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Thrombi with newly formed vessels in thirteen human umbilical arteries were studied. Red blood cells formed masses which were covered by fibrin within twelve hours after birth. By the second day, the intima including endothelial cells was denuded. In the junctional area between the thrombi and the original intima on the sixth day, red blood cells were surrounded by endothelial-like cells, which displayed junctional complexes and did not show any connection with intact endothelial cells. These cells also exhibited filaments with fusiform densities, suggesting a probable origin from vascular smooth muscle cells. Examination of older specimens indicated that these were precursor structures of functional capillaries found in mature thrombi. ACTA PATHOL. JPN. 34: 529–536, 1984.

Fresh breast and leg meat was collected from 11-wk-old pullets fed a high protein-low fat starter ration. Lipid oxidation measured in malonaldehyde (MA) equivalents in total fat extracted from meat, and in phospholipids (PL), triacylglycerol (TG), and cholesterol ester (CE) fractions of total fat was determined by an improved TBA assay with antioxidant protection. It was found that breast meat had two-fold less fat than leg. Breast fat contained 70.1% PL, 22.2% TG, and 1.2% CE; leg fat contained 42.9% PL, 51.4% TG, and 0.8% CE. After separation by thin layer chromatography, the individual lipid classes were tested for TBA reactivity. The PL fraction was found to contribute approximately 90% of the MA measured in total fat from chicken meat.

The major ovarian hormones (estradiol and progesterone), the major testicular hormone (testosterone), and the major precursor to steroid hormones (cholesterol) were fed ad libitum in various combinations for either 2 weeks or 2 months (56 days) to 5-day-old female chicks; the effects of these treatments on liver lipids and plasma lipoproteins were measured. After two weeks, chicks fed basal diet supplemented with 0.05% estradiol had significant increases in plasma total cholesterol, triglycerides, and phospholipids (P less than .01). The combined supplementation of 0.05% estradiol plus 1% cholesterol produced an additive increase in plasma total cholesterol resulting in levels higher than obtained by either treatment alone (P less than .01). The addition of 0.2% progesterone to the 1% cholesterol diet inhibited the accumulation of plasma cholesterol (P less than .05), liver cholesterol (P less than .01), and liver triglycerides (P less than .01), which were found in comparable animals fed only 1% cholesterol. Likewise, the addition of 0.2% progesterone to diet containing 0.05% estradiol inhibited (P less than .01) accumulations in all of the plasma lipid classes which were found in comparable birds fed only 0.05% estradiol. After 2 months feeding, 0.1% testosterone had no effect on plasma or liver lipids. The combination of 0.05% estradiol plus 0.1% testosterone for 2 months was not very effective in reducing the hyperlipidemia caused by estradiol alone, but this treatment did result in a peculiar dwarf chicken. The results demonstrate strong steroid sex hormone interactions which produce major changes in chick plasma and liver lipid metabolism.

Intimal thickening and lipid accumulation, which occur in atherosclerosis, were observed in fifteen human umbilical vessels. Quantification of lipid laden cells was done electron-microscopically. Within 1 month after birth, lipid laden cells originating from macrophages were observed in the umbilical artery, while those originating from smooth muscle cells were seen in the umbilical artery and vein. Lipid droplet formation appeared to be independent and different in macrophages and smooth muscle cells; the latter cells were stimulated to produce lipid droplets by hypoxia and the former cells by blood components.

Qualitative and quantitative changes in the human umbilical artery and vein were observed in 15 human specimens at different stages of development. Features such as intimal thickening and cellular lipid accumulation were found in umbilical vasculature. Cellular origin and quantification of lipid-containing cells were determined by electron microscopy. Within 1 month after birth, lipid-containing cells originating from macrophages were observed in the umbilical artery, while those originating from smooth muscle cells were observed in both the umbilical artery and vein. Lipid droplet formation appeared to be independent and different in macrophages and smooth muscle cells; the former cells were stimulated to produce lipid droplets primarily by plasma insudation and the latter cells primarily by hypoxia. These findings indicate that ultrastructural changes observed in closing umbilical vasculature may closely parallel and serve as a model for atherosclerotic changes which occur in mature vessels.

The effects of hereditary hyperlipidemia on coronary artery atherosclerosis were studied in 77 White Leghorn (DeKalb strain) chickens ranging from 4 to 13 months in age. After pubescence, the plasma levels of triglyceride and cholesterol in non-laying hens ranged 2- to 3-fold and 2- to 7-fold higher compared to layers. Serial sectioning revealed that most lesions were found in the proximal portions of both the left and right coronary arteries. Ultrastructurally, lesions in the roosters contained no foam cells, whereas some foam cells and small amounts of stainable lipid were observed in the thickened intima of layers. Half of the non-layers had stenotic lesions characterized by many foam cells, necrotic foci, and heavy stromal lipid deposits. Continuous permeation of excess plasma lipids into the arterial wall appeared to be an important factor in the development of coronary lesions.

Comparaison de 2 nouvelles methodes d'analyse de l'oxydation des lipides avec une methode classique, par distillation. La premiere methode utilise une extraction aqueuse, la seconde une extraction des lipides avant addition de BHT et mesure de l'indice TBA. La validite de chacune est testee sur de la viande fraiche, refrigeree ou congelee

Five-day-old female chicks were fed diets containing testosterone, estradiol, and cholesterol for 2 months. Cholesterol supplementation of 1 per cent. resulted in production of lipid vacuoles in the interlamellar connective tissue cells and to a lesser extent in the smooth muscle cells in the aorta; cholesterol had no effect on the coronary artery. The vasculo-toxic nature of estrogen was indicated when 0.05 per cent. dietary estradiol produced more accumulations of lipid vacuoles in smooth muscle cells, more extracellular lipid, and more smooth muscle cell death than cholesterol feeding. A dietary combination of cholesterol plus estradiol produced severe lipid deposition throughout the entire thickness of ascending aorta, and degenerative atherosclerotic changes in the coronary artery. Combined testosterone and estradiol supplementation resulted in peculiar dwarf chickens which exhibited increased vascular smooth muscle cell mitosis and degeneration.

Degenerative changes in endothelial and smooth muscle cells from fetal, 2-month-, and 6-month-old swine ductus vasculature were observed. In fetal ductus, a discontinuous internal elastic lamina and increased extracellular mucopolysaccharide deposition were initially noted. At 2 months of age, there was widespread fibromuscular intimal thickening, the appearance of modified smooth muscle cells, increased medial fibrosis, and the occurrence of cell debris and nuclear pyknosis. Early modification of smooth muscle cells was marked by increased occurrence of lysosomes, widely dilated rough endoplasmic reticulum, and Golgi bodies. Abundant aggregates of Weibel-Palade bodies occurred in early endothelial cell degeneration. At 6 months of age, after complete anatomical closure, there was abundant lipid vacuole production by degenerated medial smooth muscle cells. This study demonstrates that at various stages of occlusion, endothelial and smooth muscle cells from ductus vasculature exhibit morphological changes which are qualitatively similar to atherosclerosis.

Fibromuscular intimal thickening was seen in the ascending and thoracic aorta of the swine fed 62,500 IU of vitamin D3/kg of diet for three months duration; and after 3 months of vitamin D3 withdrawal, atherosclerotic lesions were found. In rabbits, pronounced aortic smooth muscle cell necrosis developed with the forced feeding of 10,000 IU vitamin D3 dissolved in corn oil/kg body weight/day for 14 days. Serum analyses indicated that blood calcium did not differ from that of animals fed corn oil alone, but that the level of serum 25-hydroxy-vitamin D3 measured by HPLC was 30 times that in the control animals. These data suggest that choleclaciferol (the oxidized sterol with vitamin D3 activity) has a very destructive influence on the integrity of arterial wall, and that smooth muscle cell necrosis could be caused by enhanced membrane permeability to Ca2+ following 25-hydroxy-vitamin D3 incorporation into smooth muscle cell membranes.

Partition coefficient analysis, equilibrium dialysis, and computer simulation were used to evaluate associations of twelve steroid hormones (androstanediol, androstenediol, androstenedione, androsterone, dehydroepiandrosterone, dihydrotestosterone, estradiol, estriol, estrone, hydroxyprogesterone, progesterone, and testosterone) with human plasma high density lipoproteins (HDL), low density lipoproteins (LDL), and very low density lipoproteins (VLDL). It was determined that partitioning of steroid hormones (SH) between the aqueous medium and the surfaces of lipoproteins (LP) was the initial (first order) SH-LP interaction. For some SH, especially dehydroepiandrosterone, significant second order interactions, which may involve chemical conversions, were detected. The first order binding values of the twelve SH with three LP were combined with the corresponding binding values of SH with sex hormone-binding globulin, corticosteroid-binding globulin, and albumin in a 6 X 12 matrix. The computer program TRANSPORT was used to analyze the matrix and determine the distribution of each SH among six different binding agents in the "normal" male. It was concluded that LP are important vehicles for SH conveyance in plasma and may also be important for SH entry into cells.

Specimens of ductus arteriosus and venosus from 2-month-old and 6-month-old swine were examined by electron microscope. The purpose of the study was to observe the effects of vessel closure and hypoxia on medial vascular smooth muscle cells. At 6 months of age, smooth muscle cells from the medial layer of ductus arteriosus showed signs of considerable cellular degeneration and contained lipid vacuoles which were often surrounded by granular endoplasmic reticulum. Specimens from the portal side of ductus venosus showed initial stages of smooth muscle cell degeneration and lipid vacuolization, while samples from the hepatic side of ductus venosus were nearly normal. This study contains the first reported morphological evidence of organelles in vascular smooth muscle cells which are responsible for endogenous lipid droplet production.

Ultrastructural and morphometrical studies were conducted on vascular tissue from 205 human Japanese specimens ranging in age from 15 weeks’ gestation to 90 years. Comparison of aorta size with overall body length by allometry revealed that the aging aorta has growth and involution stages comparable to other organs, and that progressive increase in aortic diameter was the major involutional change. The cellular and extracellular components of the medial sections of thoracic and abdominal aorta, renal artery, and superior mesenteric artery were quantitated from electron micrographs and compared at different ages. It was found that the renal artery rapidly accumulated extracellular material with increasing age; in the aortic tissue, however, the peak occurrence of extracellular material occurred at pubescence. Ultrastructural studies revealed a general tendency of aging medial smooth muscle cells to transform from a smooth, rounded morphology to become irregularly shaped.