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Biomedical subjects

G D Bloom

Publications and source records attributed to G D Bloom.

At least 19 recordsLinked to original sources
PubMed1991

A comparison of hyaluronan and fibronectin in the healing of tympanic membrane perforations.

Fibronectin and 1% hyaluronan, two extracellular matrix components, were applied to tympanic membrane (TM) perforations, using the laboratory rat as an animal model. The perforations occupied the upper, posterior quadrant of the TM. Saline-treated and untreated perforations of equal size served as controls. Fifty percent of the perforations treated daily with hyaluronan healed prior to the first closures of the other groups. The use of fibronectin did not enhance the healing rate. The hyaluronan-treated perforations were covered initially by a sheet of keratin and hyaluronan containing abundant inflammatory cells. Within this keratin-hyaluronan cover, hyperplastic stratified keratinizing epithelium advanced and bridged the gap of the perforation ahead of the approaching connective tissue. These findings indicate that exogenously applied hyaluronan could be valuable in the clinical situation and should be tried to improve the healing of TM perforations.

Animals↗
PubMed1985

Exogenous hyaluronic acid (Healon) accelerates the healing of experimental myringotomies.

Topical application of hyaluronic acid (Healon) onto the borders of rat tympanic membrane perforations accelerated the rate of wound healing. The closure time was roughly 60% of that of the untreated perforations. Epithelial cells fused with opposing cells slightly in advance of supporting connective tissue and thus bridged the remaining gap. It seems as if hyaluronic acid, topically applied, can serve as a supporting and orienting matrix for the proliferating squamous epithelium.

Administration, Topical↗
PubMed1984

Surface histamine receptors in rat peritoneal mast cells. Separation of receptor-bearing cells via binding to a histamine-protein conjugate, Cell-ect.

The Seragen Cell-ect Total Histamine KitTM was used to separate histamine receptor-bearing rat peritoneal mast cells from cells lacking these receptors. It was found that approximately 75% of the peritoneal mast cell population carried cell surface histamine receptors. The results further suggest that the mast cell histamine receptors present are mainly of an H1-type, as judged by the capacity of a specific H1-antagonist to reduce the histamine receptor-dependent cell adhesion. Moreover, an H1-agonist is less efficient in this respect and an H2-antagonist does not affect the cell adhesion at all. A possible functional role for these receptors, however, remains to be clarified.

Animals↗
PubMed1984

Influence of fixation and staining techniques on the ultrastructure of the insulin secretory granule.

The ultrastructure of beta-cell granules was examined after fixation of isolated mouse islets in fixatives of various compositions. Islets fixed in glutaraldehyde with or without post-fixing in osmium tetroxide, or in osmium tetroxide alone, exhibited the classical picture of electron-dense core surrounded by a lucid halo. After fixation in potassium permanganate, with or without post-fixing in osmium, the secretory vesicle was often completely filled with a fairly homogeneous material; the vesicle membrane was distinct in outline. When glutaraldehyde-fixed beta-cells were stained according to Rambourg to visualize reducing groups, possibly carbohydrates, two distinct classes of secretory granules were observed, one darkly stained and one faintly, without any noticeable precipitation of silver; the perigranular halo remained unstained in both types of granules. The perigranular halo of aldehyde and osmium fixed beta-granules also remained unstained in cells exposed to the osmiophilic amine, 5,6-dihydroxytryptamine.

Animals↗
PubMed1983

Ultrastructural changes in rat parotid acinar cells after selective beta 1-adrenoceptor agonist treatment.

Administration of the selective beta 1-adrenoceptor agonist, prenalterol, affects the acinar cell of the rat parotid in a manner similar to that observed after isoprenaline (IPR) treatment. Sixty minutes after injection of prenalterol, many cells are depleted of their zymogen granules and there is evidence of secretory protein resynthesis. Long term treatment leads to cellular hypertrophy and marked structural changes in the granule population. The cellular alterations are, however, not as pronounced as those observed after IPR injections. This may be due to the combined beta 1- and beta 2-adrenoceptor effect of IPR. With prenalterol, cell damage is obvious in acute experiments. In long term treated animals numerous characteristic autophagic vacuoles are observed, reflecting a reorganization of cytoplasmic components in superstimulated glands. Although prenalterol and IPR give rise to rather similar structural changes in parotid glands, marked differences between effects of the two drugs on gland biochemistry have been noted. It seems evident that different biochemical pathways involved in secretory activity have actions in common with respect to effects on submicroscopical structures.

Adrenergic beta-Agonists↗
PubMed1982

Cyclic nucleotide involvement in histamine release from mast cells--a reevaluation.

Secretory events in cells in general are accompanied by increased levels of cyclic AMP. In mast cells, however, the pattern is reversed. Thus histamine release is associated with a fall in cAMP. It has been suggested that the lowered levels of cAMP lead to an increase in membrane permeability towards calcium and that an influx of such ions triggers the release mechanisms. It has further been reported that high levels of cAMP inhibit histamine release by decreasing the permeability. However, evidence has now accumulated indicating that this general concept is far too simplistic. Studies are reviewed which imply that there is little or no correlation between histamine release and intracellular levels of cyclic nucleotides. A new working hypothesis with respect to the role of these nucleotides in mast cell secretion is proposed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1982

Sorting of pancreatic islet cell subpopulations by light scattering using a fluorescence-activated cell sorter.

Methods have been developed for the preparation of suspensions of viable rat pancreatic islet cells and their analysis and sorting in the fluorescence-activated cell sorter (FACS III or IV). Histograms of cell number versus light scattering in a near forward angle (1-15 degrees) demonstrated that viable islet cells produce a broad peak that is distinctly separated from the peaks generated by exocrine cells, erythrocytes, and nonviable cells. Electron microscopic examination and radioimmunoassay of hormone content in fractions collected across the peak showed that glucagon-containing (A) cells scatter less intensely and are concentrated within the left side of the islet cell peak, while somatostatin-containing (D) cells are localized to the far right side, indicating a higher intrinsic light scattering property of the D-cells. The more abundant insulin-containing (B) cells define the center of the islet cell peak. Sodium dodecyl sulfate slab gel electrophoresis and radioautography of 35S-methionine labeled cellular proteins confirmed that sorted cells are viable. Cells from the far left region contained increased amounts of labeled 18 Kd proglucagon and its 13-Kd and 10-Kd conversion intermediates, while cells from the right side were relatively enriched in labeled 12.4 Kd prosomatostatin. These results demonstrate that intrinsic light scattering alone can be used to prepare A- or D-cell enriched fractions from islets for biochemical analysis.

Animals↗
PubMed1981

Trophic effect of the sympathetic nervous system on the early development of the rat parotid gland: a quantitative ultrastructural study.

Rats were sympathetically denervated on one side by avulsion of the superior cervical ganglion either immediately after birth (within 4 hr) or when the salivary glands were fully developed. Nine weeks after ganglionectomy the parotid glands were subjects to microscopical studies. As shown by the lack of specific fluorescence, sympathetic denervation caused an almost total depletion of catecholamines in the acini. This was further substantiated at the electron microscopic level using KMnO4 as fixative. No alterations in either gland weight or in acinar cell size were noticeable after adult sympathectomy. On the other hand, neonatal denervation caused a decrease in gland weight as well as ascinar cell hypotrophy. The mean volume of individual acinar cells was reduced by roughly 25% and the granule volume density by about 50%. Also the mean volume of individual granules was decreased. These findings indicate an important role for the sympathetic nerve system in the maturation of the rat parotid gland.

Age Factors↗
PubMed1981

What - if any - is the role of adrenergic mechanisms in histamine release from mast cells?

The effects of catecholamines on histamine release from rat peritoneal mast cells, was studied in an in vitro system. It was found that norepinephrine (10(-5)-101(-3) M) exerts a significant, dose related, repressive effect on compound 48/80-induced histamine release. This effect is greatly potentiated by beta-antagonists and is noticeable throughout the concentration range 10(-11)-10(-3) M norepinephrine. Phentolamine diminishes the repressive effect that norepinephrine shows at 10(-5) M. Norepinephrine (10(-5) M) totally inhibits the progressive histamine release induced by both compound 48/80 and strontium (10 muM) in non-Ca2+-depleted cells. The release that is dependent on extracellular calcium is inhibited by norepinephrine. The repressive effect of norepinephrine at 10(-3) is counteracted by 5.6 mM D-glucose, 2-deoxyglucose abolishes this effect. The repression of histamine release by 10(-5) M norepinephrine is not influenced by D-glucose. These results suggest that the effects on histamine release, observed within a low concentration range of norepinephrine (less than 10(-3) M), may be due to alpha-adrenoreceptor mechanisms and an interference in transmembrane calcium transport. Our data further suggest that norepinephrine at 10(-3) M may inhibit oxidative phosphorylation. Isoproterenol and epinephrine (10(-9)-10(-5) M) show little effect on 48/80-induced histamine release in a normal medium. However, when calcium is excluded from the medium, histamine release is potentiated. These results seem to indicate that isoproterenol and epinephrine act by displacing intracellular calcium, making it available for the exocytosis process.

Animals↗
PubMed1981

Anomalous effects of disodium cromoglycate. A study on two secretory systems.

The effects of disodium cromoglycate (DSCG) on in vitro histamine release from peritoneal and pleural mast cells, and a possible interference with adrenergic mechanisms was studied. Parallel to this study, the effects of DSCG on the well-established adrenoceptor-mediated amylase release from parotid glands were investigated. It was found that DSCG in low concentrations potentiates histamine release from peritoneal mast cells. Further more, this potentiation is enhanced by alpha-adrenoceptor blockade and diminished by beta-adrenoceptor antagonists. Histamine release from pleural mast cells is affected inversely to peritoneal cells, that is, the secretion is inhibited by DSCG at a high concentration but not at a low one. The inhibition is unaffected by alpha-blockers but totally abolished by the beta-antagonist propranolol. The amylase release induced by norepinephrine, mediated via beta1-adrenoceptor, is depressed by DSCG. The beta-antagonist-sensitive amylase release induced by phentolamine is also inhibited by DSCG. Finally, DSCG alone induces amylase release from the parotid gland. These results would seem to indicate that DSCG exerts some alpha-adrenoceptor activity. However, it is not possible, at present, to state whether this activity is of agonistic nature. DSCG has effects which with respect to pattern, correspond well to the action of beta-adrenoceptor agonists.

Adrenergic alpha-Antagonists↗