Date of Award
Master of Science
Dr. Edward Hall
Dr. Leonard Beuving
Dr. Cecil Mclntire
Masters Thesis-Open Access
Considerable attention has focused on the role of free radicals in the pathophysiology of hemorrhagic shock. In this study, four pharmacological mechanisms for antagonizing free radical generation or reactions were compared in terms of their efficacy in attenuating post-hemorrhage (post-reinfusion) cardiovascular collapse. These included blocking arachidonic acid oxidation by cyclooxygenase (eg; ibuprofen), inhibiting superoxide radical production by xanthine oxidase (eg; oxypurinol), chelating iron (eg; desferal), and inhibiting lipid peroxidation (eg; U74006F and U78517G, Upjohn Company, Kalamazoo, Michigan).
Cardiovascular function, cerebral blood flow, arterial blood gases, serum glucose, and plasma vitamin E were examined in a hemorrhage/reperfusion model using urethane-anesthetized rats. U74006F and U785l7G attenuated the progressive cardiovascular collapse characteristic of hemorrhagic shock whereas ibuprofen, desferal, and oxypurinol were ineffective. Protection against the progressive decline in cerebral blood flow associated with hemorrhagic shock was observed only in U74006F-treated rats.
Fleckenstein, "Pathophysiology of Hemorrhagic Shock and the Protective Effects of Antioxidants" (1990). Master's Theses. 1044.