These experiments were done to learn whether Mycoplasma pulmonis
infections of the respiratory tract of rats can potentiate "
neurogenic inflammation" and whether this potentiation is amplified by factors that exacerbate the
infections. Pathogen-free F344 rats were inoculated intranasally with M. pulmonis or with sterile culture medium and then lived for 4 wk in an
ammonia-free atmosphere or in air containing
ammonia (100 parts per million).
Neurogenic inflammation was evoked by an
intravenous injection of
capsaicin, and 5 min later the magnitude of the response was quantified by measuring the amount of extravasation of two tracers, Monastral blue pigment and
Evans blue dye. We found that vascular permeability in the tracheas of all rats was normal in the absence of
capsaicin. However, a 75-micrograms/kg dose of
capsaicin, which caused almost no extravasation of
Evans blue in the tracheas of pathogen-free controls (17 +/- 3 ng/mg; mean +/- SE), produced extensive extravasation in the infected rats (135 +/- 18 ng/mg; P less than 0.001). Similarly, this dose of
capsaicin produced 30 times as much Monastral blue extravasation in the infected rats (area density = 47 +/- 8% of surface area) as it did in the pathogen-free rats (1.6 +/- 0.5%; P less than 0.001), a difference that resulted from increases in the number of Monastral blue-labeled postcapillary venules and in the amount of labeling per venule. Exposure of the infected rats to
ammonia exacerbated the
infections, further increased the number of Monastral blue-labeled vessels and the amount of labeling per vessel, and made the rats so sensitive to
capsaicin that a normally tolerable dose of 150 micrograms/kg i.v. caused fatal
apnea.
Ammonia did not have these effects in pathogen-free rats. We conclude that M. pulmonis
infections of the airway mucosa cause a potent, long-lasting potentiation of
neurogenic inflammation, which results in part from an increase in the number and responsiveness of mediator-sensitive postcapillary venules. These changes can be amplified by environmental factors such as
ammonia which exacerbate the
infections.