[Frontiers in Bioscience 14, 4618-4630, January 1, 2009]

[Frontiers in Bioscience 14, 4618-4630, January 1, 2009]

Animal models of smoke inhalation induced injuries Poon David1, Denny Dunsford1, Jia Lu1, Shabbir Moochhala¹

¹Combat Care Laboratory, Combat Care and Performance Programme, Defence Medical and Environmental Research Institute, DSO National Laboratories (Kent Ridge), 27 Medical Drive #09-01, Singapore 117510

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Pathophysiology of Smoke Inhalation: 3.1. Pulmonary edema; 3.2. Blood Flow; 3.3. Lung lymph flow; 3.4. Airway obstruction; 3.5. Metabolic changes; 3.6. Oxidative stress; 3.7. Mucin; 3.8. Cytokines
4. Clinical characteristics of smoke inhalation
5. Animal models used to study smoke inhalation induced injuries
6. Current therapy for smoke inhalation
7. Potential therapeutics: 7.1. Surfactants; 7.2. Leukotriene antagonist; 7.3. Antioxidants; 7.4. Anti-inflammatory drugs; 7.5. Anti-epileptic drug; 7.6. Inducible nitric oxide synthase inhibitor; 7.7. Nitric oxide; 7.8. Poly(adp-ribose) polymerase inhibitor; 7.9. Reducing cast formation; 7.10. Mechanical ventilation; 7.11. Bronchial circulation; 7.12. Endothelin-1 receptor blockade; 7.13. Protease inhibitor; 7.14. Antibiotics; 7.15. Thromboxane a2 synthase inhibitor; 7.16. Activated protein c
8. Summary and perspective

1. ABSTRACT

Smoke inhalation injury is the leading cause of mortality from structural fires, as a result of complications such as systemic inflammatory response syndrome and chronic obstructive pulmonary disease, which can be caused by a localized or systemic response. In this review, the pathophysiology of smoke inhalation injury, along with the characteristics found in clinical settings, common animal models, current treatment methods and future potential therapeutics are discussed.