ABSTRACT
I. Introduction 237
II. Lung Water 239
III. Amine Kinetics 239
IV. Components of the Pulmonary Inflammatory Process 240
A. Adhesion Molecule Expression 240
B. White Cell Trafficking 241
C. In Vivo Cell Labeling 242
D. Neutrophil Activation 242
E. Macrophage Kinetics 248
F. Resolution of Inflammation 252
V. Progression of Lung Disease 253
A. Fibroblast Proliferation 253
B. Control of the Extracellular Matrix 253
C. Synthesis of Matrix Proteins 253
D. Extracellular Matrix Degradation 254
VI. Summary 254
References 255
I. Introduction
Gas exchange, the primary function of the lungs, requires close contact over a
very large area, between the nonsterile external environment and the interior
environment of the organism. As a consequence of this interface, the lungs have,
out of necessity, developed extremely rapid and efficient mechanisms to control
the potentially damaging substances to which they are exposed. The air we
breathe is contaminated with infectious material including bacteria, viruses,
and other respirable material, which may be toxic or merely mechanically irritat-
ing. Optimal gas exchange, achieved by minimizing gas to blood distance,
requires that all inhaled particulate matter be cleared efficiently and that inflam-
matory responses to infection are resolved as soon as possible with no scarring.
The gas-exchanging membrane can also become thickened after exposure to cir-
culating drugs or external radiation. The responses to all these stimuli involve an
inflammatory component.
