Protective action of conjugated equine estrogen (CEE) against endotoxin shock was admitted in mice. Male DDN strain mice pretreated intraperitoneally with 2 mg of CEE showed various survival rates according to the interval between administration of CEE and endotoxin injection. Survival rates of the control were 20.4%, but in the group pretreated with CEE they were 0% at 0 hour, 26.3% at 1 hour, 33.3% at 12 hours, 55.7% at 24 hours (p<0.001), 10.5% at 36 hours, and 31.2% at 48 hours exhibited excellent resistance to 0.5 mg endotoxin. On the other hand, the hemodynamic effect of CEE was examined in six mongrel dogs, which showed little hemodynamic changes following administration of 10 mg/kg CEE for three hours observation. We speculated that the anti-shock action of CEE was due to the modification of vascular response to vasoactive substances, on the one hand it augmented the vascular contractile response to vasopressors and on the other hand it lessened the hypersensitive vasoconstriction under shock state.

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Discrepancy in coronary stenosis between angiogram and pathological specimen was moderately found. it is of a problem what is meaning by a significant narrowing. Coronary capacity per heart weight markedly reduced in multi-vessel disease and revealed an intimate relationship to sudden death and cardiac failure. Much of sclerosis in the arterial wall was relatively severe in spite of patency in lumen of the terminal artery. Intramuscular arterioles were intact even when severe extramuscular coronary atherosclerosis was seen. Well-developed collaterals were seen in much of multi-vessel disease. Muscle prevervation was relatively good even in the advanced sclerosis. It is reasonable to make an attempt on a newly construction of a vessel to introduce in to preserved arteriola with well-developed collateral, and preserved myocardium.

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Unselected 580 male and 779 female junior and senior high school students were subjected to the tilting test and informations on 11 autonomic dysregulation symptoms and complaints were taken by interviews. Results of the analyses of the data are summarized as follows: 1) Number of symptoms and complaints possessed by each individual distributes continuously but nonrandomly among testees; that is, individuals having no symptom and those having 5 or more symptoms are significantly more numerous than those expected from random distribution, indicating accumulation of the symptoms into some individuals. 2) Some specific symptoms tend to coincide with each other. 3) Principal component analyses disclosed that the first principal component can explain only 16-20% of the observed variation in the presence or absence of symptoms and complaints, suggesting that numerous factors are responsible for the occurrence of the symptoms. 4) Measurements of the blood pressures and the pulse rate, and their responses to the postural change show continous, normal distributions, and significantly correlated to each other. 5) The responses to the tilting test are increased with the increase of number of symptoms and complaints possessed by the testees.

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The hypotensive effect of 1-Sar-8-Ile-angiotensin II, a competitive antagonist of angiotensin II, and the pre-infusion level of plasma renin concentration were examined in conscious rats with various types of hypertension to assess the role of the renin-angiotensin system in the pathogenesis of experimental hypertension. The infusion of 1-Sar-8-Ile-A II (0.64 μg/min or 3.2 μg/min) caused a significant fall in blood pressure in two-kidney Goldblatt rate (4-5 weeks after clipping) and 7-8-month-old stroke-prone spontaneously hypertensive rats (SHR), while it was statistically ineffective in one-kidney Goldblatt rats (4-5 weeks after clipping), one- and two-kidney Loomis rats (2 and 4-5 weeks after induction), 5-month-old stroke-prone SHR and 2-, 5-, 8- and 14-month-old stroke-resistant SHR. A significant correlation between plasma renin concentration and the susceptibility to the antagonist was observed in Goldblatt rats and stroke-prone SHR, but not in Loomis rats and stroke-resistant SHR. Some groups of animals which had not responded to the original infusion of 1-Sar-8-Ole-A II were infused again with the same antagonist in a furosemide-induced volume-depleted state, in which plasma renin level was prominently elevated in all rats and angiotensin-II dependency of blood pressure was disclosed except in the 8-month-old stroke-resistant SHR. These data suggest that the renin-angiotensin system is critically involved in the two-kidney Goldblatt rats and the 7-8-month-old stroke-prone SHR, but that it is much less important in other hypertensive rats and other factors would be involved especially in case of stroke-resistant SHR.

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The conduction system was examined histologically in three cases whose electrocardiograms showed right bundle branch block and left axis deviation with or without PR prolongation. In two cases histological lesions were found in the right bundle branch and anterior division of the left bundle branch. In the third case histological lesions were found in the right bundle branch and anterior and posterior divisions of the left bundle branch. This case sufferred an Adams-Stokes attack. In the two patients with right bundle branch block and left axis deviation with PR prolongation, the PR prolongation was attributed to delay in atrioventricular node or His bundle in one case and to delay in left bundle branch in the other.

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