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Biomedical subjects

D E Gardner

Publications and source records attributed to D E Gardner.

At least 19 recordsLinked to original sources
PubMed1979

Nasopharyngeal removal of ozone in rabbits and guinea pigs.

In estimating pollutant concentrations responsible for observed pulmonary effects, nasopharyngeal removal of the pollutant plays an important role. The nasopharyngeal removal of ozone (O3) in anesthetized male guinea pigs and male and female rabbits was determined by drawing O3 through the isolated upper airways at a constant flow rate which approximated the animal's respiratory minute volume. The tracheal O3 concentration in rabbits and guinea pigs was markedly similar and was linearly related to the chamber concentration of O3 over a range of 196--3920 micrograms/m3 (0.1--2.0 ppm O3). Regression analyses showed that O3 removal in the nasopharyngeal region is approximately 50% in both species. Both rabbit sexes responded similarly over the concentration range studied. Exposures of guinea pigs to O3 concentrations between 3920 and 5880 micrograms/m3 (2.0 and 3.0 ppm) showed that, at these higher concentrations, relatively more O3 is removed by the upper airways.

Animals↗
PubMed1979

Effects of repeated exposures to peak concentrations of nitrogen dioxide and ozone on resistance to streptococcal pneumonia.

Exposures to various mixtures of nitrogen dioxide (NO2) and ozone (O3) reduced the resistance of mice to streptococcal pneumonia as evidenced by increased mortality rates and shortened survival time. Daily 3-h exposures (5 d/wk) for 2--6 mo to an air pollutant mixture consisting of 940 microgram/m3 (0.5 ppm) NO2 and 196 microgram/m3 (0.1 ppm) O3 were most effective in reducing the resistance to infection. The decrease in resistance to the infection occurred sooner than the mice continued to be exposed to the air pollutants instead of clean air for 14 d after the respiratory challenge with Streptococcus pyogenes aerosol. After 3 mo of exposure to the pollutant mixture, there was some decrease in the ability of mice to clear inhalated streptococci from their lungs. At the same time the total cell count in the fluid lavaged from the lungs of mice was markedly reduced, as were the viability and phagocytic activity of the alveolar macrophages. Exposure to the pollutants combined with challenge with Streptococcus aerosol resulted in marked morphological changes in lung tissues as seen by scanning electron microscopy.

Animals↗
PubMed1979

Influence of exposure mode on the toxicity of NO2.

Pollutant gases are subject to a variety of physical and chemical interactions within the atmosphere due to cyclic production and various meteorological influences. In consequence there is generally a diurnal concentration profile for NO2 which consists of peaks of short duration and irregular occurrence superimposed on a low background. Since this variation could play an important role in the toxic effect of NO2, the influences of various exposure modes was studied. Continuous and intermittent exposure studies were used to determine the relationship between biological response and length of exposure to various concentrations of NO2. As the concentration decreased, the slope of the regression line decreased. After adjusting for total differences in the product concentration x time, the response for the two exposure modes was essentially the same. When a constant concentration x time level was employed, a short-term exposure to a high concentration produced a greater effect than exposure to a lower concentration administered over a longer period. Using these curves, the relationship between level of effect, concentration, and time can be determined. Results of these studies indicated that the frequency and amplitude of short-term peaks are of significance even though the exposure is interrupted with periods of zero concentration of NO2.

Animals↗
PubMed1978

Chemiluminescence of phagocytic cells caused by N-formylmethionyl peptides.

N-formylmethionyl (F-Met) peptides, when added alone to macrophages or polymorphonuclear leukocytes (PMN), were found to induce a chemiluminescent response of shorter duration than that produced by the commonly employed particulate stimulant, zymosan. The cellular nature of F-Met peptide-induced chemiluminescence was indicated by its dependence on cell concentration, and by its inhibition by cell disruption, heat inactivation, or previous maximal stimulation by the peptides. Comparison of PMN and macrophages from different species showed that the maximal chemiluminescent response seen in the dose-response curve of F-Met- Phe was different in different cell types. Chemiluminescence reached highest values in human PMN, it was intermediate in guinea pig macrophages and PMN, and in rabbit PMN; but it was nonexistent in rabbit alveolar macrophages and very low in rabbit peritoneal macrophages. A definite relationship was observed between peptide structure and chemiluminescent activity. Met-Phe, F- Met and Phe were inactive even at millimolar concentrations, while F-Met-Phe caused chemiluminescence at micromolar concentrations. Four active peptides were tested in guinea pig, rabbit, and human PMN, and in guinea pig alveolar and peritoneal macrophages. The relative activity of these peptides was the same in all cells studied, e.g. F-Met-Leu-Phe >> F-Met-Phe > F-Met-Val > F- Met-Ala. The values of ED50 for each peptide were also comparable to previously reported ED50 values of these peptides in inducing lysosomal enzyme release. These results were seen both in the presence and absence ofthe chemiluminescent oxidant indicator, luminol. Low concentrations of superoxide dismutase (10 mug/ml) completely inhibited chemiluminescence caused by the F-Met peptides, suggesting the involvement of 0(2)(-) or O(2)(-)-derived compounds in this response. Sodium azide, an inhibitor of peroxidase reactions, had either no effect or a slight inhibitory effect on chemiluminescence. However, when the extracellular release of lysosomal enzymes was induced by cytochalasin B, an azide- inhibitable enhancement of chemiluminescence was seen in PMN, but not in macrophages. This effect appears to be correlated with the presence of granule-associated myeloperoxidase. Although azide-inhibitable peroxidases could be a potential source of light, they did not appear to be a significant contributor in these experiments. Based on these results and on those of previous investigators, we postulate that the F-Met-peptides stimulate 0(2)(-) production in addition to stimulating lysosomal enzyme release and chemotaxis. The similar structure- activity relationship which appears to exist for these processes may indicate that they are all initiated by a single receptor mechanism. Since F-Met peptides are formed in bacteria it is likely that their actions represent an important physiologic response.

Animals↗
PubMed1978

Cytotoxic effects of nickel on ciliated epithelium.

Studies were conducted to measure the effect of graded concentrations of nickel on ciliary activity in an in vitro model system using isolated hamster tracheal rings, and to compare the in vitro findings with in vivo exposures using an organ culture system. Dose-response experiments were conducted for various Ni concentrations and for various lengths of exposure. In the in vitro model, significant decreases in ciliary activity occurred at concentrations as low as 0.011 mM nickel (0.65 microgram of nickel per ml). A dose-response relationship between the concentration of nickel and ciliary action was demonstrated. A range of effects from a significant decrease of 26 beats per min (0.65 microgram of nickel per ml) to complete ciliostasis (65 microgram of nickel per ml)) was observed after 24 hours of exposure. Validation of the in vitro results occurred when hamsters were exposed to a nickel chloride aerosol at concentrations of 100 to 275 microgram of nickel per m3. Immediately after the cessation of a 2-hour in vivo exposure, a decrease in ciliary activity of 60 and 140 beats per min was observed for animals exposed to 100 and 275 microgram of nickel per m3, respectively. The length of time required for recovery from the in vivo exposure to nickel aerosol was determined. Histologic examination of the epithelial cells also showed dose-related effects. It is apparent that nickel, either administered to the whole animal or to the tracheal epithelium directly, can significantly decrease the ciliary beating frequency and interfere with the normal functioning of respiratory defense mechanisms, thereby increasing the risk of the host to respiratory infections.

Aerosols↗