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Biomedical subjects

J Wiener

Publications and source records attributed to J Wiener.

At least 91 records · Page 5Linked to original sources
PubMed1979

Diagnosis and treatment of pansinusitis: report of case.

A case of acute pansinusitis with the complication of orbital cellulitis has been described. The patient initially had pain around the maxillary right first molar. Accurate diagnosis allowed for prompt, vigorous treatment, culminating in surgical intervention. The need for dental and oral surgical practitioners to be thoroughly familiar with all of the manifestations of paranasal sinus disease cannot be overemphasized.

Cellulitis↗
PubMed1979

Primary myocardial disease in the diabetic mouse. An ultrastructural study.

The hearts from C57BL/KsJ db+/db+ mice and controls were examined by light and electron microscopy at intervals during 5 to 28 weeks of age. C57BL/6J ob/ob mice and their lean littermates served as other controls. The percentage of increase in body and heart weights of the diabetic animals was 150% and 64% greater, respectively, than that of the controls. Over the period of observation there was progressive damage to the ventricular myocytes and intramural small arteries and arterioles of the diabetic animals. Initially, the cardiac muscle cells of both ventricles contained large numbers of lipid droplets. Subsequently, there was shrinkage and increased electron density of mitochondria that were enveloped by single limiting membranes that in turn gave rise to large residual bodies. This was followed by loss of myofilaments and atrophy of myocytes. Similar changes occurred in the smooth muscle cells of intramural arteries and arterioles but not in those of epicardial arteries. Reduplicated layers of basal laminae were seen around interstitial capillaries. Degenerative changes also occurred in perivascular nerve endings. These changes are discussed in relation to the altered metabolism of the diabetic state. It is concluded that the pathologic lesions in the cardiac muscle cells and intramural arterial vessels and capillaries constitute a primary myocardial disease in the genetically diabetic mouse.

Animals↗
PubMed1978

Absolute morphometric study of myocardial hypertrophy in experimental hypertension. I. Determination of myocyte size.

A method for determining the mean absolute volume of a specific population of cells within a tissue is described and applied to the measurement of endocardial and epicardial myocytes in the left ventricle of normal and hypertensive rats. The technique, based on nuclear counts per unit area in tissue slices of different known thicknesses, measures the mean cell volume per nucleus independent of previously unknown nuclear dimensions and systematic counting errors. Duplicate determinations, demonstrating reproducibility, were made in mutually perpendicular longitudinal and transverse sections of the myocardium. Combining these light microscopic measurements with electron microscopic data enabled the evaluation of the mean diameter and length of the cylindrical myocyte nuclei showing those in the epicardial cells to be significantly longer than the nuclei in endocardial cells. It was estimated that 2 to 4 per cent of ventricular myocytes are binucleate. After 1 to 4 weeks of hypertension, induced by constriction of the left renal artery, endocardial myocytes were enlarged 21 per cent, from 10,370 +/- 410 to 12,520 +/- 490 cu. micrometer., while epicardial myocytes showed a 37 per cent hypertrophy, from 12,600 +/- 1,600 to 17,300 +/- 1,100 cu. micrometer. The availability of a reliable determination of cell volume will make possible the interpretation of much biochemical, functional, and morphometric data at the whole cell level.

Animals↗
PubMed1978

Absolute morphometric study of myocardial hypertrophy in experimental hypertension. II. Ultrastructure of myocytes and interstitium.

The left ventricular myocardium of normal and hypertensive rats has been characterized morphometrically in the endocardial and epicardial zones. Compared to the epicardial regions, the normal endocardial regions contain 30 per cent more myocytes, 27 per cent less interstitial space, 48 per cent less capillary volume, 17 per cent less capillary surface, and the same capillary length per unit tissue volume. In terms of both the relative and absolute volumes and surface areas of their organelles, the cytoplasmic composition of normal endocardial and epicardial myocytes is nearly identical. After 14 weeks of hypertension, induced by constriction of the left renal artery, left ventricular weight is increased by 30 per cent, wall thickness by 42 per cent. The number of myocytes and the total length of capillaries remain constant. The epicardial region enlarged 37 per cent with proportional increases of myocyte and interstitial volumes. In contrast, the endocardial enlargement was only 26 per cent, comprised of 21 per cent hypertrophy of myocytes and a 55 per cent increase in interstitial components. Expansion of capillary lumina accounted for much of the interstitial enlargement throughout the myocardium. Hypertrophy of myocytes is 76 per cent greater in the epicardial region and is accompanied by a reduced mitochondria to myofibril ratio and disproportionately large increases (2- to 3-fold) in both smooth endoplasmic reticulum and T-system volume and surface area. On a cellular basis the absolute morphometric characteristics of myocytes from hypertensive rats are significantly different from normal, and significant differences occur between the inner and outer layers of the myocardium for practically every cytoplasmic component.

Animals↗
PubMed1977

Morphometric analysis of hypertension-induced hypertrophy of rat thoracic aorta.

The response of the intima-media of the thoracic aorta to 1 to 4 weeks of two-kidney renal hypertension in the rat has been analyzed by morphometric techniques at light and electron microscopic levels. The increased thickness of the aorta that ensues is the result of an increase in the size but not the number of smooth muscle cell layers. The volume fractions of intima occupied by endothelium (26%), internal elastic lamina (37%), and subendothelial space (37%) in normotensive animals are not significantly altered by the hypertension. The percent increases in muscle cross-sectional area is greatest (58 to 60%) in the two innermost layers (M1 and M2). M1 is composed of nearly equal compartments of smooth muscle cells and interstitial space that expand 69% and 50%, respectively, with hypertension. Analysis of the subcellular constituents of the M1 smooth muscle cells indicates that significant changes in absolute volume include increases of caveolae (45%), myofibrils (59%), mitochondria (81%), glycogen (163%), and rough endoplasmic reticulum (221%). Factors contributing to these alterations are discussed.

Animals↗
PubMed1976

Specialized junction in the distal convoluted tubule of rat kidney.

The ultrastructure and permeability of the apical junctions between epithelial cells of the distal nephron have been studied in rat kidney using a collidal lanthanum tracer and uranyl acetate staining en bloc. The apical intercellular junctions of the macula densa and juxtaglomerular segment of the early distal convoluted tubule measure up to 0.5 mu in length and about 50 A in width. Lanthanum permeates the occluding portion of these junctions in a discontinuous manner, defining a series of closely spaced and parallel lines of fusion that run in a direction perpendicular to the apical-basal axis of the tubular cells. The apical junctions of the remainder of the distal convoluted and cortical collecting tubules are impermeable bolanthanum. This distinctive apical tight junction can account for the greater permeability to ions of the early distal convoluted vs. late distal convoluted and cortical collecting tubules.

Animals↗
PubMed1976

Effect of angiotensin-induced hypertension on rat coronary arteries and myocardium.

Acute hypertension has been produced in rats by the intravenous infusion of angiotensin amide for 4 hours. Both control and hypertensive animals were injected intravenously prior to sacrifice with either horseradish peroxidase (HRP) or colloidal carbon. Epicardial arteries and blocks of ventricular myocardium containing intramyocardial arteries and arterioles have been processed for electron microscopy. HRP appears to penetrate the endoethelium of epicardial arteries from control animals within vesicles that bypass endothelial junctions and empty into interendoethelial clefts. Peroxidase does not traverse the endothelium of intramural arteries and arterioles of controls over the 10-minute period of observation. There is acceleration of lateral vesicular transport in the endothelium of epicardial arteries after angiotensin infusion and direct permeation of interendothelial clefts of intramural arterial vessels. Medial fragmentation and more extensive necrosis are observed in intramyocardial but not in epicardial arterial vessels. Foci of myocardial damage resembling irreversible ischemic or anoxic injury followed by reflow are described. It is suggested that the increased permeability of epicardial arteries may be due to elevated pressure, while the altered permeability and vascular lesions of intramural arteries and arterioles are more readily attributable to the vasoconstriction produced by angiotension. The vascular and myocardial lesions are also discussed in relation to the regional actions of angiotensin on the coronary circulation and known effects of this vasoactive peptide on myocardium.

Angiotensin II↗
PubMed1975

Intercellular junctions of rat endocardium.

The ultrastructure of the intercellular junctions of rat endocardium has been characterized following lanthanum exposure in vitro and uranyl acetate staining en bloc. The interendothelial clefts of the endocardium run either a relatively straight or convoluted course and posses one or two loci where the plasma membranes are in close apposition or form punctate fusions. Elongate restrictions, that exhibit hexagonal arrays of subunits following lanthanum immersion (gap junctions), are also present in the intercellular endocardial clefts. The occurrence of interendothelial clefts of endocardium lacking occlusive foci can account for the permeability properties of ventricular endocardium, where the direction of diffusion of macromolecules has been attributed to pressure gradients between ventricular cavity and myocardium. The relationship of gap junctions to possible electrical phenomena within the endocardium is also discussed.

Animals↗
PubMed1974

Regional variation in the permeability of rat thoracic aorta.

The permeability and ultrastructure of the intercostal orifices and interostial regions of rat thoracic aorta have been compared in the present study. The ostial regions consist of two different portions, an annulus and an inflow tract, the latter being continuous with the intercostal artery. The wall of the inflow tract has a sharp bend, demarcating inner and outer portions. Faint blueing of the lateral portions of aortic annuli is visible from 3(1/2) to 4(1/2) hours after injection of Evans blue dye and is no longer apparent at 5(1/2) hours, when there is diffuse discoloration of the thoracic aorta. Only the annuli are labeled by horseradish peroxidase (HRP) for 1(1/2) to 3(1/2) minutes after intravenous injection. There is more extensive and progressively heavier labeling of annuli and inner halves of the inflow tracts between 5 to 12 minutes. HRP is transported across aortic endothelium within micropinocytotic vesicles. Intercellular endothelial clefts do not appear to be directly permeated from the lumen through their junctions for a period of at least 3(1/2) minutes. The present observations preclude an assessment of the penetration of the junctions by HRP at later intervals. No appreciable differences are observed in the mode of transport of peroxidase through the more permeable endothelium of the annulus and less permeable endothelium of inflow tract and interostial regions. Observations made on tissues exposed to colloidal lanthanum, and on specimens stained en bloc with uranyl acetate and subjected to a combination of rotation-tilting, fail to demonstrate appreciable differences in the ultrastructure of the endothelial cell junctions of intercostal orifices and interostial regions. Since morphologic differences do not seem to account for the greater permeability of annular regions, the role of hemodynamic forces is considered. The relationship between regional variation in permeability and the development of atherosclerotic lesions is also discussed

Animals↗
PubMed1973

The cellular pathology of experimental hypertension. 7. Structure and permeability of the mesenteric vasculature in angiotensin-induced hypertension.

Acute hypertension was produced in rats by the infusion of angiotensin amide for 2 to 4 hours. These animals were injected intravenously prior to sacrifice with either colloidal carbon or iron dextran particles. The mesenteric vessels from hypertensive and control animals were processed for electron microscopy. Ultrastructural alterations are found in dilated segments of small arteries. Initially there is severe contraction of medial smooth muscle cells and the formation of processes of smooth muscle cytoplasm. This is followed by lysis of cell processes and bodies, and passage of plasma and colloidal iron into the media. Subsequently, carbon, platelets, fibrin and cellular debris are seen within these foci of medial necrosis. These changes appear as a sequence whose severity reflects the duration of the angiotensin infusion and degree of elevation of the systolic pressure. The morphologic alterations are discussed in relation to the generalized increase in vascular permeability that is associated with the hypertensive state.

Angiotensin II↗