The regional contraction sequence of the left ventricle (LV) was analyzed by 16mm. cineangiocardiograms (in LAO, 40 frames per sec.) of 5 control subjects, 4 patients with mitral insufficiency, 2 with idiopathic hypertrophic subaortic stenosis (IHSS), 2 with idiopathic myocardial hypertrophy and 3 of myocardial disease with LV dilatation.
The LV cavity was divided into basal, middle and apical portion, and internal width (diameter) for each portion was measured on a line drawn perpendicular to the long axis at 3 equally spaced points. The time course of the length of the diameters in percentage of the initial length was compared, and circumferential shortening velocity (Vcs) and total extent of circumferential shortening were calculated for each diameter. Regional contraction sequence was also analyzed by superimpositon of serial LV silhouettes during systole.
In control subjects, a synchronized contraction sequence was suggested, and regional circumferential shortening velocity was inversely related to the initial length of corresponding diameter. In hypertrophied and dilated hearts of mitral insufficiency or in IHSS, an earlier onset and/or more rapid contraction of the basal portion were noted. The possible relationship between asynchronism of the contraction sequence and alterations of ventricular geometry and of myocardial architecture of the LV were discussed. In myocardial disease with dilated LV, both shortening velocity and extent of shortening were markedly reduced.
The method described here allows direct observation of the pattern of regional contraction sequence and also gives clinical indices of contractile state of the myocardium in normal and diseased LV in man.

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A correlation between RVP and the ratio R_A/S_B in pulmonary stenosis has been demonstrated for cases investigated in different countries.
This distinguishes between operative and non-operative cases.

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The conduction system was histologically examined in 14 cases of right bundle branch block associated with left axis deviation. Twelve cases showed marked degeneration of the central fibrous body, degeneration and interruption (fibrosis, calcification and fatty changes) of terminal portion of the bundle of His, proximal portions of the both bundle branches and intermediary portions of the right bundle branch and the anterior radiation of the left bundle branch. Some increase of acid mucopolysaccharide was frequently found in the blocked lesions, which suggested an accumulation of mechanical strain as a pathogenesis of the injuries in the conduction system. Two cases showed extensive myocardial infarction which gave total necrosis on the peripheral part of bilateral bundle branches. Histological basis of RBBB with LAD was concluded as a kind of bilateral bundle branch block.

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The effect of a large dose of epinephrine in blood was studied in dogs. Pulmonary edema resulted both in the experiments in which injections were made into the carotid artery and in those with intravenous injections. Left ventricular systolic pressures rose more with intravenous than with intracarotid infusions. Left ventricular end-diastolic pressures rose dramatically and rapidly but less with intravenous infusion. There was an increase of the dp/dt peak and ventricular dilatation in both types. Cardiac denervation followed by intracarotid infusion prevented or decreased pulmonary edema in 4 out of 8 experiments.
It is concluded that the rise of left ventricular end-diastolic pressure is a primary factor for the increased pulmonary capillary pressure causing edema. This rise seems to be caused by adrenergic action and efferent sympathetic stimuli affecting both ventricular compliance and peripheral vasoconstriction rather than by myocardial failure in the usual sense.

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Blood with epinephrine was infused into crosscirculated dogs and comparison was made between animals receiving the infusion only in their heads, only in their trunks, or in their entire circulation.
The procedure was invariably followed by pulmonary edema in all experimental animals.
Left ventricular systolic pressure elevations and increases of the dp/dt of this chamber were similar in all animals irrespective of the area infused. Left ventricular end-diastolic pressure elevations also occurred in all animals but were greater in the "trunk dogs" than in the "head dogs" or the "whole dogs".
These results suggest that both neurogenic stimuli and circulating catecholamines (either injected or secreted under the influence of nerve stimulation) contribute to the chain of events leading to formation of pulmonary edema.

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Many factors have been implicated in the etiology of hypertension. The experiments to be reported here were done to study the effects of diets on blood pressure in a total of 263 Dawley rats in which unilateral renal artery was constricted by silver clip and 82 normal rat served as controls.
As regards the environmental factors, experiment I was done under the natural condition while experiment II was made under the condition of constant temperature and constant humidity.
In experiment I, both normal control and renal hypertensive rats were divided into 9 groups respectively and fed various experimental diets by the combinations of protein, fat and salt according to the experimental design. In experiment II, they were divided into 5 groups respectively by the combination of protein and salt.
From these experiments, it was observed that low protein diet combined with high salt causes significant elevation in blood pressure of Goldblatt hypertensive rats compared to the other experimental diet, while not in the normal control rats fed the diets of similar composition. There were no significant differences in blood pressure elevation between two environmental conditions.

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Responses of the sympathetic nerves and the systemic arterial pressure to vertebral embolism were examined in rabbits anesthetized with α-chloralose under artificial respiration and the following results were obtained:
1. Following vertebral embolism, the systemic arterial pressure increased moderately at first followed by a slight decrease, then increased to much higher levels and returned gradually to the control levels, and thereafter it decreased to lower levels than the controls.
2. The sympathetic discharge increased slightly and momentarily at the onset of hypertension (the phase of the first increase), decreased to lower levels than the control (the phase of decrease), then increased markedly (the phase of the second increase) and returned gradually to the control levels in most experiments under intact buffer nerves. The phase of the second increase corresponded nearly to the second rise in blood pressure. The phase of decrease in sympathetic discharge disappeared or became slight with repeating embolism or with elevating blood pressure to much higher levels. Also, it became slight or disappeared in most experiments done after resection of the buffer nerves.
3. Both rhythmical and non-rhythmical impulses were recorded from the renal nerves. The former responded to vertebral embolism in somewhat different fashion from the latter.
4. Following embolism, the afferent impulses from the right subclavian baroreceptor increased nearly in parallel with the arterial pressure.
It was concluded that the sympathetic nerve showed various discharge patterns in response to vertebral embolism. It was supposed that the phase of decrease in sympathetic discharge was mainly due to reflex inhibition by the buffer nerves and that the excitation patterns of the sympathetic nerve following vertebral embolism were determined by the following factors: magnitude of the sympathetic nerve excitation, sympatho-inhibitory action of the buffer nerves, reactivity of the target organs of the sympathetic nerves and the control levels of both sympathetic nerve activity and blood pressure.

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The influence of blood pressure on the renal medullary osmotic pressure gradient was studied in hemorrhagic hypotension of hydropenic rabbits. Slice analysis was made for urea, sodium and potassium concentrations in the kidney slices. The tissue fluid osmolality was estimated as the sum of the urea concentration and 2×electrolyte concentrations. A drop of systemic blood pressure, induced by bleeding, resulted in decrements of urea and sodium concentrations with resultant reduced osmotic pressure gradient in the medulla, but did not significantly affect solute and osmotic concentrations in the cortex. A loss of urea from the medulla was more rapid and greater than that of sodium. The reduction of the medullary osmotic pressure gradient became greater as mean blood pressure decreased to 50-60mm.Hg, but was reduced with progressively decreased blood pressure below 50mm.Hg. Renal arterial occlusion for 1 hour gave rise to a slight decrease in the medullary osmotic pressure gradient, chiefly due to loss of urea from the medulla. The finding indicates that the depletion of the medullary osmotic pressure gradient in hemorrhagic hypotension is dependent upon the blood pressure level. The data were also discussed in relation to the renal hemodynamic alterations in hemorrhagic hypotension.

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