Mediator-dependent secondary injury after unilateral blunt thoracic trauma

Citation
Sm. Melton et al., Mediator-dependent secondary injury after unilateral blunt thoracic trauma, SHOCK, 11(6), 1999, pp. 396-402
Citations number
33
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
SHOCK
ISSN journal
10732322 → ACNP
Volume
11
Issue
6
Year of publication
1999
Pages
396 - 402
Database
ISI
SICI code
1073-2322(199906)11:6<396:MSIAUB>2.0.ZU;2-J
Abstract
The pathophysiologic sequence leading to respiratory failure after chest tr auma can be an inevitable consequence of the primary injury or a secondary, mediator-driven inflammatory process. To distinguish between these alterna tives, a simple cross-transfusion experiment was performed. A captive bolt gun injured the chest of anesthetized pigs that were mechanically ventilate d with Fio(2) =.21, .50, or .50 plus indomethacin (5 mg/kg intravenous; 15 min before injury). Tube thoracostomy immediately followed. After 30 min, b lood from these injured donors was transfused into three matched groups of naive recipients (n = 8, 6, and 4, respectively) for a 33% exchange transfu sion. Two control groups received blood from uninjured donors with tube tho racostomies only (Fio(2) = .21, n = 7; Fio(2) = .50, n = 10). Within 15-30 min after transfusion, in recipients from injured donors versus controls, l ung compliance was decreased 20%, stroke volume and cardiac output were dec reased 50%, and pulmonary vascular resistance was increased >300% (all p < .05). These changes recovered to baseline within 60-90 min. The stable meta bolite 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% O-2 which suggests that hypoxia per se is not a cause of mediator production. All responses were eliminated by indomethacin. By 24 h, histolo gic changes included atelectasis in 3/3 recipients from injured donors vers us 0/3 recipients from uninjured donors. We conclude that 1) blunt chest tr auma releases blood borne mediators, including prostanoids; 2) these mediat ors can cause secondary cardiopulmonary changes in naive recipients similar to those produced by chest trauma; 3) the progression to trauma-induced re spiratory failure is multifactorial; 4) early pharmacologic intervention, r ather than supportive care alone, may benefit some victims of severe chest trauma.