Migratory responses of pmn following intraperitoneal and intratracheal administration of lipopolysaccharide. Hirano, Seishiro. Regional Environment Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305, Japan
APStracts 3:0002L, 1996.
The present study was undertaken primarily to investigate accumulation of polymorphonuclear leukocytes (PMN) within the lung vasculature following intraperitoneal (i.p.) injection of lipopolysaccharide (LPS) and migratory responses of those intravascular PMN by intratracheally (i.t.) instilled LPS in mice. I.p. injected LPS was absorbed into the blood rapidly and the concentration of circulating LPS peaked at 1 h post injection. Tumor necrosis factor concentration in blood began to increase at 0.5 h and also peaked at 1 h post injection. The number of lung vascular-associated PMN was increased 7.5 folds at 0.5 h post i.p. injection. However, neither diapedesis of PMN nor injury was observed in the lung, while mixed cell infiltration was observed in the liver. Although i.p. injected LPS caused a significant PMN accumulation within the lung vasculature, pre-i.p. injection of LPS dramatically and dose-dependently abolished both i.t. LPS-inducible PMN infiltration and apparent plasma protein leakage into the alveolar space. On the other hand, pre-i.t. instillation of LPS enhanced rather than reduced i.p. LPS-inducible PMN infiltration into the peritoneal cavity. In rats, a sublethal dose of i.p. injected LPS caused a modest increase in alveolar PMN, and yet reduced i.t. LPS-inducible robust transpulmonary PMN infiltration. Although mechanisms of different migratory responses of the lung vasculature-associated PMN are unknown, the inhibitory effects of i.p. injected LPS on transpulmonary PMN infiltration may be applicable to treatments for septic lung diseases. 

Received 10 April 1995; accepted in final form 14 December 1995.
APS Manuscript Number L111-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96