Ratios of weight and surface area of various parts of the heart to the heart and body were determined in 18 controls. In other 52 dogs the interventricular septum was operatively replaced with 1/8 inch thick Teflon felt, and cardiac performance was studied in dogs which survived for more than 30 days. It was estimated that in the long-term survivors the resected septum was 28.3 to 44.3% of the septum in weight, dependent upon definition of the septum. In surface area it was 63% of the right ventricular side of the septum and 55% of the left. To the left ventricule the septum replaced was 12.3% in weight and 15.6% in surface area. Cardiac performance of these heart was close to normal with the competent mitral valve and was impaired in presence of mitral insufficiency. It was also suggested that paradoxical movement of the septum had special meaning in term of compromising the normal volume ratio of the ventricles, compared with that of the free ventricular wall and that the septum had a role for the normal function of the mitral valve.

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In this paper, the correlation between the maximal QRS vector or the mean electrical axis by Frank lead system and the maximal long axis or the half area long axis of the left ventricle obtained by biplane angiocardiogram in the frontal and left sagittal planes in thirty patients with various heart diseases were studied. Cases with marked ventricular hypertrophy or abnormalities in the intraventricular conducting pathways were excluded as much as possible. Compared to contemporary studies the approach utilized by the present authors appears to be more favorable, viz; (1) the mean electrical axis was calculated from the corrected orthogonal lead system, (2) the anatomical position of the left ventricle was measured exactly and minutely from the angiocardiogram in the frontal and left sagittal planes, and (3) the end-diastolic volume and the wall thickness of the left ventricle were determined from the left ventriculogram in order to assess the grade of left ventricular hypertrophy, while pressure measurements in the right heart chambers detected right ventricular hypertrophy.

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^3H-norepinephrine (NE) disappearance rate after the intraventricular injection of ³H-NE tended to be delayed in the brainstem but not in the telencephalon of spontaneously hypertensive rats (SHR) in the prehypertensive stage, while these indices were conversely accelerated in the heart and slightly so in the kidney of SHR. A similar tendency was partially noted in the brainstem, telencephalon and heart of SHR, DOC and renal hypertensive rats at the age of 10 weeks which had maintained hypertension for 1 month. The relative delay in the NE turnover of the brainstem compared with telencephalon was seemingly the common deviation of NE metabolism in these rats with genetic or experimental hypertension.

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Inactivation of vasoactive substances in pulmonary circulation were studied in vivo experiment and heart-lung preparation using rabbits. In vivo experiments, pressor substances such as angiotensin vasopression, epinephrine, and norepinephrine passed through the lung without any change on their pressor activities, but all the depressor substances, such as bradykinin, 5-hydroxytryptamine, adenosine, ATP, poly A and prostaglandin E₁ were markedly affected in their depressor activities through pulmonary circulation. In the heart-lung preparation, inactivation of bradykinin and prostaglandin E$₁, as well as the activation of angiotensin I, were observed, however other depressor substances were not inactivated.

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Shortly after the beginning of immobilization stress a remarkable elevation in the arterial pressure, a significant increase in plasma renin levels and plasma corticosterone concentrations were observed. However the changes of plasma renin levels throughout the immobilization stress did not coincided with those of plasma corticosterone concentrations and adrenocortical biosynthetic activity. There seem to be the different mechanisms to activate the renin angiotensin system and the pituitary-adrenocortical system. The changes of the EEG activity during the stress suggested that the homeostatic mechanisms mediated by the activity of the mesencephalic reticular formation and the mesencephalic central grey seemed to regulate the blood pressure. The involvement of the mesencephalic reticular formation and the mesencephalic central grey was also suggested by the stimulation experiments; that is, the mesencephalic reticular formation, the mesencephalic central grey and the posterior hypothalamic area seemed to be more effective on the release of renin than on the release of corticosterone, while the other areas in the brain such as the hippocampus, the amygdala and the anterior hypothalamic area were not so effective on the release of renin.

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In the cytoplasmic fraction (C. F.) of rats treated with DOCA plus salt, renal renin activity was already decreased before the development of hypertension and was more suppressed after that of hypertension. Renal cathepsin activity was slightly increased shortly before the development of hypertension and more elevated after that of hypertension. Increased renal β-glucuronidase activity was found after the longer duration of hypertension. Deoxyribonuclease activity was slightly increased in average after the development of hypertension, but not significantly. Ribonuclease and β-glycerophosphatese activities were not increased, rather slightly decreased after the development of hypertension. The percentage of soluble fraction (S1) or supernatant fraction (S2) to cytoplasmic fraction (C. F.) was diminished in both cathepsin and β-glucuronidase activities in rats treated with DOCA plus high salt as compared with that in the controls, but was nearly identical with that in the controls in β-glycerophosphatase activity. The probable role of lysosomal acid hydrolases in hypertensive vascular lesions was discussed.

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It was electronmicroscopically shown that thick and thin filaments similar to myosin aggregates and F-action constituting arterial natural actomyosin were present even in renal arteriolar or capillary endothelium. Amounts of Ca²⁺, Mg²⁺ and Na⁺/K⁺ contained in arterial wall appeared to be higher in renovascular hypertensive rats than those in normotensive rats, although amounts of these electrolytes in skeletal muscle were not different between them. Since it has been clarified that free ion concentrations of these electrolytes have influence on the contractile activity of arterial natural actomyosin, the role of these electrolytes in arterial wall for the induction of hypertension was discussed on the basis of a hypothesis that an augmentation in the active contractility of peripheral arterioles may play an etiological role for the essential hypertension.

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The effect of salt, high blood pressure and renal factors on the development of acute vascular lesions of small arteries and arterioles and cerebral hemorrhages was studied in rabbits through production of hypertension by means of unilateral or bilateral renal injuries. 1 . Massive cerebral hemorrhages were induced in animals with bilateral renal injuries and these were never induced in animals with one ischemic and the other intact kidneys even during advanced stage of hypertension. 2. Animals died, due to cerebral hemorrhages usually accompanied with marked high blood pressure during the advanced stage. However, cerebral hemorrhages were induced in animals with blood pressure less than 120 mmHg as well as in those with higher blood pressure during the early stage after renal manipulation. 3. Among acute arterial lesions, the most prominent lesion consisted of the fibrinoid necrosis of small arteries and arterioles with a wide distribution. The vessels of gastro-intestinal tract especially those of stomack were predominantly vulneable. 4. Fibrinoid necrosis of small arteries and arterioles in the brain was found all of the experiments with cerebral hemorrhages. The incidence of the acute arterial lesion in the brain and other tissues was higher in experimental groups in which cerebral hemorrhages developed. These results convince that the fibrinoid necrosis of small arteries and arterioles in the brain is the primary vascular lesion responsible for cerebral hemorrhages. 5. The incidence of the fibrinoid necrosis in small vessels was not related with the grade of high blood pressure especially during the early stage of hypertension. It was not clear, however, how much the high blood pressure itself contributed to the development of the acute arterial lesion during the advanced stage of hypertension. 6. Renal factors played a great role in producing the acute arterial lesion (fibrinoid necrosis). A renal factor other than renin seemed to be responsible for the acute arterial lesion and cerebral hemorrhages. The acute arterial lesion was induced in animals with one ischemic and the other intact kidneys during the early stage of hypertension. But, it was scarcely produced during the advanced stage of hypertension. Bilateral renal injuries (two ischemic kidneys or one ischemic kidney after one nephrectomy) enhanced the development of the acute arterial lesion. 7. High salt intake augumented the incidence of the acute arterial lesion.

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