1. Correlation between hemodynamics in different parts of venous system and difference in graft patency was discussed. 2. Feasibility of compilation graft made of autogenous vein and Teflon tube with external support was evaluated in experimental replacement of canine superior vena cava. 3. Clinical trial of this compilation graft would appear to be worth while.

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1) The production of a septal laceration which interrupted anterior rami of the left bundle branch caused a marked left axis shift in baboons, while far less axis shift was observed in dogs. 2) In the control state, definite differences in the configurations of ventricular complexes were observed from direct epicardial leads over some parts of the left ventricle. 3) The mode of excitation of antero-basolateral wall of left ventricle, where a marked delay of activation time was observed after the lesion, was almost the same in degree of the delay and extent of the involved area in dog and baboon. 4) A hypothesis which may reconcile the discrepancy of these experimental data is proposed.

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The effect of acute and chronic ischemia on the A-V conduction system was investigated by occluding both the anterior and posterior septal arteries in the dog. A-V block, either complete or of second degree, developed in about 90 per cent of the acute experiments. The reversibility of the acute disturbances of the A-V conduction was demonstrated by releasing the occlusion after A-V block was established. In the chronic experiment complete A-V block disappeared when the dogs survived one day or more in spite of marked destruction of the A-V conduction tissue.

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Aconitine induces the automaticity and fibrillatory activity in the vena caval muscle. The electrical activities in the vena caval muscle may have physiological significance.

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In order to evaluate a role of sympathetic nervous system in pathologic physiology of essential hypertension, an effect of autonomic ganglion blockade and noradrenaline on systemic and digital hemodynamics was observed in 55 normotensive subjects, 102 patients with essential hypertension and 18 patients with hypertension caused by glomerulonephritis (renal hypertension). Under basal condition, digital blood flow (DBF) was lowered, and digital (DVR) and total peripheral resistance (TPP) were elevated uniformly in both essential and renal hypertensives. Following the administration of hexamethonium, the increase of DBF and the decrease of DVR were significantly greater in essential hypertensives than in normotensives. These changes tended to be less remarkable in older individuals. Responses to noradrenaline were examined after the pretreatment of hexamethonium. Compared with the normotensive subjects, the elevation of DVR and TPR and the reduction of DBF was significantly greater, and the de-crease of cardiac index (CI) was observed in essential hypertensives. The majority of renal hypertensives showed the increase of DBF and CI, and no significant change in DVR and TPR. In contrast to noradrenaline, angiotensin 11 induced uniform changes of systemic and digital hemodynamics in normotensives and two hypertensive groups, i. e., the decrease of CI and DBF and the increase of DVR and TPR. Based on these findings, relationship between essential hypertension and sympathetic nervous tone was discussed. Coworkers; Dr. Osamu Iimura, Dr. Hisao Abe, Dr. Tsuyoshi Kikuiri, Dr. Tadashi Ueda, Dr. Ichiro Hirano. Dr. Takeshi Agata, Dr. Kenj Inami and Dr. Atushi Mukai.

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The pressor response to norepinephrine, which was infused intravenously using an infusion pump, was investigated in hypertensives and normotensives. The hypertensive group showed a greater response than the normotensive group. In the former group, the response increased in accordance with the progress of the disease. Under long-term antihypertensive treatment, the pressor response changed with the lapse of time. The manner of this change differed in the individual case. Such time-course changes of pressor response might give an indication of the resetting of the internal environment to the lower level induced therapeutically. The possible application of these changes in evaluating the effectiveness of antihypertensive treatment is considered.

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From our animal experiments and clinical experiences the conclusion will be as follows. ( 1 ) The increase of both renin activities and aldosterone excretion is parallely recognized in acute stadium of hypertension of GOLDBLATT'S rats. However the etiological role of both factors to hypertension is not yet clear. ( 2 ) We must say that the pressor mechanism of renal vascular hypertension in man is still also obscure. (3) We can not recognize the role of renin-angiotensin system and aldosterone as the etiology of essential hypertension. We suppose that hypersecretion of both factors is merely the secondary phenomenon. (4) Both factors are increased in secondary aldosteronism. It is still obscure why they don't cause hypertension. In conclusion the essential role of renin-angiotensin system is still not clear, but they certainly work as the electrolytes regulator (especially sodium and potassium) to renal tubules dirrectly or by means of aldosterone secretion. According to our experiments, it seems that aldosterone excretion depend entirely on the dynamics of renin-angiotensin system so far.

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(1) There is a vasoregulatory center in the basal portion of the pons besides in the medulla oblongata. The experimental evidences to support this concept were briefly described. (2) In dogs, normal responsiveness of basilar blood flow to intravenously administered vasoactive substances (norepinephrine, epinephrine and synthetic angiotensin II) requires normal function of the kidney. The responsiveness of basilar blood flow differed from that of internal carotid blood flow in dogs with renal hypertension and with nephrectomy, although the latter responded like in normal dogs. The altered responsiveness of basilar blood flow was restored towards normal when medullorenal extract was given. (3) Ligation of the basilar artery produced hypertension in dogs. (4) The significance of these findings as replated to pathogenesis of hypertension was discussed.

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