By a modification of the Byrom's method, forceful repeated injections of physiological saline or 7% gum arabic-added physiological saline (having the same viscosity with blood) was made in rats through the left carotid artery toward the aorta in order to elicit sudden rise of intra-arterial pressure.
As the result, fibrinoid degeneration and medial necrosis were found in arteries of the kidneys, pancreas and mesentery. These lesions were quite different from each other. Namely, the former was stained dark blue with PTAH (phosphotungstic acid hematoxylin), negative in fat stain, and originally developed in the intima, while the latter was unstained with PTAH, positive in fat stain, and derived from degeneration and necrosis of medial smooth muscle cells.
In arteries of animals survived a long period (4-6 weeks), after the injections, fibrocellular intimal thickening was found as a sign of healing of the fibrinoid degeneration.
When unilaterally nephrectomized rats were given 1 % saline solution as drinking water for one year, hypertension was occurred, and fibrocellular intimal thickening and fibrinoid degeneration were seen in arteries of the mesentery and kidneys.
It was concluded that fibrinoid degeneration, medial necrosis and fibrocellular intimal thickening were experimentally produced in arteries by abrupt elevation of intra-arterial pressure.

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In hypertensive rats at 615 weeks after bilateral constriction of renal arteries, the mesenteric arteries grossly presented nodose appearance (periarteritis nodosa) and histologically showed fibrinoid degeneration. These animals were intravenously injected with I¹³¹-labeled rat plasma protein, I¹³¹-labeled rat or bovine fibrinogen, radioacive chromic chloride (Cr⁵·Cl₃ ; for the purpose of labeling plasma protein with Cr⁵¹ in vivo), or radioactive colloidal suspention of metallic gold (Au¹⁹⁸), and degree of insudation of these proteins or colloidal gold into arterial wall was investigated by measuring radioactivity of the mesenteric arteries in three ways with the following results :
1) Determination with a scintillation counter revealed remarkably higer radioactivity in the mesenteric arteries of hypertensive rats with bilaterally constricted renal arteries than in those of normal controls, indicating that a large amount of I ¹³¹-plasma protein, I¹³¹-fibrinogen, Cr⁵¹-plasma protein, or colloidal Au¹⁹⁸ had insudated into arterial wall of the former.
2) Microautoradiographs disclosed high radioactivity restricted to nodose lesions which represent fibrinoid degeneration.
3) Microautoradiographs showed radioactivity in areas of fibrinoid degeneration and edematous lesions in the intima and media, indicating the presence of I¹³¹-fibrinogen or I¹³¹-Plasma protein in these lesions.
It was concluded that the permeabilily of the blood-arterial wall barrier was markdly increased in rats with bilaterally constricted renal arteries, and that in arterial fibrinoid degeneration there was conspicuous insudation of blood plasma protein and fibrinogen into the arterial wall, and in fibrinoid substanse these proteins were present as its constituents.

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1. Fibrocellular intimal thickening was produced in the left carotid arteries of rats by single ligations of them. At 2 days10weeks after the ligations, the animals were intravenously injected with thymidine-H³ and sacrificed 3 hours after the injections. And labeled and radioactive cells (proliferating cells) were autoradiographically investigated.
At 2 days after the ligation, intimal cells were not yet observed, but endothelial cells were remarkably proliferated (radioactive index, RI, i. e. % labeled cells : 6.1). At 4 and 8 days after the ligation, one to several layers of intimal cells appeared. Endothelial cells of the arteries were considerably proliferated (RI : 3.1), and the intimal cells were more conspicuously proliferated (RI : 7.5). At 5 and 10 weeks after the ligation, radioactive index of endothelial cells was 1.7, and that of intimal cells 0.6. At 2 days10 weeks after the ligation, smooth muscle cells of the media showed scarcely any proliferation (RI : 0.1). In normal control arteries, there was scarcely any proliferation of endothelial cells and medial smooth muscle cells (RI : 0.14 and 0.08).
From these results, the intimal cells are assumed to be derived from endothelial cells.
2. Thrombi formed in the vicinitiy of the ligation were investigated with the aforementioned method. The autoradiographical findings suggested that most of fibroblasts organizing the thrombi were considered to be derived from the arterial endothelial cells in the neighborhood of the formed thrombi.
3. The so-called atherosclerosis was formed in the thoracic aorta of rabbits by feeding a diet containing 1% cholesterol and 5% lard for 4-24 weeks. Slices of the aorta with lesions were incubated for 3 hours (37°C) in thymidine-H³-added whole blood or thymidine-H³-added blood plasma from these animals, and labeled cells (proliferating cells) were autoradiographically investigated.
In the animals fed with cholesterol for 4 or 7 weeks, endothelial cells and intimal cells were proliferated, but there were no radioactive cells in the media. At 13 or 24 weeks feeding, endothelial cells and cells of the superficial layer of the intimal (fibrocellular cap) were proliferated, but not in the medial cells.
In normal control rabbits, scarcely any proliferation was observed in endothelial cells and in the medial smooth muscle cells.
It has thus found that in the formation of mass of foam cells, endothelial cells and cells of the superficial layer of the intima are proliferated. Accordingly it was assumed that most of foam cells are derived from endothelial and intimal cells.

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1. In Salmonella group A there was no difference in sugar components between S. paratyphi A 1015 [1, 2, 12], which has phage-mediated antigen 1, and S. partyphi A var.durazzo [2, 12], which lacks it. Both strains contained galactose, glucose, mannose, rhamnose, paratose, hexosamine, and N-acetylhexosamine. The antigenic determinant of O-antigen I was Considered to be α-glucosyl- (1→6) -galactose-mannose-. The antigenic determinant of O-antigen 12, whlch is related to the infection of phage iota, was assumed to be α-glucose- (1→4) -galactose-mannose-rhamnose by many workers. However mannose was considered to play an important role as the antigenic determinant of O-antigen 12.
2. In Salmonella group E there was no difference in sugar components between S. anatun [3, 10], S. newington [3, 15], and S. thomasville [(3), (15), 34] which have different phage-mediated antigens. These strains all contained galactose, glucose, mannose, rhamnose, hexosamine, and N-acetyl-hexosamine. The antigenic determinants of O-antigen 10 and 15 were considered to be, respectively, α-galactosyl-mannosyl-rhamnose and β-galactosyl-mannosyl-rhamnose to both of which glucose were linked. In the case of phage conversion from O-antigen 3, 10 to 3, 15, it was considered that the change from α-anomer to β-anomer occurred in the antigenic end-determinant. The antigenic determinant of O-antigen 34 was considered to be α-glucosyl- (1→4) -β-galactosyl-mannosyl-rhamnose. In the case of phage conversion from 3, 15 to (3), (15), 34, it was considered that β-anomer of the galactose as the end determinant in O-antigen 15 was modified by the addition of an α-glucose with 1→4 linkage.
3. In Salmonella group C, galactose, glucose, hexosamine, and N-acetylhexosamine were demonstrated in the polysaccharide of S. kentucky [(8), 20] and galactose, glucose, mannose, rhamnose, abequose, hexosamine, and N-acetylhexosamine were demonstrated in the polysaccharide of S. newport var. puertorico [6, 8]. The antigenic end determinant of phage-mediated antigen 20 was considered to be the sugar like N-acetylglucosamine.

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