Platelet adherence and subsequent aggregate formation on damaged vessel walls may be fundamental events in the initiation of an atherosclerotic lesion. To clarify the molecular mechanism of the interaction between platelets and endothelial cells, we have developed an in vitro model system; a porcine arterial endothelial cell monolayer cultured on type I collagen gel was partially injured and denuded, then ⁵¹Cr-labeled platelet binding to the injured area was measured. In this study, we found that in the presence of collagen both fibronectin and fibrinogen are essential for specific and significant platelet binding to the injured area of the endothelial monolayer.

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We examined the effects of CS-514, a newly introduced inhibitor of cholesterol biosynthesis, on lipoprotein metabolism of Type III and Type III-like hyperlipoproteinemia (HLP). Two subjects were studied. Case 1 showed typical lipoprotein abnormalities of Type III HLP with apoprotein (apo) E-III deficiency and Case 2 demonstrated broad-β band on paper electrophoresis and increased concentration of intermediate density lipoprotein without apo E abnormality. LDL-cholesterol level was low in both cases. After 3 months of CS-514 treatment, they showed decreased cholesterol and triglyceride concentration in plasma. This was accompanied by a reduction in the lipid content of Sf 20-400 range. On the other hand, LDL-cholesterol rose in both cases.
Since it is unlikely that inhibition of cholesterol biosynthesis causes suppression of LDL-receptor activity, the rise in LDL-cholesterol after the treatment may indicate the accelerated conversion of VLDL-remnant to LDL. Thus, it is speculated that CS-514 can enhance the VLDL-LDL cascade by producing lipoprotein particles which are subject to degradation by lipoprotein lipase.

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This study was conducted to re-evaluate the relation between running distance and plasma high-density lipoprotein (HDL) cholesterol concentration in runners. Fifty male endurance runners, aged from 30 to 57yr., were classified into four groups according to training distance per week, with lean untrained subjects, aged from 34 to 56yr. Body fat content in each group, and training distance in each runner group were shown as follows; Untrained, lean: n=12, 13.5%, Trained, Grade I : n=11, 12.7%, 24km/wk, Grade II: n=12, 12.3%, 49km/wk, Grade III: n=13, 11.6%, 66km/wk, Grade IV: n=14, 11.5%, 99km/wk. There were no remarkable differences in the cholesterol concentrations in total plasma (194-208mg/dl) and low-density lipoprotein fraction (105-122mg/dl). Grade I runners (71mg/dl) had slightly, and Grade II, III and IV runners (76, 78, 77mg/dl) had significantly higher HDL cholesterol than untrained men (63mg/dl). This study suggests that regularly performed endurance running increases plasma HDL cholesterol with elevation of running distance up to 25-50km/week, but that further increases in running distance do not result in an additional increase in HDL cholesterol level.

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Lipid-rich lesions were produced in the ascending aorta of Japanese quail 3 months after feeding an atherogenic diet containing 2% cholesterol and 15% corn oil.
Histologically and electron microscopically, major cellular component of the thickened intima was fibroblast-like cells with or without lipid droplets. Immunoperoxidase method showed that products of myc and src oncogenes were strongly positive for proliferating intimal fibroblast-like cells and negative for fibroblast-like cells of the tunica media. These results suggest possible regulatory roles of oncogenes on intimal cell proliferation.

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Alterations of apolipoprotein levels in serum and pleural effusion in a newborn with idiopathic chylothorax were examined particularly focusing on apo A-IV and apo B-48. When he was treated with MCT (medium-chain triglyceride) milk, the pleural effusion containing chylomicrons was disappeared by the 14th hospital day. MCT has been known to be triglyceride comprising of mediumchain fatty acids (C₈-C₁₂) and to be absorbed directly into the portal vein without chylomicron formation in intestinal cells.
Serum apo A-IV level decreased in the period of receiving only 5%glucose solution, whereas it restored to the normal range after administration of MCT milk. In addition, apo A-IV level in the pleural effusion altered in the same manner as that in serum, indicating that apo A-IV i s synthesized in the intestine during absorption of MCT.
On the other hand, apo B-48/total apo B ratio in the d<1.006 fraction in the pleural effusion decreased during administration of the MCT milk, suggesting that the synthesis and/or secretion of apo B-48 is relatively suppressed during absorption of MCT.

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Although there are many reports on the effects of glycosaminoglycans (GAGs) on atherogenesis, its precise effects still remain controversial. Recently, it has been suggested that GAGs have the antiatherosclerotic effects and GAG compounds is used as antilipidemic agents.
In this experiment, we studied the effects of Mucopolysaccharide-polysulfate (MPS-L) (Arteparon^R) on 1% cholesterol-fed rabbits. MPS-L, which is used as agents for arthritis deformans, is the polysulfate ester of GAG extracted from fresh bovine lung tissue. The contents of hexosamine, uronic acid, sulfur and nitrogen in it are 21.5-23.3%, 19.4-23.3%, 12.5-13.1% and 1.67-1.91%, respectively, and its molecular weight is 5, 000-8, 000. Though the mobility of MPS-L by two-dimensional electrophoresis is similar of heparin, its negativity is more potent than that of heparin.
Twenty-one rabbits were fed on a 1% cholesterol diet with an intraperitoneal injection of saline (n=8)(control group), 25mg of MPS-L (n=7)(MPS-L 25mg group) or 50mg of MPS-L (n=6)(MPS-L 50mg group). After 10 weeks of feeding, all rabbits were sacrificed and used for further studies. Eight rabbits on a standard diet with an intraperitoneal injection of saline (n=8)(standard group) were processed as similar.
After 10 weeks feeding, the plasma total cholesterol of the MPS-L 25mg group and the MPS-L 50mg group [1, 753.9±111.1 and 1, 667.9±148.4mg/dl (mean±SE), respectively] were significantly lower than that of the control group (2, 226.0±114.9mg/dl)(p<0.05, p<0.02, respectively). The VLDL cholesterol of the MPS-L 25mg group (690.0±90.1mg/dl) and the MPS-L 50mg group (803.0±98.4mg/dl) was also significantly lower than that of the control group (1, 212.3±112.1mg/dl). There were no differences in LDL-cholesterol, HDL-cholesterol and plasma triglyceride between the groups.
ADP-induced platelet aggregability of the MPS-L groups were significantly decreased at 10 weeks when compared to that of the control group and antithrombin-III activity of the MPS-L groups were inversly increased when compared to that of the control group. These findings suggest that MPS-L might have antiplatelet and/or anticoagulant effects. Total lipoprotein lipase activity (T-LPL)(LPL+HTGL) of the MPS-L groups at 10 weeks were higher than that of the control group and especially, T-LPL of the MPS-L 50mg group was significantly higher than that of the control group. These elevated T-LPL were mainly due to an increase in the LPL from peripheral tissues. Among MPS-L and other polyanions such as heparin, chondroitin-4-sulfate, chondroitin-6-sulfate, dermatan sulfate, heparan sulfate and hyaluronic acid, the increase of T-LPL by MPS-L is most potent. These findings might suggest that MPS-L increase catabolism of VLDL to LDL. Though in regard to the surface involvements of the aorta and the aortic contents of total cholesterol and uronic acid there were no differences between the MPS-L groups and the control group, the aortic contents of hydroxyproline and calcium of the MPS-L groups were significantly decreased when compared to that of the control group. These findings suggest that MPS-L has somewhat antiatherosclerotic effects.

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The coronary risk factors and the severity of the coronary atherosclerosis were analyzed in 244 consecutive male patients who underwent coronary angiography. The patients consisted of 82 with acute myocardial infarction with prior angina pectoris (Group I), 73 with acute myocardial infarction without prior angina pectoris (Group II) and 89 with angina pectoris without myocardial infarction (Group III). As compared with Group I, Group II and Group III contained significantly greater numbers of young patients less than age 50, while the incidences of smokers and zero or single vessel disease were significantly greater in Group II and III than Group I.
On the other hand, no significant differences were observed among the 3 groups in serum total cholesterol, serum HDL-cholesterol and serum triglyceride. A significant positive correlation between serum total cholesterol and the severity of the coronary atherosclerosis was demonstrated only in Groups I and III.

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By feeding rabbits on diets containing 0, 0.1, 0.5 or 1.0% of cholesterol, the relationship between the levels of serum total cholesterol (TC) and lipid deposition in aortic surface was studied. Whereas the level of serum TC in 0.1% cholesterol-fed rabbits did not change from the basal level (about 30mg/dl), the level of serum TC in 0.5% cholesterol-fed rabbits increased to about 400mg/dl between 4 and 10 weeks after cholesterol-loading and that of serum TC in 1.0% cholesterol-fed rabbits increased continuously to a higher level. The extents of lipid deposition in aorta were related closely with the “integrated value” of TC, i. e. sum of the serum TC values obtained at each week.

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Two mouse monoclonal antibodies against human PDGF, PGF 007 (IgG₁) and PGF 033 (IgM), were prepared with immunization with a chemically synthesized peptide corresponding to positions 73 to 97 of human PDGF-B chain. In immunoblotting, these antibodies specifically reacted with purified human PDGF. By use of the synthetic peptide immobilized on microplates and these monoclonal antibodies, ELISA's for human PDGF were prepared. In these ELISA's, both antibodies were able to react with human PDGF even in the presence of human plasma.

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Restenosis is one of important problems after PTCA and may be related to marked platelet accumulation at the dilatation site. The preventive effect of dilazep, which is well known as antiplatelet drug, on thrombus formation induced by transluminal dilatation in rabbits was investigated. The drug effect was evaluated histologically and semi-quantitatively using an image analysis system. The conclusion is summarized to be as follows;
1) Marked mural thrombus constituted largely from platelet aggregates and slightly from fibrin network was observed on the injured abdominal aorta one hour after dilatation.
2) Dilazep obviously inhibited this thrombus formation.
3) These results suggest that dilazep will be clinically useful for the prevention of restenosis after PTCA.

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In the present experiment, the effects of streptozotocin diabetes on serum and liver lipid concentrations were investigated in two strains of mice with different responses of serum cholesterol to cholesterol feeding.
Serum glucose concentrations were elevated in both strains almost identically by streptozotocin administration. Although serum triglyceride concentrations increased similarly in both strains and had good correlations to serum glucose levels, the elevation of cholesterol was found only in C₃H strain, which was a good responder to cholesterol feeding. Consequently, serum cholesterol concentration in the diabetic C₃H mouse was higher than that in diabetic DBA. Liver lipid increased on both diabetic mice pallaleled with serum glucose as compared with nondiabetic controls except triglyceride in DBA mouse.
It is concluded that the latent metabolic disorder of cholesterol is emphasized in diabetic state, which may be a reason why hypercholesterolemia is not always accompanied with diabetes mellitus.

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The low plasma HDL concentration and cholesterol-rich LDL may play a role in the early onset of atherosclerosis in homozygous patient with familial hypercholesterolemia. We studied effects of plasma exchange and LDL-apheresis on cholesterol levels and lipid composition of LDL and HDL in two patients with homozygous FH (SY and YS). In case SY, plasma exchange (1/2wks) and LDL-apheresis (2/1wk) caused a decrease of LDL concentration (p<0.01) and an increase of HDL concentration (p<0.05). Cholesterol content (%) of LDL decreased from 56.7±0.9% to 53.2±0.6% by LDL-apheresis (2/1wk)(p<0.05). TC/PL mass ratio decreased from 1.690±0.036 to 1.530±0.025 (p<0.02). In case YS, LDL-apheresis caused a decrease in cholesterol content (%) of LDL and HDL, and an increase in phospholipid content (%) of HDL. The differences between HDL-cholesterol levels measured by ultracentrifugation and precipitation (Heparin-Ca) methods, decreased after LDL-apheresis treatments. HDL with apo E also examined by an immunoblotting method using human apo E anti-serum. Homozygous FH serum showed a darker band of HDL with E than a normal serum by agarose gel electrophoresis and immunoblot. The band of apo E thinned after LDL-apheresis.
These results indicated that LDL lowering by LDL-apheresis and plasma exchange may cause an increase of HDL concentration and a decrease of cholesterol content (%) in LDL and HDL. In addition, the remove of HDL with E by LDL-apheresis may activate a reverse cholesterol transport system.

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It is well recognized that chylomicron remnant is a risk factor for the development of atherosclerosis. We demonstrated in previous study that Chylomicron remnant was abnormaly accumulated in subjects with non-insulin-dependent diabetes mellitus (NIDDM). This study was designed to evaluate if its abnormality of chylomicron remnant was improved by diabetic treatment. Apolipoprotein (apo) B subfractions (apo B-100 and apo B-48) of VLDL and IDL in 19 subjects with NIDDM were analyzed before and after treatment, using SDS-PAGE method described by Kane et al. Apo B-48 ratio (apo B-48/apo B-100) was calculated. Treatment produced a significant decrease in apo B-48 ratio of VLDL from 0.042±0.014 to 0.029±0.016 (p<0.02). Apo B-48 ratio of IDL was significantly reduced from 0.023±0.012 to 0.012±0.011 (p<0.01). Total cholesterol, triglyceride and protein levels of VLDL were slightly reduced, though these changes were not significant. These levels of IDL were also changed in likewise. These results suggest that abnormal accumulation of chylomicron remnant might be improved by treatment in NIDDM.

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It has been reported by Stout et al, that hyperinsulinism might accelerate atherosclerosis. In the Zucker rat strain, made by Zucker and Zucker in 1961, the presence of the “fa” gene in the homozygous condition (fa/fa) leads to the development of hyperinsulinism of early onset.
In order to investigate how hyperinsulinism causes atherosclerosis, age-related changes in the aortic lesions were studied in Zucker fatty rats (fatty rat) and their lean littermates (lean rat) at 7, 11, 20 weeks of age. Serum glucose, cholesterol and triglyceride concentration were determined using enzymatic methods. Cholesterol contents in the aorta were analyzed by the Gas Liquid Chromatography. Morphological studies were performed light and electromicroscopically in the aorta of rats.
The following results were obtained;
1. The fatty rats showed a remarkable increase in the body weight with age.
2. The levels of serum triglyceride and cholesterol of the fatty rats were higher than those of the lean rats at the same age. But there was no significant difference in serum glucose level between the fatty rats and the lean rats at 7, 11, 20 weeks of age.
3. At 20 weeks of age, cholesterol content in the aorta of the fatty rats was significantly higher than that of the lean rats. Triglyceride content in the aorta of the fatty rats was higher than that of the lean rats at 11 weeks of age.
4. The aorta and serum of the fatty rats contained significantly higher amount of nonessential fatty acids (C₁₆, C_16-1, C_18-1) with a concomitant decrease in C_18-2, C_20-4 as compared with those in the lean rats.
5. The light microscopic examination revealed slight thickening of the intima of the aorta due to increase both in cellular components and matrixes in the fatty rats of 20 weeks of age. Electron microscopic observations demonstrated the accumulation of homogeneous substances and smooth musclelike cells in the intima of 20 weeks old fatty rats. The aorta of the lean rats was almost normal by light and electro microscopy.
These data suggest that hyperinsulinism plays an important role in development of diabetic macroangiopathy.

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Atherogenecity of triglyceride-rich lipoproteins circulating in the post-prandial state has been reported. It has been suggested that chylomicron remnants may contribute to atherogenesis. Apolipoprotein (apo) B-48, a subspecies of apo B, which is secreted only from the small intestine in human, has provided a specific marker for exogenous lipoproteins, especially for chylomicron remnants. In the present study, the effects of oral fat ingestion on plasma concentrations of lipids, lipoproteins and apolipoproteins and VLDL-apo B subspecies were studied in the fasted 7 healthy men aged 25-43 years. Butter 100g (81% fat) or margarine 100g (81.6% fat) was ingested within 10 minutes early in the morning on the different days. Blood was withdrawn at 0, 60, 120, 180, 240 and 300 minutes after fat ingestion. Lipoproteins were fractionated by sequential ultracentrifugation. Apolipoproteins were measured by single radial immunodiffusion. Apo B subspecies in VLDL (d<1.006g/ml) were analyzed by SDS-3.5 polyacrylamide gel electrophoresis. After staining, the protein bands were evaluated by densitometer and peak area was measured. Apo B-48 ratio (percent of apo B-48 in total apo B) was calculated. Fasting plasma concentrations of lipid and apolipoproteins were as follows: cholesterol (Ch); 191.5±11.0mg/dl, triglyceride (TG); 108.8±13.9mg/dl, phospholipids (PL); 195.3±6.5mg/dl, HDL-Ch; 63.6±3.3mg/dl, apo A-I; 143.8±2.6mg/dl, apo A-II; 32.3±0.8mg/dl, apo B; 76.7±6.6mg/dl, apo C-II; 3.2±0.3mg/dl, apo C-III; 7.8±0.5mg/dl and apo E; 4.0±0.2mg/dl. After fat ingestion, plasma TG increased mainly due to the increments of TG in VLDL and chylomicron (d<1.006g/ml) fraction. There was no significant difference between response of TG after butter load and that of margarine. Plasma Ch increased due to VLDL-Ch. Neither significant changes in Ch concentrations in the other lipoprotein fractions nor difference between response of plasma and lipoprotein Ch after butter load and margarine load were observed. Concentrations of any apolipoproteins showed no apparent changes either by butter or margarine load. Apo B-48 ratio in d<1.006g/ml fraction increased after fat ingestion. Degree of apo B-48 ratio response to fat ingestion varied from a subject to a subject, but there was no apparent difference between response after butter load and that of margarine. Both increment of plasma TG concentration and maximum concentration of TG after fat ingestion correlated negatively with maximum value of apo B-48 ratio, indicating that degree of TG increase after fat ingestion (i. e. magnitude of post-prandial lipemia) is partly regulated by metabolism of apo B subspecies.

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This study was aimed to clarify the relationship between autopsy findings on cardiovascular system and various clinical profiles. The former included myocardial fibrosis, stenosis of coronary arteries, weight of the heart, diameter of the aortic root and pathological changes at the aortic root. The latter included age of subjects, blood pressure, serum cholesterol, existence or absence of diabetes mellitus and electrocardiographic findings.
One hundred autopsied cases (62 males and 38 females aged 18-93 years of age) were included. Cases with congenital heart disease, valvular heart disease, cardiomyopathy, myocarditis and ischemic heart disease were excluded from this study.
Each pathological and clinical item was classified into two or three categories according to its severity and then compared by using multivariance statistical analysis.
As the results of this study, statistically significant relations were obtained between each item in the following three groups:
(1) Severe myocardial fibrosis and hypertension.
(2) Severe coronary stenosis and hypercholesterolemia.
(3) Moderate myocardial fibrosis, increased heart weight, diabetes mellitus and LVH on ECG.

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In normal male rabbits fed a cholesterol (CH) supplemented (1.5% CH) diet for a period of 12 weeks, increases in intravascular adhesiveness of leukocytes and aggregability of erythrocytes in the subcutaneous microcirculatory system within a transparent ear chamber were noticed concurrently with persistent marked increases in serum levels of total CH, β-lipoproteins, phospholipids and triglycerides, in vitro leukocyte adhesiveness, and erythrocyte sedimentation rates, with persistent decreases in erythrocyte counts, hematocrit values and hemoglobin concentrations, and with remarkable aortic accumulations of total CH. Daily administrations of nicotine (N; 0.4mg/kg, s. c.) or carbon monoxide (CO; 1 minute's inhalation of 4% air-balanced mixture) combined with CH feeding appeared to have no effect on the aortic CH accumulations, hematological and biochemical changes and to have an appreciable enhancing effect on the microcirculatory changes due to CH feeding. Although no additive effect on the aortic CH accumulations was observed, the microcirculatory findings may suggest that N and CO as main noxious substances in tobacco smoke can play certain role in atherogenic changes at least in the peripheral arteries of the skin induced by CH feeding through their enhancing effects on the microcirculatory changes due to CH feeding.

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The purpose of this study is to clarify the role of glucose and lipids metabolism in vasospastic angina. The subjects who underwent coronary angiography were 100 patients. Subjects were classified to three groups according to angiographic findings; 34 normal controls (group 1), 18 subjects (group 2) with coronary spasm and 47 subjects (group 3) of coronary atherosclerosis without coronary artery spasm. The age was younger in group 2 than in group 3. The values of serum total cholesterol and triglyceride and the prevalence of abnormal glucose tolerance, which include both diabetes mellitus and impaired glucose tolerance, were lower in group 2 than in group 3, while they were not significant statistically. The group 2 showed higher HDL-cholesterol and lower atherogenic index level than in group 3. These risk factors in group 2 were compatible with group 1 rather than in group 3. Both apo A-I and apo A-II levels of group 2 were significantly higher than group 3. Apo B level revealed higher value in group 2 and group 3 than in group 1. Apo C-II level in group 2 and group 3 showed significantly higher values than group 1. Apo E level of group 2 showed high value than in group 3.
These risk factors of vasospastic angina were compatible with in normal subjects rather in coronary atherosclerosis from the results of lipids metabolism, namely classical risk factors of coronary artery disease such as cholesterol or HDL-cholesterol were not affected. However, increased apo C-II and apo E levels in vasospastic angina suggested the abnormality of triglyceride metabolism in VLDL. On the other hand, the high prevalence of abnormal glucose tolerance was noted in vasospastic angina comparing to normal subjects. It was suggested that abnormal lipids metabolism might be related on the development and progression of vasospastic angina.

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CS-514, a new inhibitor of endogenous cholesterol biosynthesis, has been shown to reduce plasma cholesterol concentration in both healthy and hypercholesterolemic subjects. In this study we compared the effect of CS-514 and probucol on plasma lipids in hypercholesterolemic subjects. After treatment with probucol, HDL-cholesterol as well as total cholesterol tended to decrease. After a washout period probucol was replaced with comparable doses of CS-514. All the patients showed decreased plasma cholesterol levels after CS-514 treatment. HDL-cholesterol levels increased significantly after CS-514. Plasma triglyceride levels showed no significant change throughout the study period. Thus, the two drugs differed in their effects on HDL-cholesterol.

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The effects of Dextran Sulfate (MDS®) on body weight, fatty liver formation, biochemical liver function tests, serum lipids and lipoproteins were examined in ventromedial hypothalamic (VMH) obesity in rats. Twelve weeks old female rats were divided into 4 groups: 1) control, 2) control with MDS treatment (0.4% of MDS containing diet), 3) VMH lesioned and 4) VMH lesioned with MDS treatment. After 12 weeks treatment of MDS, body weight, total liver lipid content, biochemical liver function tests and serum lipids (triglyceride, cholesterol) were determined. High performance liquid chromatography developed by Hara and Okazaki were also performed to analyse lipoproteins. There were no significant differences in body weights, total liver lipids and biochemical liver function tests between two control groups, and between two VMH lesioned groups, although both VMH lesioned rats became obese. In control rats, serum triglyceride did not change after treatment of MDS: VLDL-TG was decreased but LDL-TG and HDL-TG tended to increase. Serum cholesterol did not change. In VMH obese rats, both groups showed significant increase in serum triglyceride and cholesterol compared to control groups. Triglyceride was significantly decreased due to decrease in chyromicron and VLDL after treatment of MDS. There were no significant changes in total cholesterol but plasma VLDL-C were significantly decreased. These results suggest that Dextran Sulfate improved lipid abnormalities in VMH obese rats mainly by decreasing serum triglyceride in VLDL and chyromicron.

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Two patients with marked, intractable hypertriglyceridemia under treatment for chronic renal failure by hemodialysis were treated by either an apolipoprotein B-dependent removal of lipoproteins using dextran-sulfate cellulose column plasmapheresis or a size-dependent removal of lipoproteins using hollow fibers' filtration plasmapheresis. In one patient, a column packed with hollow fibers was used as a plasma separator and a dextran-sulfate cellulose column as an adsorbent. In another patient, because the hollow fibers' column could not separate plasma from whole blood, a centrifuge-type blood cell separator was used for the plasma separation. The amounts of plasma cholesterol, triglycerides and phospholipids removed by plasmapheresis using the combination of a hollow fibers' column and a dextran-sulfate cellulose column were 30%, 33%, and 30%, respectively, and the amounts removed by the combination of the centrifuge-type blood cell separator and the hollow fibers' column were 31%, 29%, and 27%, respectively. The efficiency of lipid removal was almost at the same rate in both patients. We thus have concluded that plasmapheresis could be used for the treatment of marked hypertriglyceridemia, such as type IV and V hyperlipoproteinemia, and that we prefer the centrifuge-type blood cell separator to the hollow fibers' column for plasma separation. The second filter must be chosen for each patient, depending on the size of their lipoproteins.

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In order to evaluate the possible effects of nifedipine and trichlormethiazide on the lipid and lipoprotein metabolism, 16 patients with essential hypertension were studied before and after 16 weeks' treatment with 30mg nifedipine or 4mg trichlormethiazide daily. Eight patients were treated with nifedipine. There was no change in the concentration of serum total cholesterol, HDL-cholesterol, LDL-cholesterol and VLDL-cholesterol. The concentration of serum triglyceride decreased slightly, HDL₂-cholesterol increased slightly, HDL₃-cholesterol decreased slightly after the administration of nifedipine for 16 weeks. Eight patients were treated with trichlormethiazide. The concentration of serum total cholesterol and triglyceride increased slightly after 4 to 16 weeks. HDL-cholesterol decreased significantly after 16 weeks. HDL₂-cholesterol decreased slightly. LDL-cholesterol and VLDL-cholesterol increased slightly. Total cholesterol/HDL-cholesterol increased significantly after 16 weeks. These results could possibly suggest favorable effects of nifedipine and infavorable effects of trichlormethiazide on the lipid and lipoprotein metabolism of hypertensive patients.

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