Volume 2 Supplement 1

ESICM LIVES 2014

Open Access

0919. Effect of catecholamine immediately after blast lung injury caused by laser-induced shock wave in a mouse model

  • H Miyawaki1,
  • D Saitoh2,
  • K Hagisawa3,
  • M Noguchi2,
  • S Satoh4,
  • M Kinoshita5,
  • H Miyazaki2,
  • Y Satoh6 and
  • T Sakamoto1
Intensive Care Medicine Experimental20142(Suppl 1):O27

DOI: 10.1186/2197-425X-2-S1-O27

Published: 26 September 2014

Introduction

The physical damage inflicted by blast waves is called primary blast injury, and lungs are vulnerable to blast waves [1]. Blast lung injuries (BLI) can be extremely critical during the super-acute phase, and hypotension is supposed to be the main cause of death (1) , but its etiology has not been elucidated. Recent studies have demonstrated that hypotension is mediated by the absence of vasoconstriction [2]. However, research investigated the effectiveness of catecholamine for BLI during the super-acute phase was not identified.

Objectives

The present study aimed to establish a small-animal model of severe BLI using laser-induced shock wave (LISW) and to evaluate the effect of catecholamine on the super-acute phase of severe BLI.

Methods

The investigation comprised two parts. Study 1 assessed the validity of the BLI model using LISW as follows. Mice were randomly allocated to groups that received 1.2, 1.3 or 1.4 J/cm2 LISW. Survival rates, systolic blood pressure (sBP), heart rate (HR), and peripheral oxyhemoglobin saturation (SpO2) were monitored for up to 60 min thereafter and lung tissues were histopathologically analyzed. Study 2 evaluated the effects of catecholamines as follows. The mice were randomly assigned to groups that received 1.4 J/cm2 LISW followed by the immediate intraperitoneal administration of dobutamine, noradrenaline or normal saline. A sham group received no LISW or drugs. Survival rates were measured for 48 h. We also measured sBP, HR, and SpO2 before and 5 and 10 min after LISW, and left ventricular ejection fraction (EF) and systemic vascular resistance (SVR) before and 1 min after LISW.

Results

(Study 1) The triad of BLI (hypotension, bradycardia, and hypoxemia) was evident immediately after LISW. The degree of the triad and the survival rates were aggravated with increasing doses of LISW. The histopathological findings were compatible with BLI.

(Study 2) The survival rate was highest in the group that received noradrenaline, with significantly elevated SVR and decreased EF after LISW.

Conclusions

The LISW induced lung injury model seems to be useful as severe BLI in small animals without any large scaled equipment. The main cause of death during the super-acute phase of severe BLI might be hypotension due to the absence of peripheral vasoconstriction. The immediate administration of an α1-adrenergic receptor agonist such as noradrenaline right after exposure to blast waves might be an effective treatment during the super-acute phase of severe BLI.

Declarations

Grant acknowledgment

This work was supported by a grant-in-aid for the Special Research Program from the National Defense Medical College (D.S.).

Authors’ Affiliations

(1)
National Defense Medical College Hospital, Department of Traumatology & Critical Care Medicine
(2)
National Defense Medical College, Division of Traumatology, Research Institute
(3)
National Defense Medical College, Division of Physiology
(4)
National Defense Medical College, Division of Biomedical Information Sciences
(5)
National Defense Medical College, Department of Immunology and Microbiology
(6)
National Defense Medical College, Department of Anesthesiology

References

  1. Guy RJ, et al.: Physiologic responses to primary blast. The Journal of Trauma 1998,45(6):983–987. 10.1097/00005373-199812000-00001PubMedView ArticleGoogle Scholar
  2. Ohnishi M, et al.: Reflex nature of the cardiorespiratory response to primary thoracic blast injury in the anaesthetised rat. Experimental Physiology 2001,86(3):357–364. 10.1113/eph8602145PubMedView ArticleGoogle Scholar

Copyright

© Miyawaki et al; licensee Springer. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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