The mean systemic pressure was estimated indirectly in humans from cardiac index and right atrial pressure under a set of obviously over-simplifying assumptions that (1) "normal" venous return curve for mean systemic pressure (Pms) of 7 mmHg gives, by definition, a venous return of 3.8 lit.min ^-1M^-2 at zero right atrial pressure and (2) different human subjects have venous return curves with downslopes parallel to this "normal" venous return curve. Mean systemic pressure estimated in this manner was termed the graphically estimated mean systemic pressure (Pms.g.). Pms.g. was examined for its numeric-al relationship with the cubital venous pressure (VP). In 38 pairs of comparison which was possible in 36 patients with or without heart diseases and congestive heart failure, Pms.g. tended to rise with VP. Moreover, VP tended to approach Pms.g. on the average and slightly, when the cubital venous pressure rose above the upper limit of the "normal" range, and also when the cardiac index was low, independently of the venous pressure. If the obviously over-simplifying assumptions which formed the basis of this approach are adequate, these facts suggest that the chronic congestive right heart failure, with elevated cubital venous pressure, is associated with elevated mean systemic pressure. Possible significance of the apposition between VP and Pms.g. observed for higher VP and lower CI (cardiac index) was discussed.

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The effect of electrical stimulation of the stellate ganglion on the blood flow through the ischemic myocardium was examined in anesthetized open-chest dogs. The flow was continuously monitored by heated cross-thermocouples. The anterior descending branch of the left coronary artery was constricted in order to produce various ischemic states in the anterior wall of the left ventricle. Following stimulation, the flow through the outer half of the wall was increased before constriction, was slightly reduced during mild constriction, was markedly reduced during moderate constriction and was slightly reduced or increased during severe constriction. The flow through the inner half was not infrequently reduced before constriction, was slightly reduced or increas-ed during mild constriction and was markedly increased during moderate or severe constriction. These flow changes had a relation to the pressure gradients between the constricted and non-constricted branch. The flow through the zones adjacent to the constricted area was augmented by stimulation. Pretreatment with propranolol eliminated these flow changes. These results suggest the regional difference of sympathetic regulation of the myocardial blood flow and the dependence of its modality on the severity of ischemia. It is supposed that stimulation-induced reduction in the flow through the moderately ischemic myocardium was due to 'coronary steal' and that its occurrance is dependent on the severity of constriction of the coronary artery.

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An unusual disappearance of right bundle branch block by digitalis in a child with cretinism is described. A transient occurrence of right bundle branch block pattern in V1 and left bundle branch block pattern in V2 and V3 is also observed in the same case, and the possible mechanisms behind these findings are discussed.

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In order to elucidate the propagation process of ventricular activation in left bundle branch block (LBBB) and its resultant QRS patterns observed on the body surface, a number of experimental studies have been made. However, the site and the mechanism of block still remain a matter of debate among these reports. It is also under question whether the results obtained from animal experiments can be applied to explanation for the genesis of naturally developed LBBB within human ventricles. The purpose of this paper is to discuss the mechanism of LBBB observed with human subjects. Namely, the ventricular propagation process of excitation was simulated in a model of the human ventricles which was constructed using the human heart as a basis and stored in a computer. A variety of speculative for LBBB was provided to the model before the simulated propagation took place. The body surface QRS patterns were computational reconstructions based on these simulated ventricular propagation processes. The obtained QRS pat-terns were then compared with those of clinical cases of LBBB. Moreover QRS vector loop were obtained and they were examined correspondence with the obtained QRS patterns. Methods: 1. Simulation and QRS reconstruction By means of digital computer simulation, a number of propagation processes in excitation of the ventricles with LBBB were obtained. The scalar QRS patterns for the thus acquired propagation processes were obtained by the above means in the conventional twelve leads and X, Y and Z leads of Frank system. QRS vector loops of Frank system were plotted by hand from the scalar QRS patterns. within human ventricles. In order to provide the ventricular model with a mechanism of LBBB, the following five kinds of different assumptions (1-a, 1-b, 2, 3 and 4) were utilized respectively. In all of these five assumptions, a lesion was assumed on the left bundle branch running on the upper portion of the ventricular septum. For the remaining parts of the ventricle, a block of the excitation spread was provided to the model according to one of the following five assumptions. Each of these assumptions was pursued on the bases of various interpretation of LBBB advocated in the previous reports on animal experiments.

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The role of catecholamine-sympathetic nervous system on the genesis of essential hypertension has long been investigated, but unsettled. Ikoma reported an increase of norepinephrine excretion in the urine of patients with essential hypertention without renal insufficiency, whereas Euler demonstrated elevated levels of urinary excretion of norepinephrine in only 16.4 per cent of 500 hypertensive patients. There were also no significant differences in urinary excretion of the metabolites of catecholamines between normal controls and hypertensive patients. On the other hand, the fact that most antihypertensive agents currently used are involved in some way with catecholamine metabolism, suggests an intimate relationship between hypertension and sympathetic nervous system. Gitlow was the first who investigated the catecholamine metabolism of the essential hypertension with use of dl-beta-H³-norepinephrine. It was assumed that the accelerated turnover of norepinephrine may be present in the essential hypertensive patients. However, De'Quattro could not confirm the accelerated turnover in the hypertensive patients. This discrepancy may be the reflection of the absence of a uniform sympathetic nervous response in the different varieties of hypertension. There are posturated two stages of essential hypertension, i.e., labile and fixed. A heightened sympathetic and circulatory activity may be more characteristic in the early labile than in the fixed phase of essential hypertension. The purpose of this study was to compare the rate of norepinephrine turnover in labile hypertension and fixed hypertension and to study on the effect of fusaric acid, a potent inhibitor of dopamine beta hydroxylase, on the catecholamine turnover in the hypertensive patients.

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The present study was designed for morphologic-al investigation of the vascular abnormalities or vascular reconstruction in areas of myocardial infarction, compared with the normal vascular patterns. The vascular changes along with the time course changes of infarcts were emphasized. Studies were performed on 62 hearts obtained at random at necropsy in Tokyo Medical Examiners' Office. The age of patients including 15 cases of myocardial infarction range from 5 to 85 years. At necropsy, the heart was removed and canulae were inserted into the right and left coronary arteries at their origin. A radiopaque medium (60 wt/vol% barium sulfate) with addition of 5% gelatin was injected into the coronary arteries under hand operated pressure, at about 40°C at first into the left coronary artery followed by the right as a rule. After injection, stereo-arteriography of each intact heart, unrolled heart and transverse section of heart was carried out. Serial observation of 2mm thick sections of coronary arteries was then carried out, before clearing the heart tissue. Histological investigation of myocardium stained by Hematoxylin and Eosin, Elastica Van Gieson and Mallory-Azan staining was also carried out. Results: 1) Three fundamental intramural intramural vascular patterns were distinguished in the left ventricular free wall of the normal heart. The vessels of type I leave the extramural subepicardial artery at right angles into myocardium and quickly branch like a bamboo-broom or like an arbor with delicate fine branching, gradually losing its lumen diameter. Although smaller vessels of this type terminate themselves in middle layer of the myocardium, larger vessels penetrate deeper up to the inner one thirds or one fourths of myocardium or even to the traveculae. The vessels of type II also leave at right angles into myocardium like the vessels of type I, but are less numerous, branch infrequently and arrive directly at papillary muscles and traveculae, where they subdivide, forming large looping arcades bending upwards and downwards like a hook or a rake. The vessels of type III are rela-tively smaller ones seen in the subepicardial layer. Various intermediate or transitional vessels between typical patterns of type I and type II are recognized. Except the subendocardial layer and septum, intramural interarterial anastomoses are not found in the normal myocardium as a rule.

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Radioimmunoassay of angiotensin I and its appli-cation to the measurement of plasma renin activity (PRA) was studied. The assay method consists of the incubation of plasma at 37°C, pH 5.5 for 6 hours with disodium ethylenediamine tetraacetic acid (EDTA) and di-isopropyl fluorophosphate (DFP) and the radioimmunoassay of angiotensin I generated during the incubation. The values of PRA determined by the present method showed a good correlation with that of bioassay. We examined to find the ideal conditions in each step of this procedure and found its high specificity, sensitivity and reproducibility for routine clinical use. Materials and Methods: 1) Angiotensin I antibody Angiotensin I antiserum was supplied from Schwarz Mann which was produced by injection of copolymers of asparatyl-isoleucyl⁵-angiotensin I and succinylated poly-L-lysine in a rabbit according to Haber's method. 2) Preparation of ¹25I-angiotensin I Angiotensin I was iodinated according to the method of Hunter and Greenwood. Anion exchange resin was employed on the procedure of the purification of ¹25I-angiotensin I. 3) Angiotensin I standard solution Asparatyl-isoleucyl 5-angiotensin I supplied from the Institute for Protein Research of Osaka University was dissolved to the Concentration of 500 μg/ml with 0.1M acetic acid. This solution was used as a stock standard solution. 4) Blood sampling Blood was drawn in the morning under fasting and recumbent position. Plasma was separated by centrifugation and was stored at -20°C. 5) Incubation One milliliter of plasma was pipetted into a polyethylene tube and incubated with EDTA and DFP at 37°C, pH 5.5 for 6 hours. 6) Radioimmunoassay Tris acetate buffer 0.2M, pH 7.4 containing lysozyme 0.1%, EDTA 0.05% was used as diluent for all samples and reagents. All procedures were performed in polyethylene tube. Standard angiotensin I (10, 25, 50, 75, 100, 200, 300 and 500 pg) or 10μl of samples were mixed with 6, 000 cpm of ¹25I-angiotensin I and 50μl of dilute antiserum in 1ml of tris buffer. The mixtures were incubated at 4°C for 24 hours. After the incubation, dextran coated charcoal was added to each tube and then shaken for 20 minutes and centrifuged. The supernatant was discarded and the precipitate was counted in a well-type scintillation counter. The binding ratio of each standard solution was calculated and plotted on a semilogarithm paper (standard curve). The binding ratio was used as a quantitative indicator to estimate angiotensin I content in each sample.

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