• Department of Anesthesiology, The University of Texas Medical Branch, Shriners Burns Hospital, Galveston, Texas 77555-0833, USA.
• Am. J. Physiol. Lung Cell Mol. Physiol. 2003 Jul 1;285(1):L240-9.

AbstractWe investigated the role of the nuclear enzyme poly (ADP ribose) synthetase (PARS) in the pathogenesis of combined burn and smoke inhalation (burn/smoke) injury in an ovine model. Eighteen sheep were operatively prepared for chronic study. PARS inhibition was achieved by treatment with a novel and selective PARS inhibitor INO-1001. The PARS inhibitor attenuated 1) lung edema formation, 2) deterioration of gas exchange, 3) changes in airway blood flow, 4) changes in airway pressure, 5) lung histological injury, and 6) systemic vascular leakage. Lipid oxidation and plasma nitrite/nitrate (stable breakdown products of nitric oxide) levels were suppressed with the use of INO-1001. We conclude that PARS inhibition attenuates various aspects of the pathophysiological response in a clinically relevant experimental model of burn/smoke inhalation injury.

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