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Pulmonary blast injury in mice: A novel model for studying blast injury in the laboratory using laser‐induced stress waves
Author(s) -
Satoh Yasushi,
Sato Shunichi,
Saitoh Daizoh,
Tokuno Shinichi,
Hatano Ben,
Shimokawaji Tadasuke,
Kobayashi Hideo,
Takishima Kunio
Publication year - 2010
Publication title -
lasers in surgery and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 112
eISSN - 1096-9101
pISSN - 0196-8092
DOI - 10.1002/lsm.20899
Subject(s) - blast injury , medicine , percutaneous , blast wave , heart rate , oxygen saturation , shock (circulatory) , lung , blood pressure , shock wave , surgery , poison control , oxygen , chemistry , environmental health , organic chemistry , engineering , aerospace engineering
Background and Objectives Primary blast injury is produced by shock waves. Blast injuries to lungs are extremely critical threats to survival, but their etiology is largely undefined. The majority of animal models for these injuries use explosive or complex experimental settings, limiting the laboratory study of blast injury. The aim of this study was to establish a small‐animal model for blast injuries, using laser‐induced stress waves (LISWs) with high controllability, high reproducibility, and easy experimental settings. Study Design/Materials and Methods LISWs were used to produce isolated pulmonary blast effects in mice. An LISW was generated by the irradiation of an elastic laser target with 532‐nm nanosecond laser pulses of a Q‐switched Nd:YAG laser. Histopathological evaluations of damage to lung tissue were conducted to estimate the relevance between peak pressure and trauma intensity. Blood pressure, heart rate, and percutaneous oxygen saturation were monitored for 60 minutes. Results We could flexibly control the peak pressure of the shock wave by varying the laser energy. Non‐lethal doses of LISWs caused pulmonary contusions with alveolar hemorrhages depending on peak pressure. Pulmonary contusion was observed only in areas that were exposed to LISWs, allowing study of isolated injuries without concomitant ones. These injuries caused decreased blood pressure, heart rate, and percutaneous oxygen saturation, immediately after LISW exposure. Conclusion Mice exposed to thoracic LISWs showed pathologic and physiologic changes similar to those seen in other studies in this area, and in clinical practice. Our newly developed model allows fine management of trauma intensity, and concomitant injuries of the exposed animals were limited. This novel mouse model of blast injury using LISWs is suitable for detailed studies of blast lung contusion and other blast injuries in the laboratory. Lasers Surg. Med. 42:313–318, 2010. © 2010 Wiley‐Liss, Inc.