2001 Fiscal Year Final Research Report Summary

MILD HYPOTHERMIA ATTENUATES RAT ACID-INDUCED ACUTE LUNG INJURY MODEL

Research Project

Project/Area Number	12671481
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Anesthesiology/Resuscitation studies
Research Institution	OITA MEDICAL UNIVERSITY
Principal Investigator	NOGUCHI Takayuki OITA MEDICAL UNIVERSITY, DEPT. OF ANESTHESIOLOGY, PROFESSOR, 医学部, 教授 (90156183)
Co-Investigator(Kenkyū-buntansha)	MORI Masakazu OITA MEDICAL UNIVERSITY, LECTURER, 医学部, 講師 (20220022) KIRA Shinitiro OITA MEDICAL UNIVERSITY, STUDENT IN DOCTOR COURSE
Project Period (FY)	2000 – 2001
Keywords	lung injury / mild hypothermia / ntercellular / adhesion molecule-1 / acute respiratory distress syndrome
Research Abstract	The pathophysiology of the acute phase of acid-induced lung injury has been elucidated. However, once acute respiratory distress syndrome (ARDS) develops, the mortality rate remains high and there is, as yet, no effective therapy. There are reports that application of mild hypothermia is an effective treatment for ARDS, but, at the tissue and the molecular level, there is no clear understanding of the factors that to the positive outcome of such treatment. We studied the effects of mild hypothermia on the expression of intercellular adhesion molecule-1 (ICAM-1) and the accumulation of neutrophils after acid-induced lung injury in the rat. Oxygenation in acid-instilled rats was significantly impaired as compared to that in non-instilled groups, but induction of mild hypothermia gradually improved oxygenation. Expression of ICAM-1 was enhanced in the acid-instilled normothermic group. By contrast, no overexpression of ICAM-1 and its transcript was detected in the acid-instilled hypothermic group. In addition, accumulation of neutrophils was markedly inhibited after exposure to mild hypothermia irrespective of the instillation of acid. Our data suggest that mild hypothermia can inhibit the adhesion, activation, and accumulation of neutrophils in the acute phase of acid-induced lung injury and suggest an approach that might potentially reduce ongoing damage in patients with ARDS.