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5 1) Tsujita, Y., Kuroda, M., Shimada, Y., Tanzawa, K., Arai, M., Kaneko, I., Tanaka, M., Masuda, H., Tarumi, C., Watanabe, Y. and Fujii, S.:CS-514, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase:tissue-selective inhibition of sterol synthesis and hypolipidemic effect on various animal species. Biochim. Biophys. Acta, 877:50 (1986). 2) Nakaya, N., Homma, Y., Tamachi, H., Shigematsu, H., Hata, Y. and Goto, Y.:The effect of CS-514 on serum lipids and apolipoproteins in hypercholesterolemic subjects. J. Am. Med. Assoc., 257:3088 (1987). 3) Yamamoto, A., Matsuzawa, Y., Yokoyama, S., Funahashi, T., Yamamura, T. and Kishino, B.: Effects of probucol on xanthomata regression in familial hypercholesterolemia. 29H-35H (1986). Am. J. Cardiol., 57: 4) Nakaya, N., Homma, Y., Tamachi, H., Shigematsu, H., Hata, Y. and Goto, Y.:The effect of CS-514 on serum lipids and apolipoproteins in hypercholesterolemic subjects. J. A. M. A., 257: (1987). 5) Saku, K., Sasaki, J. and Arakawa, K.:Long-term effect of CS-514 (HMG-CoA reductase inhibitor) on serum lipids, lipoproteins, and apoproteins in patients with hypercholesterolemia. Curr. Ther. Res., 42: (1987). 6) Le Lorier, J., De Breuil-Quidor, S., Lussier-Cacan, S., Huang, Y. S. and Davignon, J.:Diet and probucol in lowering cholesterol concentrations. Arch. Intern. Med., 137: (1977). 7) Riesen, W. F., Keller, M. and Mordasini, R.: Probucol in hypercholesterolemia:a double blind study. Atherosclerosis, 36: (1980). 8) Strandberg, T., Kuusi, T., Tilvis, R. and Miettinen, T.:Effect of probucol on cholesterol synthesis, plasma lipoproteins and the activities of lipoprotein and hepatic lipase in the rat. Atherosclerosis, 40: (1981). 9) Nikkila, E. A., Taskinen, M.-R. and Kekki, M.: Relation of plasma high-density lipoprotein cholesterol to lipoprotein-lipase activity in adipose tissue and skeletal muscle of man. Atherosclerosis, 29: (1978). 10) Matsuzawa, Y., Yamasbita, S., Funahashi, T.,
6 Yamamoto, A. and Tarui, S.:Selective reduction of cholesterol in HDL2 fraction by probucol in familial hypercholesterolemia and hyper HDL2 cholesterolemia with abnormal cholesteryl ester transfer. Am. J. Cardiol., 62:66B-72B (1988). 11) Sirtori, C. R., Sirtori, M., Calabresi, L. and Franceschini, G.:Changes in high-density lipoprotein subfraction distribution and increased cholesteryl ester transfer after probucol. Am. J. Cardiol., 62:73B-76B (1988). 12) Nestel, P. J. and Billington, T.:Effect of probucol on low density lipoprotein removal and high density lipoprotein synthesis. Atherosclerosis, 38: (1981). 13) Atmeh, R. E., Stewart, J. M., Boag, D. E., Packard, C. J., Lorimer, A. R. and Shepherd, J.:The hypolipidemic action of probucol:a study of its effects on high and low density lipoproteins. J. Lipid Res., 24: (1983). 14) Aburatani, H., Matsumoto, A., Kodama, T., Takaku, F., Fukazawa, C. and Itakura, H.:Increased levels of messenger ribonucleic acid for apolipoprotein E in the spleen of probucol-treated rabbits. Am. J. Cardiol., 62:60B-65B (1988). Summary Effects of Pravastatin (CS-514) and Probucol on Plasma Lipids, Lipoproteins and Postheparin Lipolytic Activities in Hypercholesterolemic Subjects Pravastatin is a new derivative of compactin and has been found to be a specific inhibitor of hydroxymethylglutaryl-coenzyme A reductase. In this study, the effectiveness of pravastatin and probucol was tested in patients with primary hypercholesterolemia in crossover design. Special attention was paid to the erects on HDL-cholesterol levels since they have been shown to be a major factor in predicting the risk of coronary heart disease. Because available evidence suggests that the activities of the lipoprotein lipase system and LCAT are related to the level of plasma HDL and the HDL subpopulation distribution, the effects of these drugs on postheparin lipolytic activity and LCAT activity were measured. HDL particles were also examined by gradient gel electrophoresis to determine the effects of these drugs on particle size distribution. We obtained the following results. 1. Treatment with pravastatin reduced mean total plasma cholesterol, triglyceride and phospholipid levels by 16% (p<0.05), 30% (N. S.) and 13% (p<0.05), respectively. 2. In the probucol group, mean total plasma cholesterol and phospholipid levels were decreased by 24% (p<0.01) and 20% (p<0.01), respectively. 3. As for he effects on HDL-cholesterol before drug-crossover (at period B), probucol reduced HDL-cholesterol levels significantly (p<0.01) while pravastatin had no significant effect on HDLcholesterol. 4. In contrast to the effects of these drugs on HDL, we noted a decrease in the activities of LPL, and no significant change in LCAT activities were seen in either group. 5. Gradient gel electrophoretic profiles of HDL particles after probucol treatment showed a reduction of larger HDL2 particles and a prevalence of smaller HDL2 particles and HDL3 particles when compared with the controls. In the pravastatin group, HDL2 particles were larger than those of the controls. These results showed the effects of our test drugs on HDL particles. Further study is needed to find which HDL changes are favorable to prevent atherosclerosis. Key words:pravastatin, probucol, HDL particles, postheparin lipolytic activities.
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