The role of catecholamines in the accumulation of sodium and water in the vascular walls of hypertensive patients was examined. The excess production of catecholamines was not found in hypertensive patients. During the rise of blood pressure induced by norepinephrine, the concentration of plasma sodium decreased and that of plasma potassium increased. No significant difference could be found between hypertensive patients and normal subjects in these cationic shifts. Water also moved into intracellular space during the rise of blood pressure. The influx of ²²Na in the aorta strips of rats was found to be potentiated by norepinephrine, while that of ⁸⁶Rb seemed to be hindered. The influx of ²²Na in the aorta strips in the group of hypertensive rats was significantly greater than that seen in the group of normotensive rats. The relationship of these cationic shifts to the pathogeneses of "essential" hypertension has been discussed.

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Cholesterol level of normal subjects with 499 men and 331 women in Kyoto area were examine 1) Cholasterol level increased with age in both sexes. 2) Cholasterol level increased with obesity. 3) Cholesterol level in mental worker was higher than that in non-mental one. 4) Relationship between cholesterol level and such factors as age, workness and body-weight was discissed.

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Though our experiments are still on the way and have much to be done, tentative conclusion may be as follows : 1) In experimental right heart failure with dogs produced by the injection of lycopodium spores, total hepatic blood flow was shown to decrease with the distributional change of relative increase of hepatic arterial flow (and consequently relative decrease of portal venous one).

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1) Hepatic circulation in hemorrhagic and anaphylactic shock was studied upon dog experiments, with special emphasis on its relation to systemic circulation. 2) The results on hemorrhagic shock are diagrammatically summarized in Fig. 1 2. During the stage of "simple hypotension ", concomitant changes were observed in the main features of hepatic and systemic circulation, as indicated in the Figure. However, during sub-sequent irreversible phase, the changes in hepatic circulation were no more in parallel with systemic hemodynamic alterations. In particular, the more pronounced diminution was revealed in hepatic blood flow than in cardiac out-put with a resultant " gap" between those two variables. This gap seems to be the most characteristic feature of this critical state of shock, and may result from increased splanchnic vascular resistance. Other problems such as the significance of the blood pooling in the splanchnic bed were discussed in connection with the foregoing events. 3) During anaphylactic shock, the features of hepatic circulation varied in parallel with systemic hemodynamic alterations, except at a brief period just after the provocation to shock. At this cirtical period, hepatic blood flow was reduced pronouncedly with the accompanying but less pronounced diminution in cardiac out-put, and, there was a sharp rise in portal vein pressure, a marked increase in splanchnic vas-cular resistance and a simultaneous fall in inferior vena caval pressure. All of these phenomena may be ascribed to " hepatic sluice mechanism" due to the constriction of the hepatic venous sphincters. Marked congestion and plasma extravasation was observed in the liver. 4) Splanchnic oxygen utilization became significantly impaired, in both types of shock, despite the increased arterio-venous oxygen difference. 5) Catecholamine concentration in arterial blood rised continuously throughout the course of hemorrhagic shock, but it rised temporarily in anaphylactic shock just after the provocating injection. The possible role of the fact was discussed in connection with its action on splanchnic vascular resistance. The details of the present investigation will be submitted by our collaborators as separate publications.

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