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Biomedical subjects

G Majno

Publications and source records attributed to G Majno.

At least 19 recordsLinked to original sources
PubMed1992

Acute endothelial cell contraction in vitro: a comparison with vascular smooth muscle cells and fibroblasts.

The contractile responses of cultured rat and calf endothelial cells (EC), vascular smooth muscle cells (VSMC), and fibroblasts (FB) to vasoactive mediators (thrombin, serotonin, bradykinin, and histamine), forskolin, and cytochalasin B were compared. Cells were grown on a pliable silicone membrane, and contraction was assessed, using time-lapse video microscopy, by recording changes in the wrinkling of the silicone as the cells exerted tension on the surface. We found that all cells contracted in the presence of serum or thrombin and that VSMC and FB also contracted with serotonin stimulation. Bradykinin and histamine were not contractants in this system. Discrepancies between these results and reports of changes in permeability of endothelial layers in vitro and in vivo may be due to (1) the vascular segment from which EC were studied or (2) the possibility that certain mediators may provoke a noncontractile response that results in gap formation. Thus changes in vascular permeability, which occur during inflammation, may have both contractile and noncontractile components. Forskolin, known to indirectly inhibit myosin light-chain kinase activity, and cytochalasin B were potent relaxants, suggesting a similar smooth muscle-like contractile mechanism for all three cell types.

Actin Cytoskeleton↗
PubMed1992

Maude Abbott Lecture--1991. The capillary then and now: an overview of capillary pathology.

The concept of capillary is traced through its historical development, beginning with the pathologic "synanastomoses" between arteries and veins as proposed by the ancient Greeks. Harvey assumed that arteriovenous connections existed but never saw them. Malpighi and van Leeuwenhoek were the first to observe the capillary circulation in vivo. In the 1800s, pathologists contributed two advances: a method for proving that capillaries have a structured wall (von Recklinghausen) and the notion of "capillary leakage" in inflammation (Cohnheim). Then physiologists took over for half a century (Starling, Krogh, Pappenheimer) until electron microscopy created a new viewpoint (Palade). Several topics of capillary pathophysiology are discussed: vascular labeling and the capillary as a privileged vessel; capillary versus venular leakage in inflammation; endothelial tone. The overview concludes with a summary of 15 pathologic events that may occur in capillaries.

Anatomy↗
PubMed1991

Lipid deposition and intimal stress and strain. A study in rats with aortic stenosis.

These experiments were designed to study the topography of lipid deposition in the stenotic aorta of hypercholesterolemic rats, and to correlate it with flow conditions and intimal stresses and strains studied in a scale biophysical model and in a computer model. A 69% +/- 5% stenosis was produced with a U-shaped metal clip. One month to 8 months later, the aorta was studied en face by light microscopy after fixation and lipid staining. The intima in the throat of the stenosis was almost completely free of lipid, whereas symmetric lipid deposits occurred as bands just above and especially just below the stenosis; elsewhere lipid deposits appeared to be random. The flow data obtained from the scale model showed that the intima in the throat of the stenosis was subjected to an increase of as much as 20 times in shear stress, whereas the lipid deposits just above and just below the stenosis were associated with asymmetric flow conditions: the proximal area corresponded to a region of rapidly increasing shear stress, the distal area to a region of low to normal shear stress and separated flow. A finite element computer model based on the aortic deformations indicated that the endothelium at the inlet and outlet of the stenosis is subjected to a symmetric pattern of elevated stresses and strains. These results indicate that 1) the pattern of lipid deposition can not be adequately explained by a hypothesis based solely on flow conditions, and 2) lipid deposits can develop in areas of increased fluid shear stress, decreased fluid shear stress, and increased intimal strains.

Animals↗
PubMed1990

Morphological and physiological characteristics of pancreas-specific venular permeability induced by Monastral blue B.

Leaky blood vessels in the microcirculation can be detected in vivo by injecting an animal with colloidal pigments such as Monastral blue B (MbB) or carbon black. We have previously used the MbB labeling method in the spontaneously diabetic BB/W or rat and detected increased vascular permeability restricted to the venules of the pancreas. We now report the morphological and physiological characteristics of this phenomenon in additional rat strains. Susceptibility to pancreatic labeling with MbB among strains was found to be a highly variable, heritable characteristic, but in no strain did vessels label in any organ other than the pancreas. Pancreatic labeling by MbB was dose dependent, was observed in both inbred and outbred rats, and was not related to major histocompatibility complex haplotype. Enhanced permeability was induced by MbB within minutes of its administration as a result of the formation of gaps between endothelial cells; these gaps then closed within 15 min. Pretreatment with silica or carrageenan, agents known to affect macrophage function, completely blocked pancreatic MbB venular labeling, but the effect was reversible over a period of several days. We hypothesize that presence of MbB in the pancreatic circulation induces organ-specific venular leakage either by a direct effect on pancreatic endothelial cells or via the local release of a mediator.

Animals↗
PubMed1979

Lymphocytes and monocytes in the aortic intima--An electron-microscopic study in the rat.

In an electron-microscopic survey of the aorta in the adult rat, white blood cells were found adhering to the intima; these were invariably lymphocytes or monocytes. Similar cells were also found beneath the endothelium. Counts were not made, but published data indicate that mononuclear cells lying over or within the rat aortic intima are approximately 1 for every 9 endothelial cells. This infiltration by blood-borne cells is interpreted as a pathologic event, possibly in response to a chemical message (antigen?) originating from the underlying media.

Animals↗
PubMed1979

A myofibroblastic tumor. Infantile digital fibroma (recurrent digital fibrous tumor of childhood).

Infantile digital fibromas are distinctive tumors both clinically and morphologically. A unique light microscopic features in the presence of intracytoplasmic, spherical, eosinophilic inclusion bodies. Previous electron microscopic studies have shown these bodies to consist of fibrils; bundles of fibrils have also been described in the cytoplasm. We have examined one such tumor, confirmed earlier findings, and established that the component cells are typical myofibroblasts. The latter are a variety of fibroblasts first described in granulation tissue; they are endowed with contractile properties and are characterized ultrastructurally by bundles of fibrils containing "dense bodies" such as are found in smooth muscle cells. Since our case is identical to those previously described, we propose that this tumor be called infantile digital myofibroblastoma.

Basement Membrane↗
PubMed1978

Ultrastructure of the myocardium after pulmonary embolism. A study in the rat.

The purpose of this study was to find out whether acute massive pulmonary embolism can produce myocardial changes visible by light and electron microscopy. Ww therefore produced pulmonary embolism in rats using plastic microspheres (diameter, 15 +/- 5 mu). Two experimental protocols were used: lethal embolism, with a dose of microspheres known to kill in 3 to 15 hours (these rats were killed after 1 hour), and sublethal embolism, with a dose compatible with 100% survival (these rats were killed after 24 hours). In both groups, the left ventricle was normal. The right ventricle showed two tyes of changes: a) A distinctive lesion of the myocytes, more diffuse after lethal enbolism and different from the "zonal lesion" of shock. It consisted primarily in a localized shredding of the myofibrillar system; hence, the name shredding is proposed. Earlier stages of this lesion were represented by focal dissolution of the Z line (Z lysis). The pathogenesis of these lesions appeared to be primarily mechanical. b) Necrosis was already apparent at 1 hour and was more extensive after 24 hours. The pathogensis of the necrotic lesions is best explained by a temporary ischemia followed by delayed reflow; a possible potentiating role of endogenous catecholamines cannot be excluded. Most capilaries in the necrotic foci remained functional; this explains the rapid rate of the healing process of such lesions. A comparison is drawn between the observed foci of necrosis and the human myocardial lesions knowns as "miliary infarcts" and "myocytolysis." It is proposed that a factor common to all three is the preservation of the microcirculatory vessels and that our experimental model helps illuminate the pathogenesis of the human lesions. It is concluded that the right ventricle of acute cor pulmonale may develop cellular changes with a complex pathologenesis (mechanical, ischemic, and possibly hormonal). The nature of the changes found in our model could represent the morphologic substrate of right-sided failure; it can be correlated with the electrocardiographic abnormalities found in the comparable human condition.

Animals↗
PubMed1977

Binding of anti-actin autoantibodies to platelets.

Normal platelets incubated with anti-actin autoantibodies (AAA) (from the serum of patients with chronic aggressive hepatitis) do not show binding of these antibodies as seen by indirect immunofluorescence. AAA serum does not inhibit thrombin-induced clot retraction, despite the binding of the antibodies to platelets in the clot. Similarly, AAA serum does not affect "reversible" or "irreversible" aggregation (induced by ADP, collagen or epinephrine), despite the binding of the antibodies to platelet actin under such circumstances. AAA also bind to platelets when aggregation is inhibited by EDTA. The incubation of "reversibly" aggregated platelet with AAA results in a small but definite binding of AAA to platelets. These findings suggest that during "irreversible" and/or "reversible" aggregation, changes take place at the surface of platelets which expose the antigen at the surface of the cell.

Actins↗
PubMed1977

Cell-to-cell herniae in the arterial wall. I. The pathogenesis of vacuoles in the normal media.

Vacuoles were observed by light microscopy in the smooth muscle cells of the media in normal rat arteries. By electron microscopy these vacuoles were limited by two membranes; they usually contained myelin figures, a few organelles (especially mitochondria and microfilaments), and an amorphous background material that varied greatly in density. Morphologic evidence indicates that these structures arise by herniation of one smooth muscle cell into another; it is presumed that herniation occurs during contraction at weak points corresponding to areas where adjacent cells come in close contact. Such cell-to-cell herniae were mostly seen in small arteries (arterioles) with a diameter of 0.4 to 0.2 mm; however, none was found in coronary arteries of this size. This discrepancy suggests that the pathogenesis of cell-to-cell herniae is correlated not only with the caliber of the artery but also with functional demands. (Am J Pathol 87:375-398).

Animals↗
PubMed1977

Effect of occlusion on large vessels. I. A study of the rat carotid artery.

The effect of permanent occlusion on the carotid artery of the rat was studied by light and by electron microscopy. A segment between two ligatures was examined at times from 2 minutes to 1 year. Between 2 and 15 minutes after occlusion, the red blood cells adjacent to the wall formed radially arranged rouleaux; within 24 hours the endothelium disappeared, while platelets (despite the lack of flow) accumulated against the denuded elastica. This behavior of formed blood elements may have been the result of electric forces (injury potential). By 3 days, undifferentiated cells were found lining the elastica interna or free in the lumen; they apparently were derived from medial smooth muscle.In the media, by 3 days some smooth muscle cells had become necrotic, while "undifferentiated" cells appeared; strong circumstantial evidence suggested that these were smooth muscle cells which had lost their specific characteristics and had thus become dedifferentiated (a phenomenon also known to occur in striated muscle cells); by 1 month they had matured into smooth muscle, but the media from then on contained fewer cells and more collagen than normal.In the lumen, the undifferentiated cells also matured into typical smooth muscle cells from 15 days onward, while collagen and elastin appeared between them. After 1 month these cells began to accumulate droplets of fat, which thereafter increased in number (at 6 months they were associated with cholesterol clefts) and then declined. This accumulation of fat in smooth muscle cells (also seen in atherosclerosis) was interesting because it occurred in the absence of blood flow.

Arterial Occlusive Diseases↗