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Biomedical subjects

I Joris

Publications and source records attributed to I Joris.

At least 37 records · Page 2Linked to original sources
PubMed1987

The mechanism of vascular leakage induced by leukotriene E4. Endothelial contraction.

This study identifies the microvascular target of leukotriene E4 (LTE4) by vascular labeling with carbon black and establishes the mechanism of its action at the cellular level by electron microscopy. LTE4 and its tripeptide precursor, leukotriene C4 (LTC4) were injected subcutaneously in guinea pigs. With LTE4, venular labeling was intense at 1000 and 100 ng and slight at 10 ng, with extinction at 1 ng. LTC4 induced a ring of labeled venules around a blank central area, suggestive of vasospasm. The nonpeptidyl leukotriene LTB4 induced no labeling. Histamine (1000 ng) induced an area of vascular labeling about equal to that by 1000 ng LTE4, but the labeling of individual venules was more intense. By electron microscopy, LTE4 was found to induce gaps in the endothelium of the venules; the endothelial cells adjacent to the gaps bulged into the lumen and showed wrinkled nuclei, consistent with cellular contraction. This ultrastructural evidence suggests that LTE4 increases vascular permeability by contraction of endothelial cells selectively, in the postcapillary venules, as was previously demonstrated for other inflammatory mediators, including histamine, serotonin, and bradykinin.

Animals↗
PubMed1987

Focal arteriolar insudation. A response of arterioles to chronic nonspecific irritation.

The subcutaneous insertion of sterile, inert plastic pellets over the cremaster muscles of rats induces characteristic focal lesions of the arterioles at a distance from the pellets. These lesions appear with a delay of about 6 hours; by light microscopy they are characterized by a focal dilatation accompanied by endothelial damage and increased permeability. They are more severe if the pellets are loaded with histamine and are inhibited if the pellets are loaded with serotonin. Electron microscopy shows interendothelial gaps; the media is massively infiltrated with blood components and fibrin. The medial smooth muscle cells are stretched and at times necrotic; inflammatory cells are scarce. On the basis of these features the lesion was named focal arteriolar insudation (FAI). Although its pathogenesis is not yet clear, the data at hand suggest that it is caused by endogenous mediators affecting the smooth muscle cells and/or the endothelium. FAI appears to be a specific arteriolar response to chronic nonspecific irritation.

Animals↗
PubMed1987

A pancreatic venular defect in the BB/Wor rat.

BB rats develop spontaneous autoimmune diabetes mellitus characterized morphologically by insulitis, an inflammatory lymphocytic infiltration of the islets of Langerhans. To investigate the role of the vascular endothelium of the pancreas in this destructive process, the authors injected diabetes-prone (DP) and diabetes-resistant (DR) BB/Wor rats as well as other nondiabetic strains of rats with Monastral blue B, a colloidal pigment that identifies leaky microvasculature. They found evidence of a venular defect limited to the pancreas that is specific to the BB rat. Light- and electron-microscopic evidence suggests that this defect is due to a population of trapped (marginating) intravascular monocytes, which may be activated by the colloidal pigment and release vasoactive mediators.

Animals↗
PubMed1986

Cellular changes during hypertension: a quantitative study of the rat aorta.

Using rats made hypertensive by aortic ligation or by the one kidney--one clip method, we searched the aorta for morphologic clues that could explain why hypertension aggravates atherosclerosis. Both atherosclerosis and hypertension are characterized by an increased migration of mononuclear cells into the aortic intima; we therefore quantitated this phenomenon and studied its time course. In the thoracic aorta of hypertensive rats intimal cells (emigrated mononuclear cells) increased up to 15 times 2 weeks after surgery and remained stationary thereafter. In both control and experimental rats, leukocyte emigration was heavier in the thoracic aorta than in the abdominal region. A two- to threefold increase in medial smooth muscle herniae into the intima (myointimal herniae) was also found at 8 weeks, indicating a smooth muscle cell dysfunction. Electron microscopic study of the intima showed that its thickening was due to blood-borne material and also to extracellular matrix synthesized by the endothelium. Heightened secretion reflects cell activation, a condition that (in the endothelium) leads also to leukocyte adhesion. These data suggest that, in renovascular hypertension, the aortic endothelium is in an activated state, possibly through a hormonal stimulus.

Animals↗
PubMed1985

The significance of endothelial stomata and stigmata in the rat aorta. An electron microscopic study.

Perfusion of arteries with dilute silver nitrate produces in the endothelium (a) a pattern of pericellular black lines, which we earlier interpreted as a marker of the physiological electrolyte pathway (Zand et al. 1982), and (b) focal black deposits on or between the cells, either ring-shaped (stomata) or solid (stigmata). The purpose of this study was to clarify the nature and significance of these controversial structures. A glutaraldehyde-fixed normal rat aorta was perfused with silver nitrate; 17 typical stomata and stigmata were photographed en face, then studied on ultrathin serial sections. When seen en face, they fell into three groups: (I) 4 stomata in endothelial cells; (II) 6 stigmata in endothelial cells; (III) 7 stigmata on intercellular junctions. By electron microscopy, (I) all the stomata in endothelial cells corresponded to myoendothelial herniae. (II) Of the 6 stigmata in endothelial cells, 4 corresponded again to myoendothelial herniae, 2 corresponded to blebs (it seemed likely that these blebs had existed in vivo, but the possibility of a fixation artefact could not be excluded). (III) Of the 7 stigmata on intercellular junctions, one corresponded to the diapedesis of a mononuclear cell; the other 6 did not correspond to visible endothelial changes and are best interpreted as points of normally higher permeability. We conclude that stomata and stigmata (under the conditions of our experiments) can be explained in at least 4 different ways, depending in part on their location (in cells, on junctions). These ancient terms therefore remain useful for descriptive purposes, as long as it is realized that their significance in any given case must be determined by electron microscopic study.

Animals↗
PubMed1985

Necrosis of adipose tissue induced by sequential infections with unrelated viruses.

Vaccinia virus infection in mice previously infected with and immune to lymphocytic choriomeningitis virus resulted in a clinical illness which neither virus alone induced. The main pathologic finding was extensive fat necrosis with a cellular infiltrate suggestive of delayed type hypersensitivity. Vaccinia virus titers in adipose tissue of clinically ill mice were not higher than those in relevant control groups. This indicates that an unusual virus-induced disease can arise in an animal with a history of unrelated virus infection, and that this disease may be due to an altered host response to infection. The experimental model presented here suggests that chronic inflammation and necrosis of a given tissue may depend on sequential infection with two viruses, neither of which would be capable of inducing such a lesion.

Adipose Tissue↗
PubMed1984

Adriamycin impairs phagocytic function and induces morphologic alterations in human neutrophils.

Normal human polymorphonuclear leukocytes (PMNL) were preincubated in vitro with methotrexate, 5-fluorouracil, vincristine, cisplatin, Adriamycin (doxorubicin), and daunomycin for 15 hours before being tested in a phagocytic-bactericidal assay. Anthracycline-treated PMNL were defective in phagocytosis and killing of the bacteria, in contrast to the other chemotherapeutic agents which allowed the PMNL to remain functional. The defect of Adriamycin-treated PMNL resulted from decreased ingestion: 3 micrograms/ml Adriamycin inhibited by 50% of the uptake of Oil Red-O particles. In this assay, the proportion of noningesting PMNL increased from less than or equal to 20% with 0.62 micrograms/ml to greater than or equal to 90% with 10 micrograms/ml Adriamycin. Electron microscopy revealed that Adriamycin-inactivated PMNL had rounded up, were depleted in glycogen, and had undergone profound nuclear changes. RNA and protein synthesis in PMNL were also affected. Adriamycin, besides producing neutropenia, may decrease the phagocytic function of circulating PMNL.

Antineoplastic Agents↗
PubMed1983

The intracerebral microcirculation of the rat in hemorrhagic shock.

The intracerebral microcirculation of the isocortex was studied in unanesthetized rats under hemorrhagic shock. To observe the microvessels, three markers were separately injected intravenously during the shock period: (a) Evans blue for fluorescence microscopic visualization of the vessels. (b) India ink for gross and light microscopic evidence of retention of carbon. (c) Horseradish peroxidase (HRP) for light and electron microscopic study. Lack of spontaneous recovery from shock was associated with: (a) 55-65% blood loss, a low blood pressure (30-40 mm Hg), and a dramatic increase in pulse rate; (b) marked Evans blue fluorescence along the vessels; (c) no retention of India ink in the microcirculation; (d) peroxidase activity on the luminal surface of the endothelium. Absence of India ink in the microcirculation of the isocortex during the shock period, as shown by light and electron microscopy, suggests that there is sufficient cerebral blood flow to clear the carbon particles from the blood stream and that there are no openings greater than 30 nm in the endothelial layer allowing seepage of carbon particles through or between endothelial cells. Vascular Evans blue fluorescence and peroxidase activity were both demonstrated on the luminal surface of the endothelial cells, by light microscopy, indicating that these markers are abnormally retained. Ultrastructural demonstration of increased HRP uptake and adherence onto the endothelial cells confirms these observations. These results show that regional endothelial alterations occur in this model of hemorrhagic shock.

Anesthesia, Inhalation↗
PubMed1983

Studies on the pathogenesis of atherosclerosis. I. Adhesion and emigration of mononuclear cells in the aorta of hypercholesterolemic rats.

In rats with diet-induced hypercholesterolemia, two concomitant changes began to occur within 1 week and persisted for 1 year: an increase in total plasma cholesterol and an increase in the number of mononuclear cells adhering to the aortic intima (up to values 50 times normal). Adherent cells were approximately 90% monocytes and approximately 10% lymphocytes. Adhesion was focal, with some preference for ostia of aortic branches; it was followed by migration into the subendothelial space. The subendothelial monocytes/macrophages progressively became foam cells, thus giving rise to microscopic "fatty streaks." Ultimately, typical atherosclerotic plaques were formed. Four possible mechanisms of increased cell adhesion are suggested. Endothelial changes were mild; myelin figures arising from the endothelial surface were seen by electron microscopy. Endothelial denudation was never observed, neither in light-microscopic preparations stained with AgNO3 nor by ultrastructure. Platelet participation was minimal. It is concluded that in this model atherosclerotic plaques are initiated by mononuclear cell adhesion and emigration; endothelial denudation is not a necessary step in their pathogenesis.

Animals↗
PubMed1982

Endothelium and "silver lines". An electron microscopic study.

The significance of endothelial "silver lines" was studied by TEM in rat aortas after perfusion with glutaraldehyde followed by silver nitrate. Standard TEM technique proved unsatisfactory (coarse silver granules, imprecise localization, artefacts). Exposure of the silver-treated aortas to photographic fixer markedly improved the image of the deposits leaving fine, stable, uniform "residual granules" about 100 A in diameter. Most of these granules were localized along the intercellular junctions; they also tended to pool in the basement membrane beneath each junction. This image suggests that the Ag+ ions pass through the junction, and react with its contents as well as with the basement membrane beyond it. A scheme is proposed to explain the reaction of Ag+ ions with anions and negatively charged radicals within the junction. It is concluded that the "silver lines" represent not only a histochemical effect, but also the visualization of a transendothelial electrolyte pathway.

Animals↗
PubMed1982

Vascular labelling with monastral blue B.

Vascular labelling is an established technique of experimental pathology whereby leaky vessels can be identified in vivo. A suspension of a suitable colloidal pigment is injected intravenously; the pigment is then trapped in the wall of the leaky vessels. The colloidal preparation of carbon black, which has been used for many years for this purpose, is no longer commercially available. This communication introduces a substitute: Monastral blue B which gives beautiful preparations in whole mounts, is readily visible in paraffin and plastic embedded histologic sections, has a distinctive appearance in electron micrographs, and is nontoxic in the required dosage.

Animals↗
PubMed1982

Hydrodynamic injury of the endothelium in acute aortic stenosis.

The acute effects of increased shear stress on the endothelium were studied by reducing the lumen of the rat aorta to 20-25% of normal by means of metal clips. Intimal damage in the stenotic area was assessed by light microscopy after perfusion with AgNo3 and study of the endothelium en face. Most of the endothelium was lost within 3 minutes; the extent of the damage was not increased after 1 hour. Electron-microscopic examination showed that some endothelial cells became permeable to tracers (thorium dioxide and horseradish peroxidase); platelets adhered to the exposed internal elastic membrane. Focal endothelial changes were represented by myelin figures of various kinds arising from the luminal surface and by "cellular ulcers," superficial erosions of the endothelial cells accompanied by localized cytoplasmic changes. These "ulcers" occurred more frequently over the nucleus and near junctions; they have not been described in other forms of arterial injury.

Animals↗
PubMed1981

Endothelial changes induced by arterial spasm.

Prolonged arterial constriction can cause damage to the artery itself. The purpose of this study was to define the intimal changes. Two muscular arteries of the rat were studied by electron microscopy 15 minutes to 7 days after L-norepinephrine had been dripped over the vessels. Endothelial damage was caused by the tight folding of the internal elastic lamina, which mechanically squeezed the cells. As the artery relaxed, the endothelium showed gaps, patches of thinned cytoplasm, and many adhesions between cells on opposite sides of intimal folds. The adhesions involved whole cells of cytoplasmic bridges stretched across the intimal "valleys." They were present up to one day; later they seemed to snap and disappear without causing further cellular damage. A survey of the literature shows that such adhesions can also develop in collapsed arteries postmortem. They explain the endothelial "bridges" previously described by others as a normal intimal structure.

Animals↗
PubMed1981

Medial changes in arterial spasm induced by L-norepinephrine.

In normal rats, the media of small arteries (0.4--0.2 mm in diameter) previously was shown to contain intracellular vacuoles, identified ultrastructurally as herniations of one smooth muscle cell into another. The hypothesis that intense vasoconstriction would increase the number of such vacuoles has been tested. In the media of the saphenous artery and its distal branch, vasoconstriction induced by L-norepinephrine produced many cell-to-cell hernias within 15 minutes. At 1 day their number was reduced to about 1/10 of the original number. By 7 days the vessel was almost restored to normal. Triple stimulation over 1 day induced more severe changes in the media. These findings suggest that smooth muscle cells are susceptible to damage in the course of their specific function. The experimental data are discussed in relation to medial changes observed in other instances of arterial spasm. Endothelial changes that developed in the same experimental model were described in a previous paper.

Animals↗