Publications

Inhalation of inhaled environmental chemicals has long been recognized as a cause of acute increases in airway responsiveness. Extensive studies of the mechanisms of action of two of these chemicals, ozone and toluene diisocyanate, have been conducted during the past decade. The results of these studies suggest that acute airway inflammation plays an important role in the effect of inhaled chemicals but that the specific aspects of the inflammatory response that lead to the development of airway hyperresponsiveness are different for different stimuli and among different mammalian species. These observations suggest that in vivo airway hyperresponsiveness can arise via several different mechanisms and is thus not likely to reflect a single underlying defect.

1. In the absence of intraluminal inducers, low "basal" levels of cytochrome P-450 and its dependent MFO activities are detected in the rat intestinal mucosa, and may be regulated by endogenous hormones. 2. Rats were nutritionally maintained by either short term (48 hr) intravenous glucose infusion or chronic (8 days) intravenous hyperalimentation, and were treated with various doses of pentagastrin in the infusate. 3. Regardless of the dose (6-90 micrograms/kg/hr) or duration of infusion (2-8 days), pentagastrin had no effect on small intestinal cytochrome P-450, its dependent MFO activity, or the activity of delta-aminolevulinic acid synthetase. 4. The intestinal trophic peptide hormone, gastrin, apparently does not regulate the cytochrome P-450-dependent MFO system of the small intestine.