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J Van Reempts

Publications and source records attributed to J Van Reempts.

46 records · Page 3Linked to original sources

Oxatomide protects against degranulation of rat peritoneal mast cells during in vitro challenge with antigen or compound 48/80. Ultrastructural aspects.

The ultrastructure of isolated rat peritoneal mast cells was evaluated after in vitro degranulation and treatment with oxatomide, a new anti-allergic compound. In a first series of experiments, mast cells of rats infected with Trichinella spiralis larvae were incubated with Trichinella larvae somatic antigen to produce histamine release. The release was visualized in the electron microscope by exocytosis of the peripheral amine-containing granules, which resulted from fusion between several perigranular membranes and fusion of these membranes with the plasma membrane. A more drastic degranulation was provoked in a second series by incubation of unsensitized mast cells in the presence of the amine liberator compound 48/80. This treatment led to a complete extrusion of the granules in most of the cells, while in a smaller number of cells, only large vacuoles containing remnants of several granules were seen. The plasma membrane of these cells however was intact and there were no signs of exocytosis. The effect of oxatomide against mast cell degranulation was dose-dependent and comparable for the two types of histamine release. After incubation with high doses (10(-4) M, 5.10(-5) M) granule liberation was rarely observed in antigen-challenged and compound 48/80-challenged cells. Protection was apparently situated at the level of the plasma membrane which seemed to be unable to fuse with the perigranular membranes while fusion of perigranular membranes of individual granules was still possible. None of the tested concentrations of oxatomide induced spontaneous degranulation. High doses, however, led in a number of cells to some ultrastructural alterations such as partial disappearance of plasmalemmal folds, slight cytoplasmic oedema and the appearance of intranuclear microtubules. The latter were also seen in oxatomide-treated challenged mast cells.

Animals↗

Comparative effects of oxatomide on the release of histamine from rat peritoneal mast cells.

Oxatomide inhibits the release of histamine from rat peritoneal mast cells in vitro induced by C 48/80, antigen, anti-IgE and ionophore A 23 187, without effect on non-specific release by n-decylamine. Its effect is concentration- and pH-dependent and decreases with increasing extracellular Ca2+-concentrations. Prolonged incubation does not enhance the inhibition, which is lost after one single wash-out. Aminophylline and isoproterenol are not potentiated by oxatomide. The present study points to an effect of oxatomide on a Ca2+-dependent process at the level of cell membrane common to antigen, C 48/80 and ionophore A 23 187.

Animals↗

Intranuclear microtubules in lung mast cells of guinea pigs in anaphylactic shock.

Intranuclear microtubules were found in lung mast cells during anaphylactic shock following ovalbumin challenge of guinea pigs passively sensitized with homocytotropic antibodies. Simultaneously, such cells showed mitochondrial swelling with a clear matrix and partially disrupted cristae. Although a decreased number of mast cell granules generally accompanied these observations, the degree of degranulation and the morphologic appearance of the granules are less reliable criteria to indicate the immediate participation of a cell in the anaphylactic phenomenon. The cells that presented intranuclear microtubules were mainly found in the vicinity of the bronchiolar smooth muscle. The distribution of cations has been investigated in these tissues with a combined oxalate-pyroantimonate method. Whereas in controls the reaction product is located mainly in the nucleus and the mitochondria of mast cells, these sites become almost completely devoid of precipitate during the anaphylactic reaction. A hypothetical link between histamine release, intracellular distribution of cations, possibly calcium, and the appearance of intranuclear microtubules in mast cells is proposed.

Anaphylaxis↗

Early myocardial ischaemia: evaluation of the histochemical haematoxylin-basic fuchsin-picric acid (HBFP) staining technique.

A series of experiments, carried out to evaluate the histochemical method for the morphological diagnosis of early stages of myocardial ischaemis (HBFP) is reported. The experiments were performed on dog hearts in which ischaemia was induced by coronary artery ligation for different periods of time. The original procedure or modifications of the HBFP-technique, including different staining, rinsing, and differentiation times, the use of different commercial brands of chemicals and preparatory changes of routine histological procedures such as fixation, embedding, cutting, and mounting, did not give satisfactory results. False positive and negative staining was frequent. Very equivocal results were obtained on serial sections of ischaemic tissue samples. Therefore this method was regarded as unreliable and non-reproducible.

Animals↗

A simple polychrome stain for conventionally fixed Epon-embedded tissues.

The described technique, based upon a one-step Mallory-Heidenhain stain, can be applied as a routine stain for glutaraldehyde or OsO4 fixed, Epon embedded tissues of various organs. The technique consists of a short treatment of the sections with H2O2, a nuclear staining with celestine blue B and a final staining in a modified Cason's solution. The different tissue and cell components are displayed as follows: dark brown nuclei, yellow cytoplasm, red collagen fibers and blue elastic fibers. Intracytoplasmic components as glycogen and mucus are stained respectively blue and violet, whereas other inclusions such as leucocyte granules are colored orange to red.

Animals↗

Flunarizine reduces cerebral infarct size after photochemically induced thrombosis in spontaneously hypertensive rats.

The cerebroprotective effect of flunarizine was studied in a minimally invasive model of photochemically induced cerebral infarction in spontaneously hypertensive rats. Intravenous administration of the photosensitizing dye rose bengal and intense focal illumination of the brain produced a deep cortical infarction that resulted from singlet oxygen-induced peroxidative injury to the endothelial membrane, subsequent platelet adhesion, and eventual thrombus formation. The infarct size was calculated from area measurements on consecutive histologic sections prepared from the brain cortex 4 hours after the onset of the insult. Oral treatment with 40 mg/kg flunarizine 3 hours before photoexcitation resulted in a significant reduction of the median infarct size from 11.75 mm3 in the untreated group to 6.40 mm3 in the treated group (n = 13, p less than 0.001). At this dose, flunarizine had no effect on systemic blood pressure. In a separate experiment the area of thrombotic obstruction was quantified 30 minutes after the onset of light exposure. Flunarizine did not significantly reduce early thrombus formation (2.28 mm3 in the untreated and 1.78 mm3 in the treated group) (n = 12, p = 0.2). The infarcted area at 4 hours was considerably larger than the initial thrombotic area. Protection with flunarizine against development of cortical infarction has been unequivocally shown. Although some effect may already be present at the early stage of lesion formation, the major protective action admittedly occurred in the later postinsult period when the lesion was expanding.(ABSTRACT TRUNCATED AT 250 WORDS)

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