Neurtrophil degranulation in cadmium-chloride-induced acute lung inflammation.

Lobar intrabronchial instillation of cadmium chloride (200 micrograms/ml) in saline causes a reproducible acute pulmonary inflammation in dogs. The influx of inflammatory neutrophils from the circulation into the alveolar spaces reaches a maximum approximately 16 hours after the cadmium chloride treatment in the treated lobe, while the controlateral lung appears normal. Morphometric quantitation of peroxidase-positive (azurophilic) granules in the inflammatory neutrophils shows a 74% loss of these granules, with little or no loss of the peroxidase-negative (specific) granules.

A model of decreased functional alpha-1-proteinase inhibitor. Pulmonary pathology of dogs exposed to chloramine T.

The objective of this study was to develop an animal model representative of chronic human alpha-1-proteinase inhibitor deficiency. Eight dogs were treated with a mild oxidizing agent, chloramine T, with varying regimens for 3--27 wk. The capacity of the serum to inhibit both trypsin and elastase was examined and found to respond differently.

Emphysema induced in vitro and in vivo in dogs by a purified elastase from homologous leukocytes.

The protease hypothesis of emphysema development evolved from systems using intratracheal instillation or aerosols of heterologous enzymes, such as papain or porcine pancreatic elastase, which bear no relation to the animal species treated. Although these enzymes did produce experimental emphysema, their exogenous origin and superphysiological dosages limit their use in definitive model systems. The observation that dog leukocyte homogenates could induce canine emphysema led us to purify the causative agent from canine neutrophils.