Why the study?
Does PARS inhibition with INO-1001 attenuate pathophysiological responses in an ovine model of burn and smoke inhalation injury?
Does PARS inhibition with INO-1001 attenuate pathophysiological responses in an ovine model of burn and smoke inhalation injury?
PARS inhibition with INO-1001 attenuates lung and systemic injury in a sheep model of burn and smoke inhalation.
Extends PARS inhibition evidence to ovine burn-smoke injury; leaves open translation to human therapy.
We 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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Shimoda et al. (2003) studied this question.
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