Elastase (30% or 50%, namely 12 or 20 unit/mg by Sachar's method) and mice were used. The following results were obtained. A. Blood total cholesterol: When normal animals were injected at a rate of 1mg/kg/day for 15 days, no changes were seen, while cholesterol or puromycin induced hypercholesterolemia were inhibited by the joint usage of administration of elastase. B. Biosynthesis of liver cholesterol in vitro and in vivo: Addition of elastase to liver homogenate inhibited the incorporation of both acetate-14C and mevalonate-14C into cholesterol. As regards the biosynthesis of liver cholesterol in the case of injection of elastase, the incorporation of acetate-14C increased, while the incorporation into cholesterol from mevalonate-14C showed no changes. C. The decrease of cholesterol induced liver oxygen consumption was inhibited by the administration of elastase. D. The intestinal absorption of cholesterol-4-14C showed no changes by the administration of elastase. E. Total activity in bile comming from cholesterol-4-14C administration increased in animals injected with elastase at a rate of 4mg/kg/day for 5 days. F. The oxidation of cholesterol-26-14C by liver mitochondria increased by administration of elastase. G. The excretion of total bile acid-14C in faeces after cholesterol-4-14C administration increased in both normal and cholesterol fed animals by administration of elastase. From the above data it may be said that the blood cholesterol-lowering act of elastase appers to be due mainly the increase of the catabolism of cholesterol and fecal excretion of bile acids.
Normal values of changes in jugular O2 tension (PjO2) and cerebral blood flow (CBF) induced by carotid compression were measured in 9 healthy young men. The normal changing value of PjO2 was 0.3±1.0mmHg, CBF 2.9±3.5ml/100g Brain/min. There were no effects on electroencephalogram (EEG) during carotid compression in the healthy young men. In normal cerebral blood flow group, CBF changed from 59.9 to 62.9, PjO2 from 33.3 to 32.9 on ipsilateral compression, and CBF changed from 59.9 to 59.1, PjO2 from 33.3 to 32.9 on contralateral compression. In this group, there were no influences on PjO2, CBF and EEG during carotid compression. In low cerebral blood flow group, CBF was reduced from 41.7 to 34.8, PjO2 from 35.4 to 32.3 on ipsilaterat compression, and CBF from 41.7 to 40.0, PjO2 from 35.4 to 35.1 on contralateral compression. During ipsilateral compression, it showed tendency of decreasing on CBF and PjO2, and ΔCBF was -6.7, ΔPjO2-3.1. 7 cases with EEG slowing on carotid compression exsisted in this group. The cases with EEG slowing, who were certified occlusions and/or stenosis of carotid arteries or main cerebral arteries, had the significant CBF and PjO2 reduction on carotid compression, and ΔCBF was -9.0, ΔPjO2-3.5. It is concluded that digital compression of the carotid artery in the neck is the very useful method for testing the adequancy of cerebral collateral circulation observating PjO2 and EEG. Effects of respiration and blood pressure during carotid compression have to be kept in mind.
Aortic calcification was examined by routine chest film and abdominal lateral film on 639 cases in which glucose tolerance test was made. Incidence of aortic calcification in non-hypertensive and non-diabetic cases was 1.9% on those of 40-49 years of age, 9.1% on those of 50-59 years of age and 27.9% on those of 60-69 years of age; that in hypertensive cases was 16.7% on those of 40-49 years of age, 36.4% on those of 50-59 years of age and 50.0% on those of 60-69 years of age; and that in diabetic cases was 0% on those of 40-49 years of age, 42.9% on those of 50-59 years of age and 47.1% on those of 60-69 years of age. These results indicate that the aortic calcification develops about 10 years earlier in hypertensive or diabetic cases than in non-hypertensive and non-diabetic cases. Incidence of hypertension or diabetes was about the same in cases with calcification only in aortic arch as in cases without aortic calcification. However, the incidence of hypertension was significantly higher in cases with calcification in both aortic arch and abdominal aorta than in those without aortic calcification. The incidence of diabetes was also significantly higher in cases with calcification of abdominal aorta than in those without aortic calcification.