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Biomedical subjects

A A Gashi

Publications and source records attributed to A A Gashi.

6 recordsLinked to original sources
PubMed1989

Tracheal gland mucous cells stimulated in vitro with adrenergic and cholinergic drugs.

To determine the responsiveness of tracheal mucous cells to adrenergic and cholinergic stimulation, we analyzed changes in their structure induced by neurotransmitter-like agonists. Ferret tracheal rings were exposed for 30 min in vitro to one of the following: phenylephrine, isoproterenol, or bethanechol (all at 10(-5) M), in the presence of absence of appropriate antagonists. Electron microscopy and morphometric analysis revealed that the volume density of mucous cells (Vvmc, i.e. the space occupied by mucous cells in the submucosa) significantly decreased, and the surface density of mucous cell apical membrane (Svam) increased in response to isoproterenol and bethanechol but not to phenylephrine. In metabolic labeling experiments, the morphological changes were accompanied by secretagogue-evoked release of 35S-labeled macromolecules. Taken together, these data suggest that tracheal mucous cells secrete 35S-labeled macromolecules in response to beta-adrenergic and muscarinic agonists by an exocytotic process that involves a reduction in cell size.

Animals↗
PubMed1987

Autoradiographic studies of the distribution of 35sulfate label in ferret trachea: effects of stimulation.

Na2(35)SO4 is among the common isotopic mucin precursors used to label airway secretory cells and monitor their active discharge in response to drugs. Previous work has established that 35S is taken up by multiple cell types in the trachea, yet there is no direct evidence linking 35S release with secretory activity by any specific cell type. In this study, we have used autoradiography to identify the sites of uptake and release of 35S in ferret trachea. Confirming work performed in other species, we found uptake sites include surface epithelium (ciliated and goblet cells), submucosal glands (serous and mucous cells) and cartilage. Extending these findings using a "pulse-chase" protocol, we found that 35S turns over very rapidly in ciliated but not submucosal gland cells or cartilage. Specific grain density over epithelium declined from 0.12 +/-0.006 grains/micron 2 immediately after the pulse to 0.05 +/- 0.004 grains/micron 2 at 4 h. In contrast, corresponding figures for the glands and cartilage showed no spontaneous loss of label during the same period. At 4 h, when the epithelium contained very little 35S label, we exposed tracheal rings in vitro to neurotransmitter receptor agonists (bethanechol, phenylephrine, and isoproterenol; all at 10(-5) M). Counts in the medium (determined by scintillation spectrometry) increased 2-3 times in response to each agonist. These increases were prevented by preincubating tracheal rings with appropriate antagonists. Autoradiography showed that stimulated glands contained many fewer silver grains than untreated or antagonist-blocked glands. In contrast, neither cartilage nor epithelium showed decreased labeling after stimulation. These results indicate that (a) sulfated glycoconjugates turn over rapidly in the tracheal epithelium and may account for much sulfated material spontaneously released into organ culture medium and into the tracheal lumen, and (b) 4 h after Na2(35)SO4 incubation, the major source of 35S-labeled macromolecules released from ferret trachea by neural agonists is the submucosal glands.

Animals↗
PubMed1986

Neuropeptides degranulate serous cells of ferret tracheal glands.

To determine whether serous or mucous cells in tracheal submucosal glands respond to the neuropeptides substance P (SP) and vasoactive intestinal peptide (VIP), we studied the peptide-induced changes in gland cell morphology accompanying release of 35SO4-labeled macromolecules from tracheal explants of ferrets. Explants were labeled for 1 h in medium containing 35SO4 and washed for 3.5 additional hours. Base-line secretion in the absence of drugs declined between 1.5 and 3.5 h after the pulse. Between 2.5 and 3.5 h, the average percent change in counts per minute recovered per sample period was not significantly different from zero (P greater than 0.3; n = 6). Substance P (10(-5) M) and VIP (2 X 10(-6) M) added 4 h after labeling each increased greatly the release of 35SO4-labeled macromolecules (SP, 219%; VIP, 180%) above base line. Bethanechol, a muscarinic-cholinergic agonist (10(-5) M), increased secretion by an average of 142% above base line (each effect, P less than 0.05; n = 6 each). Light and electron microscopy of the control tissues showed glands with narrow lumens and numerous secretory granules. Glands treated with SP or VIP had enlarged lumens and the serous cells were markedly degranulated. These phenomena were documented by morphometry and suggest that SP and VIP cause secretion from glands at least partially by stimulating exocytosis from serous cells.

Animals↗
PubMed1986

Structural changes associated with fluid absorption by dog tracheal epithelium.

During fluid absorption induced by amphotericin B, the lateral intercellular spaces (LIS) of the dog tracheal epithelium were widely dilated as compared to untreated time controls. When fluid absorption was inhibited by ouabain, or by replacement of luminal Na by choline, amphotericin B failed to cause dilation of the LIS. These data suggest that, as in other epithelia, a significant amount of transepithelial fluid flow passes down the LIS, and that these spaces may provide the local osmotic compartment which is responsible for linking transepithelial fluid movement to active ion transport.

Absorption↗