Search PubMed⌕ Search

Biomedical subjects

J R Sheller

Publications and source records attributed to J R Sheller.

60 records · Page 4Linked to original sources
PubMed1982

Barbiturates depress vagal motor pathway to ferret trachea at ganglia.

To determine which site in the vagal motor pathway to airway smooth muscle is most sensitive to depression by barbiturates, we recorded isometric muscle tension in vitro and stimulated the vagal motor pathway at four different sites before and after exposure to barbiturates. In isolated tracheal rings from ferrets, we stimulated muscarinic receptors in the neuromuscular junction by exogenous acetylcholine, postganglionic nerve fibers by electrical fluid stimulation, and the postsynaptic membrane in ganglia by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP). We also developed a tracheal nerve-muscle preparation to stimulate preganglionic fibers in the vagus nerve electrically. Activation of ganglia by DMPP or by vagus nerve stimulation was depressed by barbiturates at 10-fold lower concentrations than those depressing the activation of postganglionic nerves or the neuromuscular junction. These findings suggest that the postsynaptic membrane in parasympathetic ganglia is the site in the vagal motor pathway most sensitive to depression by barbiturates.

Animals↗
PubMed1982

Bronchomotor responses of isolated sheep airways to electrical field stimulation.

To determine the functional innervation of sheep airway smooth muscle, we measured the isometric tension developed by sheep tracheal segments, bronchial rings, and lung parenchymal strips in response to electrical field stimulation (ES) in tissue chambers. The contractions caused by ES were abolished in trachea and bronchi by atropine 10(-6) M or tetrodotoxin 1.6 X 10(-6) M. The small contractions evoked in lung parenchymal strips were not affected by tetrodotoxin. Electrical stimulation in the presence of atropine 10(-6) M and phentolamine 10(-6) M caused a frequency-dependent reduction in serotonin-induced tension in tracheal segments and bronchial rings. Electrical stimulation had little or no effect on the tension evoked in lung parenchymal strips by acetylcholine 10(-5) M or to histamine 10(-6) M. Propranolol 10(-6) M or guanethidine 10(-5) M caused a shift to the right in the frequency-response curve of trachea and bronchi. These findings suggest the presence of cholinergic excitatory and adrenergic inhibitory innervation in larger sheep airways. A concomitant nonadrenergic inhibitory system may be present. The terminal bronchioles present in lung parenchymal strips do not appear to have an effective bronchomotor innervation.

Animals↗
PubMed1981

Threshold concentration of ozone causing an increase in bronchial reactivity in humans and adaptation with repeated exposures.

To determine the lowest concentration of ozone that causes an increase in bronchial reactivity to histamine and to determine whether adaptation to this effect of ozone develops with repeated exposures, we studied 19 healthy adult subjects. Bronchial reactivity was assessed by measuring the rise in specific airway resistance (delta SRaw) produced by inhalation of 10 breaths of histamine aerosol (1.6% solution). In 5 subjects, bronchial reactivity was determined at 9:00 and 11:30 A.M. on 4 consecutive days without exposure to ozone (Group I). In 7 other subjects (Group II), bronchial reactivity was assessed at 9:00 and 11:30 A.M. on 3 consecutive days, and subjects were exposed to 0.2 ppm of ozone from 9:30 to 11:30 A.M. on the third day. Seven additional subjects (Group III) had bronchial reactivity assessed in a similar fashion for 2 days and then again on 3 consecutive days of 2-h exposures to 0.4 ppm of ozone. Pre-exposure bronchial reactivity of the groups was the same, and no change in bronchial reactivity occurred in the group tested repeatedly but not exposed to ozone. An increase in delta SRaw provoked by histamine was noted after the first exposure to 0.4 ppm but not to 0.2 ppm of ozone (p less than 0.025). With 3 repeated 2-h exposures to 0.4 ppm on consecutive days, however, the delta SRaw produced by histamine progressively decreased, returning to pre-exposure values after the third exposure. Our results indicate that the threshold concentration of ozone causing an increase in bronchial reactivity in healthy human subjects is between 0.2 and 0.4 ppm, and that adaptation to this effect of ozone develops with repeated exposures. The threshold concentration of ozone identified in other studies as causing changes in symptoms, lung volumes, or airway resistance was also between 0.2 and 0.4 ppm, and the time course of the development of tolerance to ozone in these other studies was similar to hat observed in our study. We propose that the appearance of symptoms, changes in pulmonary function, and the increase in bronchial reactivity may be caused by a change in the activity of afferent nerve endings in the airway epithelium.

Adaptation, Physiological↗
PubMed1980

Effect of ganglionic blockade on bronchial reactivity in atopic subjects.

To determine the site in the parasympathetic pathway responsible for the increased bronchial reactivity in 5 atopic subjects, we studied the effect of premedication with aerosols of hexamethonium, a ganglionic blocking agent, and atropine, a postganglionic blocking agent, on the bronchomotor responses to histamine and methacholine aerosols. After 7 mg of aerosolized atropine, baseline specific airway resistance (SRaw) decreased, and the increases in SRaw produced by histamine and by methacholine were prevented in each subject (p < 0.001). After 1 g of hexamethonium, baseline SRaw was decreased to a similar level, and the increase in SRaw produced by histamine was again Prevented in each subject (P < 0.001); However, the increase in SRaw produced by methacholine was not affected significantly in 3 subjects (p > 0.5) and was increased or decreased only slightly in 2 subjects (p < 0.05). These results suggest that bronchial hyperreactivity in atopic subjects may be due to a change in the characteristics of the efferent parasympathetic pathway at a site distal to the ganglion, possibly at the smooth muscle, and that bronchodilation caused by atropine and hexamethonium cannot, by itself, account for their effects on bronchomotor responses.

Adult↗