title: Mediator-dependent secondary injury after unilateral blunt thoracic trauma.
abstract: The pathophysiologic sequence leading to respiratory failure after chest trauma can be an inevitable consequence of the primary injury or a secondary, mediator-driven inflammatory process. To distinguish between these alternatives, a simple cross-transfusion experiment was performed. A captive bolt gun injured the chest of anesthetized pigs that were mechanically ventilated with FiO2 = .21, .50, or .50 plus indomethacin (5 mg/kg intravenous; 15 min before injury). Tube thoracostomy immediately followed. After 30 min, blood from these injured donors was transfused into three matched groups of naive recipients (n = 8, 6, and 4, respectively) for a 33% exchange transfusion. Two control groups received blood from uninjured donors with tube thoracostomies only (FiO2 = .21, n = 7; FiO2 = .50, n = 10). Within 15-30 min after transfusion, in recipients from injured donors versus controls, lung compliance was decreased 20%, stroke volume and cardiac output were decreased 50%, and pulmonary vascular resistance was increased >300% (all p < .05). These changes recovered to baseline within 60-90 min. The stable metabolite of thromboxane A2, thromboxane B2, increased >500% in plasma within 15 min and remained elevated for >120 min. All responses were similar at 21 % or 50% O2, which suggests that hypoxia per se is not a cause of mediator production. All responses were eliminated by indomethacin. By 24 h, histologic changes included atelectasis in 3/3 recipients from injured donors versus 0/3 recipients from uninjured donors. We conclude that 1) blunt chest trauma releases blood borne mediators, including prostanoids; 2) these mediators can cause secondary cardiopulmonary changes in naive recipients similar to those produced by chest trauma; 3) the progression to trauma-induced respiratory failure is multifactorial; 4) early pharmacologic intervention, rather than supportive care alone, may benefit some victims of severe chest trauma.
authors.affiliation: Department of Surgery, University of Tennessee Health Science Center, Memphis 38163, USA. sherry.melton@ccc.uab.edu
authors.forename: S M
authors.initials: SM
authors.lastname: Melton
authors.forename: K A
authors.initials: KA
authors.lastname: Davis
authors.forename: C B
authors.initials: CB
authors.lastname: Moomey
authors.forename: T C
authors.initials: TC
authors.lastname: Fabian
authors.forename: K G
authors.initials: KG
authors.lastname: Proctor
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001803:Blood Transfusion; D002561:Cerebrovascular Disorders / Q000209:etiology; D003288:Contusions / Q000150:complications / Q000503:physiopathology*; D004487:Edema / Q000209:etiology; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D010101:Oxygen Consumption; D011014:Pneumonia / Q000209:etiology; D011651:Pulmonary Artery / Q000502:physiology; D013552:Swine; D013898:Thoracic Injuries / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D013929:Thromboxane B2 / Q000097:blood*; D014655:Vascular Resistance
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D013929:Thromboxane B2; D007213:Indomethacin