Effect of soysterol on experimental atherosclerosis in rabbits fed cholesterol diet for 24 weeks was investigated. The doses of cholesterol and soysterol was 0.3g/kg and 1.2g/kg body weight, respectively. In cholesterol treated group, serum cholesterol and serum phospholipid increased to 1, 800mg/dl and 800mg/dl at 8th week, respectively. After 9th week, they however did not increase. In soysterol and cholesterol treated group, the increase in both serum lipids were inhibited prior to 14th week. On the other hand, the volume elastic modulus (Ev value) obtained by the non-invasive optical measurement was found to increase with the increases in transmural pressure (40 and 60mmHg) in cholesterol treated group. This increased Ev value was inhibited in soysterol and cholesterol treated group. The increased atherosclerotic legions were also inhibited in soysterol and cholesterol treated group. Total cholesterol, phospholipid and hydroxyproline contents in the vascular wall, those increased in cholesterol treated group, were inhibited in soysterol and cholesterol treated group. These data show that soysterol inhibits the hyperlipidemia and atherosclerosis induced by high cholesterol diet.

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Arteriosclerosis is a silently progressive disease for a long period of time. To elucidate the initial changes, whether pathological or not, might be very useful to prevent its progress. Therefore the left main trunk and the proximal portion of the left anterior descending artery in eleven cases of newborns, composed of four cases of extremely immature newborns, three cases of newborns with very low birth weight, a case of low birth weight newborn, and three cases of mature newborns, died in and about the day of birth were examined light and electron microscopically.
Not only discontinuation and splitting of the internal elastic lamina but also factor VIII related antigen suggests that intimal thickening is not an artificial but a really organic change. The absence of the intimal changes mentioned above in the interlobar arteries of the kidneys, muscular arteries as large as the proximal portion of the coronary arteries, proved that they are independent of postmortem autolysis. Since degrees of the intimal changes are independent of duration of the life, they may manifest themselves in the gestational period. In some cases with fairly marked eccentric intimal thickening the change may play a role of a congenital predilection for ischemic heart disease, lowering the threshould of clinical manifestation of the disease due to luminal stenosis in the other points of the artery.

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In order to elucidate the role of apolipoprotein H in lipoprotein metabolism, we determined plasma apolipoprotein H levels in patients with various types of hyperlipoproteinemia by the SRID method. The relationships of lipoprotein lipid and the other apolipoprotein levels to apolipoprotein H levels were also investigated. The mean plasma apolipoprotein H level in 14 patients with only hypercholesterolemia (T-Ch≥250mg/dl) was 24.2±6.4mg/dl and did not differ from those in 22 healthy subjects (21.9±2.4mg/dl). However, the mean plasma apolipoprotein H level in 14 patients with both hypercholesterolemia and hypertriglyceridemia (T-Ch≥250 and TG≥180mg/dl) and in 36 patients with only hypertriglyceridemia (TG≥180mg/dl) were 26.5±4.9 and 25.6±6.5mg/dl, respectively, and significantly higher than healthy subjects (p<0.01, p<0.02). Even in hyperlipoproteinemic patients, the mean plasma apolipoprotein H level of the patients with liver disease was significantly lower than those mean level in patients without liver disease (23.7±4.2 versus 26.6±5.9mg/dl, p<0.05). Apolipoprotein H levels showed a positive correlation between triglyceride, apolipoprotein C-II, C-III and E levels (r=0.344, p<0.01; r=0.332, p<0.02; r=0.482, p<0.001; r=0.330, p<0.02, respectively).
These results indicated that apolipoprotein H levels varied with TG-rich lipoprotein levels. On the basis of the data and previous investigations (Nakaya, et al.) in which apolipoprotein H acts as an activator of lipoprotein lipase, it was suggested that apolipoprotein H may play an important role in TG-rich lipoprotein catabolism. In addition, liver function may play a role in the changes of apolipoprotein H levels.

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