It was studied by various methods that disturbance of microcirculation in the vascular wall caused vascular lesions. Influences of disturbed microcirculation on the metabolism in the vascular wall and etiological factors for vascular lesions were discussed.

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In order to clarify the characteristic features of arterial contractile protein, natural actomyosin (myosin B), myosin A, actin and native tropomyosin were extracted from bovine carotid arteries and their characteristic features were compared with those from bovine cardiac muscle and from rabbit's skeletal muscle. In this study, the following points were clarified: l) Arterial contractile protein mainly consisted of myosin A, actin and native tropomyosin, regulatory protein respondent to Ca²⁺ just as having been observed in those from striated muscle. 2) Arterial myosin A, actin and native tropomyosin possessed the similar features characteristic of myosin A, act-in and native tropomyosin from striated muscle, respectively, as shown with following items; effect of divalent cations on ATP-ase activity of myosin A, G&nrarr;F transformation in actin the formation of "arrow-head structure" m F-actin by reaction with arterial and skeletal H-meromyosins and the demonstration of the intraction of myosin A and F-actin with regardless of their origins. 3) The optimal concentration of Mg²⁺ necessary for the interaction of myosin A and F-actin was much high (10-20 mM) in myosin A from arterial wall and very low (< 0.5 mM) in myosin A from striated muscle regardless of origin of the F-actin. 4) In electronmicrographic structures, arterial myosin aggregates were shorter in the length compared with that of striated muscle, having rod shape without tapering and possessed the fine projections only at the both ends. However, any difference has not been observed between arterial F-actin and F-actin from striated muscle which held helical structure with the pitch of about 350 A and the width of about 80 A. 5) The thin filaments containing actin were located not only at muscular layer of arterial wall but also at endothelium of renal capillary. Through the above findings, it was understood that the contraction - relaxation of arterial wall, even in capillary, contributory to the performance of blood circulation was based on the association - dissociation of myosin aggregate and F-actin together with native tropomyosin respondent to Ca²⁺ through increase - decrease of Ca²⁺, which is associated with hydrolysis of ATP in the presence of Mg²⁺.

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Three hundred and eighty nine autopsied human aortas were studied for lipid and fibrosis area at the 6 segments which were expected to receive different grade of mechanical stimuli. The fibrosis area was increasing with age with a jump-up at 50 years-old male and 60 years-old female. It was most prominent at lower half of the aortic arch and anterior half of the abdominal aorta with an acceleration by hypertension, and showed a female predominancy at the abdominal aorta in higher age. The aMPS content estimated by both chemical and histochemical techniques, was increased at 30 to 40 years-old male and at 40 to 50 years-old female and decreased thereafter. The aMPS-age curve was identified as a differential of the fibrosis-age curve, and it means that aMPS promoted progression of fibrosis. Histochemical study proved proliferating fine collagen fibers in the location where aMPS was accumulated. Abundant aMPS was present at the intimamedia junction and its main components were chondroitin sulfates AC and B, and heparitin sulfate. Hyaluronic acid existed mainly along the elastic layers of media. They were decreasing after middle age, and atheromatous and old fibrotic lesions with poor cellularity contained less aMPS than the intact area.

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1. Contents of triglyceride in the grossly normal intima preparations of the coronary artery obtained from Japanese autopsies (41-60 yrs) were approximately 5 mg per gm of defatted and dried tissue weight, which were not significantly high compared with those in the other arterial specimens. The previous results showing a high content of triglyceride in the coronary artery were considered to be resulted from the contamination of the adipose tissue, because less than a few percentage contamination of the adipose tissue can result in a significant increase of triglyceride content of the artery. 2. The incorporations of (1-C¹⁴) acetate into digitonine precipitable sterol and bound lipids as well as FFA, PL and TG were significantly observed in the arterial wall.

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Transport of fatty acids was investigated in human aorta, aiming to analyze the esterification of cholesterol and the structure of glycerides. PC was found to be a source of supplying fatty acids to cholesterol through the participation of phospholipase. LCAT seemed to be less active in this aspect. Structure of TG was different especially at 1 and 3 position in between plasma and atheromatous plaque. This could indicate that deposited TG was modified either by transferring FFA in various position or by the biosynthesis in situ.

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At right heart catheterization, a catheter with a platinum electrode was used for recording bipolar electrocardiograms between each of the outflow tract, mid and inflow tract of the right ventricle and precordium. In the individual clinical cases including those of chronic obstructive pulmonary disease, the ratio right ventrcular element to left ventricular element was calculated, which anther named A ratio. Whether or not there was right ventricular predominance was examined by employing the A ratio as the index. Examination for correlationship was made between the A ratio, pulmonary arterial mean pressure (PAm) and cardiac index (CI), and the following conclusions have been obtained. 1) At the right ventricular outflow tract or mid, between the pulmonary arterial mean pressure and A ratio there was observed an significant positive correlationship (outflow, P<0.02; mid, p<0.01). In all but one of the cases whose pulmonary arterial mean pressure exceeded 17 mmHg, the A ratio at the outflow tract or mid was over 0.9. Dividing the cases into two groups, one showing over 0.9 as the A ratio at the right ventricular outflow tract or mid the other under 0.9, the T test, too, a difference of statistical significance (p<0.01) was observed between two groups. Thus, the A ratio has become known as an useful critical value for judgment whether or not there is pulmonary hypertension and/or right ventricular systolic overloading. 2) The A ratio at the right ventricular inflow tract exhibits a postive correlationship (p<0.02) with cardiac index. Especially in the cases of congenital heart disease accompanied by left to right shunt that pulmonary blood flow increased, the A ratio at the inflow tract tended distinctly to rise. 3) All the cases satisfied with the conventional electrocardiographic criteria for right ventricular hypertrophy (Roman et al. and WHO) showed the A ratio over 0.9. The increased A ratio may be interpreted to precede the right ventricular hypertrophy. The A ratio at the right ventricular outflow tract or mid seems to be useful as an index for early diagnosis of right ventricular hypertrophy. Increase in the A ratio at the outlfow tract or mid may be interpreted to represent the right ventricular overloading in not only cardiac disease but also chronic obstructive pulmonary disease, making it possible to evaluate to the aggravation from chronic obstructive pulmonary disease without pulmonary hypertension to chronic cor pulmonale.

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The cardiotoxicities produced by a continuous infusion of desacetyl-lanato-side C (deslanoside) alone in guinea pigs were definitely suppressed by concomitant infusion of a beta-adrenoceptor blocking agent, alprenolol (aptin, H56/28). However, the antagonistic potency of alprenolol was smaller than that of propranolol, although according to the literatures the potency of beta-adrenoceptor blocking activity of the former was said to be no less than that of the latter. That is, the correlation between the antagonistic potency against deslanoside-induced cardiotoxicities and the potency of beta-adrenoceptor blocking activity of alprenolol did not run parallel in contrary to that of propranolol. It seems probable that the suppressive activity of alprenolol against deslanoside-induced cardiotoxicities is not based on the specific action on the beta-adrenoceptor.

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