Myointimal Cells Research Articles

Über die Organisation von Thromben nach Arterienverletzungen durch wandernde 4. Larvenstadien von Strongylus vulgaris beim Pferd (licht- und elektronenmikroskopische Untersuchungen)

Migrating fourth-stage larvae of Strongylus vulgaris, a parasite of equines, damage the intima of the anterior mesenteric artery and its larger branches and induce thrombus formation on the injured sites. As the time of larval passage through each of these branches has been exactly determined in earlier experiments, the aim of the present studies is to contribute to a more complete understanding of repair mechanisms in the process of time after thrombotic vascular injuries. five foals were separated individually to specially cleaned stables and given anthelmintic treatment till the age of one year. One foal was infected per os with 350, the second with 500 and the remaining three with 1,000 third-stage larvae of Strongylus vulgaris...

Platelet embolic injury; the healing process

The impaction of emboli composed mainly of platelets at the bifurcation of arterioles in the renal cortex has been shown previously to produce severe endothelial injury and lipid accumulation in arteriolar smooth muscle, followed by a marked thickening of the intima. In this study magnesium aluminum wire was inserted into the rabbit aorta as a source of emboli composed of platelet aggregates. The healing of renal arteriolar lesions produced by the emboli was examined at intervals from 3 to 21 days. The distinctive electron microscopic features of the mononuclear cells, endothelial cells, and smooth muscle cells were described. The mononuclear cells were found to remove fibrin, red cell and platelet remnants, and to produce a mucopolysaccharide matrix. Endothelium then grew into the matrix displacing the monocytes. Lipid in smooth muscle was always associated with myofilament fragmentation and mitochondrial vacuolization suggesting that the lipid accumulation is a result of injury. Plaques of concentric intimal thickening were found to consist of condensed matrix and myointimal cells. At each stage the cell types remained distinctive and there was no suggestion that monocytes are transformed to endothelial cells. These lesions serve as a model for some of the features of the encrustation concept of atherosclerosis, in that intimal thickening follows on thrombosis, in this case thromboemoblism and is associated with lipid accumulation in smooth muscle cells. The injury begins with endothelial damage and disruption. The subsequent intimal thickening resembles the vascular lesion in chronic allograft rejection and malignant nephrosclerosis and also involves the intertubular arterioles and small arteries of the kidney.

Ultrastructural intimal changes in the rabbit aorta after a moderate carbon monoxide exposure

<h2>Abstract</h2> <ul><li>1.(1) Eight rabbits were fed a normal diet and placed in exposure chambers. Four were exposed to 0.018 vol. % carbon monoxide for 2 weeks, while the other 4 served as controls and were exposed to atmospheric air. At the end of the study tissue from arch and thoracic aorta was taken for transmission and scanning electron microscopy.</li><li>2.(2) The luminal aortic coats of the experimental animals showed pronounced changes, characterized first of all by a severe edematous reaction with extensive swelling, formation of subendothelial blisters, and plaque formation. Furthermore, the myointimal cells showed vacuolation and occasionally the endothelial cells showed severe degeneration with cytolysis and condensation. Apart from actual plaque formation, the surface structures were markedly swollen and irregular. Occasionally spotty or streaky lesions occurred, where the normal folding architecture had changed into a characteristic "cobblestone-like" picture formed by protruding, grossly edematous endothelial cells.</li><li>3.(3) The results support earlier findings of toxic effects of low concentrations of carboxyhaemoglobin on the arterial walls, thereby provoking increased endothelial permeability and formation of edema, leading to changes indistinguishable from early atherosclerosis.</li></ul>

Ultrastructure, fatty acid content, and metabolic activity of foam cells and other fractions separated from rabbit atherosclerotic lesions

Abstract Foam cells and other fractions, separated after incubation of atherosclerotic aortas from cholesterol-fed rabbits with collagenase and elastase, have been investigated with respect to their ultrastructure, cholesterol ester and phospholipid fatty acid composition, DNA content, and metabolic activity as indicated by the uptake and incorporation of 14C-labeled oleic acid into combined lipid. These studies were concerned with obtaining some information regarding the structural integrity and nature of the isolated foam cells obtained by this method and with determining whether significant breakdown of such cells occurred during the isolation procedure. The foam cell fraction contained typical foam cells with numerous large lipid vacuoles. All cells contained some evidence of myofilaments. The particle fraction (25,000g, 15-minute deposit) consisted disrupted cell organelles, while the remaining fractions appeared to contain more free lipid and liposomes. Both the cholesterol ester and phospholipid fatty acid composition of the particles resembled that of the cells. When 14C-labeled oleic acid was incubated with the various fractions, significant metabolic activity with respect to uptake of oleic acid and its incorporation into cholesterol ester and phospholipid occurred in the particle fraction, but not in the lipid skin fraction (25,000g, 15-minute floating fat layer). Determination of the DNA content of the cells and other fractions indicated that of the DNA present in the original intima, less than 20% was recovered in the foam cells isolated. The data obtained were consistent with the conclusion that the cells isolated were structurally intact, consisted primarily of myointimal cells and that significant breakdown of foam cells had occurred during the isolation procedure.

A dynamic pathology of atherosclerosis

Currently available evidence indicates that atherosclerosis of large and medium arteries is associated with the influx and trapping of low-density plasma lipoprotein within the myointimal and medial cells of the arterial wall. Many factors, including hyperlipemia, hemodynamic arterial injury and hypoxia, hasten and facilitate this process, but too little is known of the factors and mechanisms responsible. The role of local platelet aggregation in initiating localized vascular injury and increased vascular permeability is yet to be fully clarified. Blood vessels can no longer be viewed as mere blood conduits. They are composed mainly of actively metabolizing smooth muscle cells, which have a wide range of metabolic potentialities, summarized diagrammatically in Figure 6. An understanding of the metabolism of these cells is central for an appreciation of the pathogenesis of atherosclerosis for it is within these cells that low-density lipoprotein is first entrapped and accumulates. These cells, especially in the deeper layers of the inner media, exist on the brink of hypoxia and are therefore particularly susceptible to a variety of noxious stimuli. The exact identity of the factors responsible for the initiation of a particular smooth muscle cell response to injury remains unknown. However, from the experimental evidence of the characteristic smooth muscle cell response to various food fats it seems likely that certain components of the low-density lipoproteins in appropriate experimental animals elicit the typical vascular response associated with the feeding of a given food fat. Identification of the lipoprotein components important for the development of a particular cellular reaction pattern is a major problem in atherosclerosis research. A thorough study of the enzymatic potentialities and responses of smooth muscle cells is necessary for at least three reasons: 1.(1) Detailed knowledge of the metabolic characteristics of these cells will be provided. 2.(2) Such studies may also uncover a suitable quantitative measure of the incipient atherosclerotic process—a measure which would be most useful for experimental elucidation of the early pathogenesis of this disease. 3.(3) It is through such studies that we can hope to gain a better appreciation of the potentialities for dealing with this serious health hazard.

Myointimal cells as a possible source of replacement for endothelial cells in the rabbit.

Regeneration of damaged endothelium has been studied by means of mechanical injury to rabbit abdominal aorta and inferior vena cava. Ultrastructural evidence suggests that myointimal cells can become endothelial cells. It is postulated that such a myogenic replacement of endothelial cells may occur under normal circumstances in the aorta. Injury to blood vessels merely accelerates this process.

Ultrastructural changes of large rabbit blood vessels following mild mechanical trauma

The morphological changes of the abdominal aorta and inferior vena cava were studied from one to seven days following application of mild mechanical trauma (compression of the vessel wall with a clamp covered by rubber tubing). Both light microscopy of silver-stained surface preparations and electron microscopy of sectioned vessels were performed. The following morphological changes were observed in both the vena cava and abdominal aorta at all time sequences investigated: focal necrosis, abnormal overlapping of endothelial cells and pseudopod-formation from them usually directed into the lumen; and pseudopod-formation from medial smooth muscle cells, often passing into the intima via fenestrations in the elastic membrane. Leucocytes accumulated in the vessel wall only in the vena cava, whereas the ground substance increased only around myointimal cells of the aorta. The genesis and significance of the above changes are discussed.

In vitro studies of phospholipid synthesis in experimental atherosclerosis. Possible role of myo-intimal cells.

Using in vitro techniques and labeled linoleic acid and glucose, alterations in phospholipid synthesis in the aorta were correlated with electron microscopic studies at various intervals of time after feeding rabbits cholesterol. After 4 to 8 weeks of feeding, more phospholipid precursors were incorporated into the phospholipids of atherosclerotic blood vessels than of normal vessels. Concomitant with the metabolic alterations, the following ultrastructural changes occur. Smooth muscle cells of the plaque (myo-intimal cells) evolve into highly vacuolated cells containing a profusion of cytoplasmic organelles. The increase in membranous organelles suggests that the increase in phospholipid synthesis may be the result of a cellular requirement for increased intracytoplasmic structural phospholipid.