The purpose of this study was to establish experimental arteriosclerosis in rabbit, not by hypercholesterolemia but by normolipidemic method, and further to investigate whether or not sclerotic arteries of rabbits by this method have the same properties in the function (viscoelastic properties) and the structure as human arteries with arteriosclerosis. The materials used consisted of 118 rabbits including 75 sclerotic rabbits and 277 cases dissected. Arteriosclerosis of rabbits were induced by the following two methods, namely injury method using 0.1% epinephrine injection and hypoxic method using pure nitrogen gas inhalation. In each material, basic data such as body weight, length of aorta, diameter and thickness of thoracic aorta were measured and also examined were aortic pulse wave velosity (PWV) showing viscoelastic property of arterial wall and medial elastin content of thoracic aorta as a factor of the structure of arterial wall.
Results
1. In comparison with human aorta, rabbit aorta was relatively longer and slender, and the ratio of the length of abdominal aorta to thoracic aorta was higher than that of human aorta. But the ratio of thickness to diameter was almost same in both materials.
2. In the control group, mean value of PWVs was 7.3m/sec in human and 5.7m/sec in rabbit. PWV of sclerotic group was higher than that of control group and human gave higher values than rabbits.
3. In control group, the mean value of medial elastin content of human thoracic aorta was 34v/v% and the corresponding value of rabbits was 44v/v%. The value was poorer in the sclerotic group than in the control group, and in human than in rabbits.
4. The relationship of PWV—1/Elastin in human and rabbit showed almost the same tendency, as PWV increased along with a decrease of medial elastin content, and so, in the final analysis, we could not distinguish human and rabbit in this respect. Namely, we could say that, from a view point of the function and the structure, both arteries had almost the same character.

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A series of 203 specimens of human aorta was investigated by three different procedures of detecting and quantitatively determining sclerotic lesions, i. e. examination of the pathological findings of intima by point counting method, measurement of the medial elastin content by the MSP procedure and measurement of the mechanical properties of the wall by the pulse wave velocity, in order to assess the interrelationship between the ageing-related trend and individual characteristics of the various factors, and between the pathological changes of the aortic intima, media and elastic properties of the wall. (MSP: Microspectrophotometry)
1. In subjects below 40 years of age neither the tunica intima nor the tunica media was observed to show any noticeably sclerotic changes. Nor were there any significant individual variations.
2. Demonstrable sclerotic changes of these layers of the aorta were noted to appear and progress, in keeping with advancing age, in those over 40 years of age. Individual variations of the progress of those changes were prominent.
3. There was evidence of diminution of medial elastin content, proceeding the development of atheromatous plaques in the intima.
4. The degree of intimal and medial sclerotic changes was noted to be remarkably correlated with the pulse wave velocity.

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As the noninvasive indices of arteriosclerosis, the pulse wave velocity and the volume elasticity have been usually used. But there is a possibility that these indices are influenced by the functional factors as well as organic factors. The purpose of this paper is to investigate the validity and the limitation in the use of these parameters as the indices of arteriosclerosis.
The subjects were composed of 86 younger cases with normotension, 18 younger cases with hypotension and 37 old-aged cases with normotension. Hemodynamic analysis was performed in supine position with Wezler's method. Furthermore, in younger hypotensive cases, such analysis was performed at active standing position to examine the influence of the tonus of the autonomic nerve on the pulse wave velocity and the volume elasticity.
In the relation between the pulse wave velocity and the total peripheral resistance of the normotensive cases in supine position, the pulse wave velocity showed a tendency to increase in propotion to the total peripheral resistance with a little dispersion, and the value of the pulse wave velocity was at higher level in the old-aged group than its corresponding value to the total peripheral resistance in the younger goup. The same relation was appreciated in the relation between the volume elasticity and the total peripheral resistance. And the results that some cases of the younger group showed the considerable high value of the pulse wave velocity, and that the pulse wave velocity had the moderate positive correlation to the total peripheral resistance which is influenced by functional and organic changes suggest that the pulse wave velocity and the volume elasticity were altered by the organic and functional factors. In the active, standing position in hypotensive younger cases who had no clinical sign of arteriosclerosis, the pulse wave velocity increased obviously. Changes in cardiac output little influenced upon the pulse wave velocity and the volume elasticity.
In conclusion, the volume elasticity and the pulse wave velocity are the indices of vascular rigidity. But the rigidity is influenced by the functional factors as well as the organic factors, and especially the pulse wave velocity is affected by the vascular rigidity, the intravascular pressure and many other factors. Consequently it is necessary to estimate these indices carefully.

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The relationship of urinary low-molecular binding hexoses to hypertension or diabetes has been reported by our clinic.
The binding hexoses in urine were fractionated into FrI, FrII and FrIII by Sephadex G-100 column chromatography. The molecular weight of the three fractions was in the order of FrI>FrII>FrIII. Though there was much low-molecular binding hexose (FrIII) in urine, there was little in serum and blood corpuscles.
By the column chromatography, the FrIII was demonstrated as a clear peak in the extraction of the renal cortex, but only as an unclear one in that of the renal medulla.
The FrIII of urine or renal cortex obtained by Sephadex G-100 column chromatography was then divided into four fractions by Sephadex G-15 column rechromatography, the patterns of which were similar in both materials.
The molecular weight of the first peak in the Sephadex G-15 chromatography was thought slightly larger than that of raffinose.
It is concluded that the renal cortex seems to be one of the main sources of the FrIII in urine.

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With recent progress in knowledge of the structure and function of apolipoproteins, much attention has been paid to the significance of apolipoprotein-B (apo-B) in the pathogenesis of atherosclerosis. From this point of view, we attempted to establish the procedure of the double antibody radioimmunoassay of human apolipoprotein-B, the dominant apolipoprotein of low density lipoprotein (LDL). LDL (d: 1.025-1.050) was obtained from healthy adult men by sequential ultracentrifugation. Antiserum was prepared from rabbits biweekly immunized with LDL and stored at -70°C. The sera yielded a single immunoprecipitin band with LDL and also with human whole sreum on double immunodiffusion and immunoelectrophoresis. Radiolabelled apo-B which was iodinated with ¹²⁵I by chloramin T method and purified Sephadex G-200 column, could be bound by the antibody. The radioimmunoassay sensitivity for LDL using this radio-apo-B was from 0.5 to 3μg. Specifisity of the immunoassay for apo-B was established by displacement curves of very low density lipoprotein (VLDL), LDL and whole serum, both of these curves were to be parallel to the standard curve.

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1) Monoglyceride hydrolase (MGH) from human post-heparin plasma was purified 535-fold by the removal of triglyceride lipase-substrate complex and affinity chromatography on Sepharose 4B column containing covalently bound heparin.
2) The partially purified enzyme was highly unstable. This enzyme preparation could be stabilized by the addition of either glycerol to a final concentration of 20% or albumin of 1%.
3) Bile salts, triglyceride, phospholipid and serum markedly inhibited the enzyme activity.
4) Effect of preincubation with NaCl on MGH activity was similar to that on hepatic triglyceride lipase. On the contrary, effect of protamine sulfate was same as that on extrahepatic triglyceride lipase.
5) The physiological significance of post-heparin MGH are discussed in relation to the mechanism of triglyceride lipase reaction and to the breakdown of monoglyceride at the membrane of adipose cells.

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The conventional diet in Japan is characterized by high carbohydrate-content. Our previous reports represented that the diet impaired catabolism of very low density lipoprotein (VLDL). In this study, hyperlipidemia with plasma cholesterol reduced by low caloric diet has been divided into three groups according to VLDL-triglyceride concentration (under 180mg/100ml, between 180 and 260mg/100ml, and over 260mg/100ml) for clarifying characteristics of plasma lipoprotein metabolism in hyperlipidemia.
Fifty-two hospitarized subjects consumed the formula diet, which was 1000 calories containing 140g of carbohydrate and 80g of protein, for four weeks. Blood sample was drown in the morning after overnight fast at the beginning of the diet therapy and at the 4th week after the diet therapy, and plasma lipoprotein was separated by preparative ultracentrifugation.
Range of plasma cholesterol levels before treatment were similar in three different triglyceride concentration groups and group with plasma cholesterol unchanged by the diet (non effective group), and mean difference of plasma cholesterol reduced by the diet were also similar in three different triglyceride concentration groups. Decreased plasma triglyceride levels were in proportion to each initial levels. In the groups with VLDL-triglyceride levels over 180mg/100ml and also non effective group, VLDL-triglyceride was significantly decreased with decreasing in VLDL-cholesterol. The results were suggested that much calory-in-take especially from carbohydrate might be a major determinant of VLDL in plasma lipoprotein metabolism.
On the other hand initial value of free cholesterol in VLDL was 27.9% and 31.1% in group with VLDL-triglyceride level under 180mg/100ml, and non effective group, respectively. These values were low as compared with other groups. Additionally, these low values became similar after the diet therapy. So we suggest that conversion of VLDL to LDL might be controlled by the rate of exchange of free cholesterol with esterified cholesterol rather than hydrolysis and removal of VLDL-triglyceride. Namely, excess triglyceride in VLDL might inhibied the release of free cholesterol from VLDL, and then VLDL catabolism itself was impaired.
There was decreased in triglyceride of low density lipoprotein (LDL) with a decreasing cholesterol in only group with VLDL-triglyceride between 180 and 260mg/100ml. In the group with VLDL-triglyceride under 180mg/100ml only cholesterol in LDL decreased. On the other hand cholesterol level was reversivily increased by the diet therapy in group with the highest VLDL-triglyceride. These results might be suggested that there existed in two different mechanism for LDL carabolism.

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Effects of hypovitamin C on lipid contents in serum, aorta and liver were studied. Guinea pigs were made hypovitamin C by scorbutogenic diet (group 1) or cholesterol added scorbutogenic diet (group 3) for two weeks. The control for the experimental animal was fed with the similar diet and supplemented with 25mg of vitamin C daily (group 2 and 4).
Total lipids in the serum, liver and aorta were estimated with conventional methods desceribed elsewhere. Serum lipoprotein were divided into high density lipoprotein (HDL) fraction, and low plus very low density lipoprotein (LDL+VLDL) fraction with Burstein's heparin sedimentation method. Lipid constituents in the two lipoprotein fractions were separated with thin layer chromatography following the method of Stahl, and determined lipid content of the each subfraction by densitometry.
Serum lipids of group 1 were significantly elevated as compared with the control. An increase of cholesterol and phospholipids observed in group 3 was partially prevented by vitamin C administration (group 4) as shown in Fig. 1. There was no statistical difference of lipid content in both HDL and LDL+VLDL fraction between group 1 and 2. Significant decrease of all of the lipid constituents in HDL and an increase of total lipids, free cholesterol, triglyceride in LDL+VLDL were observed in cholestrol fed hypovitamin C (group 3) animals as shown in Fig. 2. The content of lipid in the aorta was also elevated in group 3 (see Fig. 3), while slight decrease of hepatic lipid content were observed in group 3 (Fig. 4).
These findings suggest that vitamin C plays an important role of lipoprotein metabolism. High dose of cholesterol intake and existance of hypovitamin C may induces an increase of LDL+VLDL, and promote lipid deposition in the aorta and finally enhance the progress of aherosclerosis.

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It has been recognized that serum lipids play the important rolls to the development of atherosclerosis, and many studies about hyperlipidemia have been made from the aspects of the lipid metabolism, epidemiology and pathology.
Ninety ambulatory patients, in Urban residents consist of 25 male and 25 female with age range of 30 to 90 year-old, and suburban residents (fishing village) consist of 15 male and 25 female with age range of 34 to 80 year-old, have been followed up for full 2 years, from April 1973 to March 1975, to survey the serum total cholesterol levels and its seasonal changes between the two groups and to check relationship to coronary heart disease, hypertension, obesty and other diseases.
1) The serum total cholesterol level of patients in urban and suburban residents were essentially unchanged (Fig 1).
In large city; 235.8±35.9mg/dl→204.8+33.3mg/dl
In fishing village; 206.8±37.0mg/dl→217.0+39.1mg/dl
2) There were no remarkable changes in serum total cholesterol levels depended upon basic diseases.
3) Fifty-five of ninety (60 percent) showed unstable levels of serum total cholesterol (Labile group).
4) Thirty-five out of ninety (40 percent) showed nonseasonal change (nonseasonal labile group).
These results indicate that it is neccessary to check the serum cholesterol levels more frequently to decide if hyperlipemia exists or not.

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This paper deals with the relationship between serum lipoprotein electrophoretic pattern and serum lipids in case with hyperlipidemia. Heparin was injected intravenously hyperlipidemic patients with diabetes mellitus, coronary sclerosis, and cerebral thrombosis. All of subjects showed serum total lipids of more than 500mg/dl. The blood was collected before, 15, 30 and 60min after heparin injection. The lipoprotein electrophoresis on cellulose acetate and chemical analysis of serum lipids were done.
The patterns of lipoprotein electrophoresis were classified into five types by pre-β band findings: type A having small pre-β band; type B, wide pre-β without dark staining; type C, wide pre-β with dark staining; type D, wider pre-β migrating into α band; type E, less dark staining in pre-β with wide α band. Triglyceride concentration was lowest in type A, and rising in types B, C, D and E order. The density of faster mobility in pre-β band increased corresponding with hypertriglyceridemia. After heparin injection, however, the density of this band showed to decrease and the mobility became slower. Namely, the change of type C electrophoretic pattern induced by heparin injection was showed to resemble the pattern of type III. Type A was often observed in diabetics without vascular complication, types A, B and C in diabetics with vascular complication, types B, C and D in patients with coronary sclerosis, types C and D in patients with cerebral thrombosis. The density of pre-β band was stronger in patients with less post heparin lipolytic activity, and few of these cases showed the decrease of pre-β band exceeding more than 60% after heparin.
In hyperlipidemia, the mobility of pre-β band got increase in parallel with triglyceride concentration. After heparin injection, the mobility and the density of pre-β band were decreased.

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Analysis of serum lipoprotein was performed in normal subjects and patients with ischemic heart disuse, cerebral arteriosclerosis, cholelithiasis and obesity.
There were several differences between male and female; (1) Female showed a significantly higher level of α-lipoprotein cholesterol and a lower β/α ratio than male. (2) An increase in β/α ratio took place with an increase in concentration of total serum cholesterol in male but there was no correlation between total cholesterol and β/α ratio in female.
Not only in ischemic heart disease which is usually accompanied with hypercholesterolemia but in cerebral arteriosclerosis, cholelithiasis and obesity, even if the serum cholesterol level was in normal range, the concentration of α-lipoprotein cholesterol in serum was lower and the β/α ratio of lipoprotein cholesterol was significantly higher than in normal subjects.
The effect of estrogen on serum lipoprotein was followed in six hypercholesterolemic subjects (Type IIa). α-Lipoprotein cholesterol was increased and the β/α ratio decreased in two female at early climacteric stage. But, two male and two aged female did not show a change in serum lipid pattern.
Following the weight reduction in obese patients, there were decreases in total cholesterol, β-lipoprotein cholesterol and triglyceride and an increase in α-lipoprotein cholesterol.

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Total cholesterol levels in serum α-lipoproteins were determined in the supernatant after centrifuge of the mixture of serum and heparin solution containing CaCl₂. On the other hand, α-lipoprotein concentration was determined by immunochemical method following Laurell's report. As the results, it was found that serum α-lipoprotein concentration didn't show significant difference between young and old healthy controls. However, significant decrease of α-lipoprotein concentration was noted in hyperlipidemic subjects of Type IIb and Type IV by WHO-classification compared with those in controls. It is suggested that decrease of serum α-lipoprotein may related to the disturbance of clearance mechanism of triglyceride in pre-β-lipoprotein, and the phenomenon may result to the increase of pre-β-lipoprotein in serum.

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A fatty diet containing two eggs, the yolk of three eggs and fifty grams of butter was ingested in the fasting state of the normal and atherosclerotic subjects in order to detect the variability in responses to the loading based on the analysis of serum lipid increments. The effects of clofibrate on the serum lipid levels after the fat loading were investigated following the clofibrate treatment for 8 weeks. The results were as follows. Although all subjects showed a rise in serum triglyceride levels by the diet, large absolute increments were confined to atherosclerotic subjects and the gradual increments were persisted until 6 hours after the loading. The normal subjects didn't readily develop hypertriglyceridemia and the maximum levels were found to reach 4th or 6th hour after the fat loading. Maximum increments of serum cholesterol were found to reach 4th or 6th hour in the atherosclerotic subjects. By contrast, in the normal subjects, serum cholesterol concentrations weren't reached to the peak levels during observation period.
Changes in serum β-lipoprotein levels analysed by the immunocrit method were much the same as those in serum triglyceride levels. Clofibrate was effective in reducing elevated serum lipid levels after the loading, and the tolerance curve of both triglyceride and phospholipid levels in the atherosclerotic subjects was similar to those in the normal subjects not received clofibrate treatment. This test would be available not only to detect abnormal dietary hyperlipidemias but also to determine the effectiveness of lipid lowering drugs.

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The effect of free fatty acids (FFAs) on fibrinolysis and platelet aggregation was studied and pathological roles of FFAs were discussed in relation to FFA regulating enzymes in blood vessel wall. Fibrinolysis was estimated in vitro using suspension of fine particles of human fibrin as a substrate. Unsaturated FFAs suppressed fibrinolytic action of plasmin. The most potent inhibitor among tested was oleic acid (66% inhibition at 5mM). Saturated FFAs were far less effective. The inhibitory effect of oleic acid was not seen when fibrin was replaced by casein or TAMe. Binding of oleic acid to fibrin showed a direct relation to its antifibrinolytic activity. Also, formation of plasmin-fibrin complex in the reaction mixture was augmented by oleic acid. Thus the FFA effect seems to be exerted through modification of E-S complesx formation. Some FFAs, particularly saturated ones, are known to aggregates human platelets. Stearic acid enhanced the epinephrine-induced aggregation at low concentrations in which it by itself has no effect on platelets. Although these effects of FFAs may be diminished in the presence of albumin, a thrombotic nature of FFAs in a certain circumstance is suggested. Lipase and triglyceride synthetase in the low-speed supernatant fraction of rat aorta were greatly modified by Ca⁺⁺; i. e. the former was enhanced and the latter inhibited. These findings implies the importance of relationship between platelet functions (adhesion, aggregation and release reaction) and FFA mobilization at the surface of atheromatous lesion.

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A potent cyclic AMP phosphodiesterase inhibitory effect of EG-626 has been reported by Shimamoto and Hidaka in 1974. In this paper the preventive effect of EG-626 on the enhancement of platelet aggregability as well as the deterioration of cardiac function induced by isometric exercise in arteriosclerotic patients has been reported.
Fifteen healthy adults, 27 coronary sclerotic and 8 cerebral arteriosclerotic patients were subjected to the 50% maximal voluntary handgrip exercise for 2 minutes. Before and after the exercise, platelet sensitivity to ADP-aggregation (Thrombos. Diathes. haemorrh. 25: 524, 1971) employing a new method and the left ventricular function by non-invasive technique, systolic time intervals were measured.
A statistically significant enhancement of platelet sensitivity to ADP-aggregation (P<0.005) was found in the patients, but not in healthy controls. This change was prevented by pretreatment with EG-626, 300mg P. O..
LVETi decreased significantly (P<0.005) by exercise on placebo, but did not change significantly on EG-626. PEPi and PEPi/LVETi did not change significantly by exercise on placebo, but decreased significantly (P<0.005) on EG-626. The results indicated probable increase in cardiac output and/or myocardial contractility on EG-626.
These effects of EG-626 on platelet aggregability and the left ventricular function could be attributed to the elevation of cyclic AMP level in platelet and myocardium.

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The ischemic symptoms of the extremities are considered to be caused by the disturbed blood flow of the main blood vessels. However, comparison of angiographic films of the lower limbs with A S O before and after amputation revealed quite difference in the patency of visible blood vessels. In order to clarify such discrepancy of vascular pattern, microcirculation in 20 patients with A S O was studied. For this purpose, pathological studies of arterioles and venules in the cutis and subcutaneous tissues from amputated toes were made. Using the dye dilution technique, the injected dye pattern from the ischemic toes was analyzed with simultaneous photoelectric plethysmographic recordings. And radioangioscintigrams of both foot with Technecium-99m MAA were taken. The apparent rich blood vessels with red cells in the pathological specimens were interpreted to be stagnation of blood. The stagnant flow could be accellerated by intravenous injection of several circulatory drugs, i. e., Esberiven, Dexascheroson, etc. Pyridinol carbamate (ANGININ) also showed similar improvement of microcirculation, which was substantiated with changes of dye curves and scintigrams before and after the drug was administered.

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血小板凝集能の測定方法には数多くの報告があるが, われわれは全血を用いて血小板ADP (Adenosine 5′-diphosphate) 凝集能を測定する Screen Filtration Pressure (SFP) 法 (Swank 1961年) を用い, 健康老年者36例, 回復期脳血栓213例, 脳出血101例の血小板ADP凝集能 (SFP) を検討した. あわせて血清脂質を測定し, SFPとの関連を検討した. 健康老年者のSFPならびに総コレステロール,β-リポ蛋白, トリグリセライド値は, それぞれ148.7±53.5mmHg (平均値±標準偏差), 201.3±30.4mg/dl, 326.7±87.3mg/dl, 98.2±35.3mg/dlであった. 回復期脳血栓症では, それぞれ213.0±60.6mmHg, 212.9±35.9mg/dl, 399.4±106.7mg/dl, 147.4±61.5mg/dl, 回復期脳出血症では196.1±63.4mmHg, 208.3±42.1mg/dl, 400.8±99.4mg/dl, 138.0±64.6mg/dlであった. これら各疾患群のSFPならびに血清脂質は, 健康老年者に比べて有意 (P<0.05～0.01) に高い値を示した. 回復期脳血栓症における健康老年者の平均値+2SD以上の高コレステローノヒ血症, 高β-リポ蛋白血症, 高トリグリセライド血症を示す率は, それぞれ11.3%, 15.5%, 27.7%であった. 回復期脳出血症では, それぞれ11.0%, 9.9%, 23.8%であった. これら疾患群において, 高トリグリセライド血症を示す例が, 高コレステロール, 高β-リポ蛋白血症を示す例よりも有意 (P<0.05～0.01) に高率であった. 一方, 高脂血症を示す疾患群のSFPと高脂血症を示さない例のSFPとの平均値はほぼ等しく, 両者間に有意差は認められなかった. また, 症患群におけるSFPと血清脂質の間に有意の相関関係は認められず, 血清脂質は直接的には血小板ADP凝集能に影響を与えないことを知った.

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高脂血症におけるリポ蛋白代謝の変化を検討する目的で, 血漿中のアポ蛋白A-Iおよびアポ蛋白Bの濃度を正常者および高脂血症患者において測定した. 測定はapo A-Iおよびapo Bに対する特異抗血清を用いるロケット免疫電気泳動法によった. この定量法は我々の研究室で開発したものであり, これらのアポ蛋白の定量には簡便でしかも良好な測定成績を示した.
正常者におけるapo A濃度は18～22歳の男性9人では102±18単位/100ml (平均±標準偏差), 同年の女性11人では111±7単位/100mlであった. さらに, これら若年正常人のapo B濃度は男性で99±29, 女性で101±21単位/100mlであった. 35～60歳の高年正常男性18人ではapo A-Iは112±20, apo Bは124±24は単位/100mlであった. 同じく35～60歳の男性高脂血症患者においてはapo A-IはII型7例で98±15, IV型16例で119±25単位/100mlであり, II型においてやや低下傾向を示した. 一方, apo Bはこれら高脂血症で著しく増加しており, II型では203±26, IV型では208±16単位/100mlであった.
Apo Bとコレステロール濃度との間には有意の相関関係が認められた. 一方, apo A-Iとコレステロールの関係は, 正常者では正の相関, 高脂血症患者では逆相関関係であった. 以上のことより, 高コレステロール血症の成因にapo A-I濃度の低下が関与している可能性が示唆された.

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血清脂質に影響を与える最も大きな因子が食餌であることはいうまでもない. 年齢, 疾患およびその stage を限局した165人において, 蛋白質のみ80gに維持し, カロリーを1000とする療法, すなわち糖質および脂質の影響がほとんどないと考えられる食餌療法を4週間行った結果から血清中性脂肪および血清コレステロールの basal lipid level の決定を試みた. この basal lipid level は治療の対象あるいは効果の1つの判定基準とされる値である. このレベルを基準にリポ蛋白代謝の面かち食餌による血清脂質の反応を検討すると共に, 食餌療法に反応しないいわゆる内因性因子によって生じていると考えられる高脂血症の成因について若干の考案をした. 血清中性脂肪の basal lipid level は90.3±27.1mg/dlであった. 高中性脂肪血症は約90%が calory dependent hypertriglyceridgmia であり, 残りは超低比重リポ蛋白の中性脂肪の異化障害が考えられた. 食餌療法4週後, 血清中性脂肪値がさらに増加し, basal lipid level の上限以上になる例は, 全例の体重変化と比べ減少が緩慢であり中性脂肪の唯一の前駆物質である脂肪酸の貯蔵組織からの放出機序にその要因がある事が示唆された. 血清コレステロールの basal lipid level は165.6±26.5mg/dlであった. calory dependent hypercholesterolemia を除いた高コレステロール血症は低比重リポ蛋白の異化過程の障害と考えられる.

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ウサギ総頸動脈の二個所にクリップをかけて, 一時的に血流を遮断し, その間の Segment に生理的食塩水を注入し, 動脈内圧を下記のごとく統御した後, 血流を再開し, その動脈壁を光顕的, 電顕的, 免疫組織化学的, オートラジオグラフ的に研究した.
1.180±10mmHg (1分間, 10回) に内圧を統御した群: 術後1日の動脈壁では, 中膜筋細胞壊死, IgG, 線維素原, エバンス青の滲入, 沈着が認められた. 電顕的に, 内皮細胞間接合部の開大と, carbon の内皮下への滲入を見た. 3～5日においては, 中膜筋細胞の ³H-thymidine による標識率は著明に増加し, 以後徐々に減衰した. 内皮細胞や内膜細胞の標識率は, 3日後においては高かったが, 以後速やかに減衰した. 3日以後, 細胞性内膜肥厚が発生し, 同部にIgG, 線維素原, エバンス青がび漫性に沈着していた. さらに, 高脂肪食を負荷した群では, Oil red O 陽性物質や泡沫細胞も, 内, 中膜に見られた. 10日以降, 中膜に石灰沈着と肉芽腫様細胞増殖巣が認められ, 電顕的にこれらの細胞は, 線維芽細胞様細胞と modified smooth muscle cell であった.
2. 110±10mmHg (1分間, 10回) に内圧を統御した群: IgGや線維素原の壁内沈着はなく, エバンス青の滲入もごく軽度だった. 中膜筋細胞壊死はなく, ごく少数の内膜細胞がまれに見られた. 壁細胞の ³H-thymidine による標識率は上昇しなかった.
以上の成績から, 機械的内圧上昇により, 中膜筋細胞壊死や内皮細胞の透過性亢進 (血漿浸潤) が起こり, その結果, 内膜肥厚が生じたと考えられる. 中膜筋細胞壊死後, 中膜再生にあずかる細胞は中膜筋細胞であった.

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