Meningism due to intravenous iron dextran.
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Adult↗
Biomedical subjects
R Slade
Publications and source records attributed to R Slade.
Correlation of effects of inhaled versus intratracheally injected males on susceptibility to respiratory infection in mice.
Effects of intratracheally administered air pollutant chemicals on susceptibility of mice to infection by aerosolized bacteria were compared with effects of the same chemical previously studied by the inhalation route. Out of 22 compounds previously studied by inhalation, the same 3 (CdSO4, CuSO4, and ZnSO4) that caused significantly increased mortality because of infection after a 3-h exposure to 1 to 2 mg/m3 showed large (greater than or equal to 40% over sham injected) mortality increases when administered by intratracheal injection at lung concentrations calculated to be equivalent to those achieved during inhalation exposures (0.6 to 1.2 microgram). Dose-effect curves of these compounds were similar by the 2 routes. Five of the compounds caused a moderate (20 to 30%) enhancement in the mean excess mortality at concentrations of 2 to 3 microgram/animal. The remaining compounds, which showed no significant effect by inhalation, also showed no effect when given by intratracheal injection. Thus, similar effects on susceptibility to lung bacterial infection were seen whether chemicals were deposited in te lung by inhalation or by intratracheal injection.
Aerosols↗
A simple method for plasma exchange.
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Exchange Transfusion, Whole Blood↗
Comparison of antioxidant substances in bronchoalveolar lavage cells and fluid from humans, guinea pigs, and rats.
Antioxidants located in the lining layer of the respiratory tract may be important in determining sensitivity of lung tissues to inhaled pollutants. This study addressed species differences in the amounts of ascorbic acid (AH2), glutathione (GSH), uric acid (UA), and alpha-tocopherol (AT) in bronchoalveolar lavage (BAL) fluid and cells of humans, guinea pigs, and rats. Protein and lipid phosphorus (lipid P) were used as normalizing factors. More than 90% of the lavageable AH2, UA, GSH, protein, and lipid P was present in the extracellular fraction of BAL in rats and guinea pigs, while over 95% of the lavageable AT was located in the BAL cells. BAL fluid AH2/protein in rats was 7- to 9-fold higher than in humans and guinea pigs. However, human BAL fluid had 2- to 8-fold higher UA/protein, GSH/protein, and AT/protein ratios than rats and guinea pigs. In BAL cells, rats had higher AH2/protein and AT/protein ratios than guinea pigs and humans, and both rats and guinea pigs had higher GSH and AT/protein ratios than humans. Individual variability among humans in the BAL fluid and cellular antioxidants was generally greater than in the laboratory animals. These data demonstrate that some large species differences exist in BAL fluid and cellular antioxidants which could affect susceptibility to oxidant pollutants.
Adult↗
Antioxidants in bronchoalveolar lavage fluid cells isolated from ozone--exposed normal and ascorbate-deficient guinea pigs.
Previous studies have indicated that systemic deficiency in one of the critical antioxidants, ascorbate, does not significantly exacerbate ozone-induced lung injury and changes in lung antioxidants following longer-term exposure. Because alveolar cells encounter the highest ozone dose upon exposure and lack direct blood supply, systemic ascorbate deficiency may exacerbate ozone response on antioxidants within these cells. Female Hartley guinea pigs (30 days old) were fed either a regular guinea pig chow or chow that lacked ascorbate. The dietary regimen was started 1 week prior to exposure, continued through ozone exposure (0, 0.2, 0.4, or 0.8 ppm, 23 h/day, 1 week), and during 1 week recovery in clean air following exposure. Immediately after 1 week of exposure or recovery, lungs were lavaged and cells were counted in bronchoalveolar lavage fluid (BALF). Protein, ascorbate, uric acid, total glutathione (GSH), and alpha-tocopherol were analyzed in these cells. Ozone caused an increase in total BALF cells and total cellular protein after 0.4 and 0.8 ppm ozone. The increase was more pronounced in ascorbate-deficient guinea pigs. Protein per million cells, however, was not changed by ozone or diet. In ascorbate-sufficient guinea pigs, ascorbate levels were increased only after 0.2 ppm ozone. However, uric acid (at 0.4 and 0.8 ppm ozone) and GSH (at all concentrations of ozone) levels were increased in both dietary groups. Ascorbate deficiency did not affect basal uric acid or GSH levels in BALF cells. There was a small diet-related depletion in cellular alpha-tocopherol. Ozone exposure also decreased alpha-tocopherol regardless of diet. The above changes except for alpha-tocopherol appeared to be reversed after 1 week of recovery in both dietary groups. In summary, ozone is capable of inducing a mechanism that increases antioxidants such as ascorbate, GSH, and uric acid. GSH and uric acid are not affected by ascorbate deficiency, but alpha-tocopherol is depleted. GSH and uric acid may be critical in ozone-induced adaptation during ascorbate deficiency.
Adaptation, Physiological↗
A study of platelet aggregation and adhesion in gout.
Platelet aggregation and adhesion were measured in twelve male patients with gout. Tests were performed with the patients off all treatment for six weeks and after the serum uric had been lowered with allopurinol. Results of aggregation and adhesion tests were normal and not influenced by the uric acid level. The increased cardiovascular disease risk in gout is unlikely to be due to an increased thrombotic tendency.
Adult↗