Sixty-six cases with bilateral cerebrovascular lesions among 141 autopsy cases examined at Harunaso Hospital during the past four years were analysed from a clinico-pathological point of view with special reference to the degree and mode of onset of motor disturbance. These cases (84.6% of cases with cerebrovascular lesion) were classified into three groups I, II and III, depending on the state of motor disturbance. Group I: Cases with tetraplegia (or paresis) were designated as group I, which was further divided into four types, A, B, C and D, according to the mode of development of motor disturbance. Type A: Separate attacks of hemiplegia on both sides with resulting tetraplegia (or paresis). Type B: Acute onset of hemiplegia on one side with gradual development of motor paresis on the other side. Type C: Gradual development of tetraparesis (or plegia) Type D: Acute onset of tetraplegia (or paresis) Group II: This group comprised cases showing hemiplegia without motor disturbance on the other side (Hemiplegia with contralateral silent type). Group III: Cases with no motor disturbance were included in group III (silent group). Pathological findings revealed that all cases of type A had their lesions in the basal ganglia including the internal capsule and 25% of these had lesions in the pons too. Lesions of type B were chiefly of lacunes of basal ganglia and the responsible lesions for the evident hemiplegia were small softenings in the pons. Cases belonging to type C were observed to have small softenings in the basal ganglia. In type D, acute onset of tetraplegia was caused by intracranial hemorrhage, i. e. cerebral (2 cases), cerebellar (1 case), pontine (1 case) and subarachnoid (3 cases) hemorrhages. Lacunes in the claustrum were the main lesions of neurologically silent side of cases belonging to group II. In group III, lacunar softenings or the cortical lesions in the silent area of the non-dominant hemisphere were the main lesions, while the other factors including diseases other than CVD, or secondary changes such as deformities of the limbs, edema or malnutrition made the diagnosis difficult in this group.
1) 14C-cholesterol incorporation into arterial tissues and the release from the tissues were studied under various conditions of the tissue culture. The arterial tissues of various portions of human arteries as well as monkey aorta were used for the experiment. In addition, 14C-cholesterol uptake into the cells was examined at cellular level using the monolayer cultures of chick aortic cells and HeLa cell lines. 2) 14C-cholesterol uptake in human aortic tissue was associated with the incubation time for 36 hours. Moreover, the linear relationship between incorporation rate and incubation time also observed in chick aortic cells for 7 hours and also in HeLa cells for 36 hours. 3) Thus, the incorporation of 14C-cholesterol was shown over 72 hours but the rate decreased gradually afterwards. Contrariwise, the release of 14C-cholesterol from arterial tissue into media was clearly observed for several hours, and then the releasing rate was decreased. 4) The uptake of 14C-cholesterol was compartively higher in the ascending and arch portions than thoracic aorta and the greatest uptake was found in the coronary artery. The incorporation rate in the thoracic aorta trended to be much higher in young subjects than aged ones and it was demonstrably high in monkey thoracic aorta prepared immediately at postmortem.
A single intraperitoneal administration of Na-Sulf-acetylthiazole (SAT), 0.5g/kg body weight as 5% aqueous solution into rats caused interstitial nephritis leading to obstructive nephropathy, which induced medionecrosis with medial calcification of the aorta, interstitial myocarditis and nephrocalcinosis in rats above the age of 4 months but not in 40 day old immature animals. Calcium content of the aorta, heart and kidneys and 24hrs. uptake of 45Ca by those organs 3 days after. SAT treatment were significantly increased in adult rats. Microautoradiogram of the aorta showed the localization of the grains of 45Ca in the media in correspondence to the histological findings. In the microautoradiogram of the kidney, the grains of Ca aggregated in the tubular canals and in the tubular epithels, and also scattered in the degenerated interstitial tissues but not in the foci of the cell infiltration without degenerative changes. Such histological changes and increase of the calcium content and 24hrs. uptake of 45Ca by the heart and aorta were prevented by prior parathyroidectomy. The content of 45Ca administered 2 weeks before SAT treatment to label the stable fration of the femur was markedly decreased in response to the administration of SAT in intact adult rats but not in immature or parathyroidectomized adult animals. These changes in calcium metabolism are probably due to the increased parathyroid hormone activity secondary to ranal injury. The greater susceptibility of older rats to SAT-induced cardiovascular changes than younger ones might be due to the increased avidity of soft tissues to calcium salts.
The prophylactic effects of thyrocalcitonin, high cholesterol diet and conjugated estrogen on the Na-Sulfacetylthiazole (SAT)-induced cardiovascular changes were studied in rats. (i) Effect of thyrocalcitonin: Daily subcutaneous injection of 200 MRC mU of thyro calcitonin dissolved in 16% gelatin prevented the increase in the calcium content of the heart after SAT treatment, but not prevented histological changes and 24hrs. 45Ca uptake. (ii) Effect of feeding with high cholesterol diet: Feeding adult rats with high cholesterol diet for 4 weeks prior to the administration of SAT and thereafter untill the day of sacrifice prevented the histological changes and abnormal calcium metabolism in the aorta and heart but not in the kidneys. The 24 hrs. uptake of 45Ca by the femur was markedly decreased through feeding with high cholesterol diet as compared with control animals. Serum total cholesterol was markedly elevated. (iii) Effect of conjugated estrogen: Daily subcutaneous injection of 100r/100g body weight of conjugated eatrogen in rats failed to prevent the SAT-induced cardiovascular changes and increased the 24hrs, uptake of 45Ca by the heart and kidneys. Serum 45Ca was also increased. (iv) Effect of the cholesterol feeding and conjugated estrogen: SAT-induced cardiovascular changes and abnormal calcium metabolism were prevented in the aorta and heart but not in the kidneys by such treatment. The 24hrs. uptake of 45Ca by the fumer was markedy decreased through such treatment as compared with control animals.
A clinicopathological study was performed in a total of 592 consecutively autopsied cases (244 men and 348 women) at Tokyo Yoiku-in Hospital between January, 1967 and December, 1969, to characterize the causes of death in the aged. Direct cause of death was single in 456 cases (77%) and multiple in 136 cases (23%). Diseases of respiratory system was the leading cause of death, which amounted to 49.2%, including various kinds of pneumonias, followed by those of central nervous system (27.7%), circulatory system (15.3%), malignant neoplasm (9.6 %), those of digestive tract (9.6%) and urinary tract (8.6%). Principal underlying diseases were consistent with the direct cause of death in 383 cases (64.7%), and different in 209 cases (35.3%). Principal underlying disease was single in 463 cases (78.2%) and multiple in 129 cases (21.8%). Among them diseases of central nervous system was the highest (38.2%), followed by respiratory system (24.5%), circulatory system (23.6%), malignant neoplasm (15.5%), digestive tract (8.4%) and urinary tract (5.9%). Comparison of these results with the vital statistics in Japan showed that there was no cases of senility in our statistics, and that importance of respiratory disease as the direct cause of death in the aged group should be emphasized. Sudden death was defined as (1) sudden death terminating within 1 hour, and (2) unexpected death terminating within 24 hours. Sudden death (38 cases) and unexpected death (65 cases) made a total of 103 cases, which corresponded to an incidence of 17.4%. Incidence of sudden death was highest in diseases of circulatory system (40.4%), followed by those of respiratory system (12.9%), and central nervous system (12.8%). Cardiac rupture (5 cases), aortic rupture (7 cases), myocardial infarction (13 cases) and valvular disease (7 cases) were the main lesions of cardiovascular origin. Essential features of respiratory disease was suffocation in sudden death and latent progress of pneumonia in unexpected death. Most of the sudden death in disease of central nervous system was unexpected, including 16 cases of bleeding. Retrospective analysis of a total of 554 electrocardiograms revealed that the incidenoes of advanced degree of A-V block, left axis deviation, right bundle branch block, myocardial infarction and ventricular premature beat were high in sudden cardiac death.