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D Sheppard

Publications and source records attributed to D Sheppard.

151 records · Page 9Linked to original sources
PubMed1981

Exercise increases sulfur dioxide-induced bronchoconstriction in asthmatic subjects.

We undertook a study to determine whether moderate exercise modifies the bronchoconstriction produced by sulfur dioxide (SO2) in subjects with mild asthma. In 7 subjects, we compared the changes in specific airway resistance (SRaw) produced by 10 min of exercise alone (400 kpm/min on a cycle ergometer), inhalation of SO2 alone, and the combination of exercise and SO2. During all studies, a subject breathed SO2 and/or air from a mouthpiece. In 6 additional subjects, we compared the increase in SRaw produced by inhalation of SO2 during exercise with that produced by eucapnic hyperventilation with SO2. Neither inhalation of 0.05 ppm of SO2 at rest nor exercise or hyperventilation alone had any effect on SRaw. Inhalation of SO2 during exercise, however, significantly increased SRaw (from 8.46 +/- 3.58 L x cm H2O/L/s (mean +/- SD) to 18.16 +/- 10.05 at 0.05 ppm and from 8.07 +/- 2.69 to 10.48 +/- 4.49 at 0.25 ppm (p less than 0.05)). In the 2 most responsive subjects, inhalation of 0.10 ppm of SO2 during exercise also significantly increased SRaw. The SRaw increased by the same amount whether SO2 was inhaled during exercise or during eucapnic hyperventilation at the same minute ventilation, but the time course of the increase in SRaw was different. The SRaw was at or near maximal values at the first measurement (30 s) after hyperventilation but not until 2 to 4 min after exercise. When 4 subjects took larger breaths after inhaling SO2 during eucapnic hyperventilation to more closely match the volume of the breaths taken after exercise, the time courses of SO2-induced bronchoconstriction after hyperventilation and after exercise were nearly identical. These results suggested that exercise increases the bronchoconstriction produced by a given concentration of SO2 in subjects with asthma by increasing the minute volume of ventilation and that the delay in bronchoconstriction after exercise is due to the large tidal volumes that persist for some minutes during recovery.

Adult↗
PubMed1981

Inhibition of sulfur dioxide-induced bronchoconstriction by disodium cromoglycate in asthmatic subjects.

To determine whether disodium cromoglycate (cromolyn) inhibits the bronchoconstriction produced by inhalation of sulfur dioxide (SO2) in people with asthma, we undertook a study of 6 asthmatic subjects. Each subject inhaled 40 mg of cromolyn on one day and lactose placebo on another day 20 min before inhaling SO2 for 10 min while exercising at a moderate rate (400 kpm/min) on a bicycle ergometer. Sulfur dioxide was delivered in humidified air at ambient temperature in concentrations of 0.5 ppm (3 subjects) or 1.0 ppm (3 subjects). Cromolyn and lactose treatments were given to each subject in a randomized sequence and in a double-blind manner. On a third day, each subject exercised at the same work rate breathing humidified air without SO2 at ambient temperature. We measured specific airway resistance (SRaw) in a body plethysmograph every 30 s for 10 min before and after each of the 3 periods of exercise. After treatment with lactose, SO2 inhalation significantly increased SRaw in all 6 subjects (from a baseline of 6.5 +/- 0.9 to 19.0 +/- 4.8 L x cm H2O/L/s (mean +/- SE) after SO2). After treatment with cromolyn, SO2 inhalation caused no increase in SRaw in 4 subjects and a small rise in 2 subjects. The mean increase in SRaw (from a baseline of 7.3 +/- 0.9 to 10.0 +/- 1.5 L x cm H2O/L/s after SO2) was significantly smaller than after lactose treatment (p less than 0.025). Exercise alone had no effect on SRaw in any subject. Thus, cromolyn inhibits SO2-induced bronchoconstriction in subjects with asthma. This finding suggests either that SO2 induces bronchoconstriction by stimulating the release of mediators from mast cells or that cromolyn inhibits bronchoconstriction by a mechanism independent of its effect on mast cells.

Adult↗
PubMed1980

Lower threshold and greater bronchomotor responsiveness of asthmatic subjects to sulfur dioxide.

To determine whether subjects with mild asthma or seasonal rhinitis have greater bronchomotor responses to sulfur dioxide (SO2) than normal subjects, we undertook a study in 7 asthmatic, 7 atopic, and 7 normal subjects, 23 to 37 yr of age. We measured the change in specific airways resistance (SRaw) provoked by 10 min of breathing 1, 3, and 5 ppm of SO2 delivered by mouthpiece on separate days at least 48 h apart. To assess the significance of parasympathetic pathways in the bronchomotor responses to SO2, we also measured the change in SRaw provoked by 5 ppm of SO2 in 17 of the subjects after they inhaled atropine sulfate aerosol (0.1 mg/kg). We found that in the asthmatic subjects, SRaw increased only at 5 ppm. In the asthmatic group, SRaw increased more than in either of the other groups at 5 ppm (p < 0.005), and was sometimes associated with marked dyspnea requiring bronchodilator therapy. The increases in SRaw produced by inhalation of SO2 were prevented by treatment with atropine in asthmatic and nonasthmatic subjects, which suggested the involvement of parasympathetic pathways. These results indicated that subjects with mild asthma develop bronchoconstriction after exposure to concentrations of SO2 well below currently accepted standards for occupational exposure, and that SO2-induced bronchoconstriction is mediated by parasympathetic pathways.

Adult↗
PubMedDate not supplied

Characterization of integrin beta6 and thrombospondin-1 double-null mice.

To identify overlapping and non-overlapping functions for TSP-1 and alphavbeta6, we crossed TSP-1-null and beta6-null mice and compared the phenotype of the double-null mice with those of wild-type and single-null mice. The double-null mice exhibited focal acute and organizing pneumonia that was more severe than the wild-type and single-null mice as well as a significantly higher incidence of inflammation in tissues other than the lung. The TSP-1-null and beta6-null mice exhibited a five to eight-fold increase in granulocyte recruitment to the lung three days after exposure to lipopolysaccharide. They also had abnormalities that were infrequently observed in the wild-type and single-null mice, including heart degeneration (8.35% in wild-type and 28.1% in double-null mice), hyperplasia of the glandular of the stomach (2.8% in wild-type and 21.1% in double-null mice) and endometrial hyperplasia (0% in wild-type and 38.5% in double-null females). Furthermore, the beta6-null and double-null mice displayed a significant elevation in benign and malignant cancers. Stomach papillomas, squamous cell carcinomas of the ear and stomach, and adenocarcinomas of the lungs, vagina/cervix and colon were observed with the highest frequency. These data demonstrate that TSP-1 and alphavbeta6 are involved in regulation of the immune system and epithelial homeostasis. They also indicate that alphavbeta6 functions as a tumor suppressor gene and that activation of TGFbeta by TSP-1 and alphavbeta6 contributes to normal tissue architecture and function.

Alopecia↗