In an attempt to elucidate the pathophysiological significance of the sympathetic hyperactivity in the acute stage ofmyocardial infarction, the author observed changes in the urinary excretion of CA, the CA content in the myocardium and the hemodynamics in both clinical and experimental myocardial infarction, and the following were found: 1) In clinical myocardial infarction, the urinary excretion of CA was markedly increased immediately after an attack, and the assay ofmyocardial specimens form the autopsied patients of acute myocardial infarction revealed that the CA content in the non-infarcted area was lower than that in the infarcted area. 2) In the experiments on rabbits with ligated coronary artery, the increase in cardiac contractility and rise in blood pressure in response to CA was suppressed after the ligation of coronary artery. In the early stage of experimental myocardial infarction, the decrease of myocardial CA content in the non-infarcted area was as in autopsied patients, predominant over the decrease of that in the infarcted areaL In the chronic stage (more than one week after the coronary ligation), the CA content in the infarcted area showed further decrease, but in the non-infarcted area it was recovered to the level in the control animals. The uptake of exogenous NA into the non-infarcted area decreased in the acute stage, and in the infarcted area it showed marked decreased in the chronic stage. The urinary excretion of CA was increased in the acute stage of myocardial infarction. 3) The administration of betamethasone suppressed the decrease in the CA content in the myocardium following the ligation of coronary artery. Based on these findings, the author came to a postulation that the sympathetic hyperactivity which is suggested by increased urinary excretion of CA and decreased CA content in the myocardium results from the reasonable biophylactic reaction so as to supplement the cardiac hypofunction derived from myocardial infarction.

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The hypothesis that plasma renin is a major risk factor in the development of cardiovascular complications of hypertension was evaluated in a model animal, the spontaneously hypertensive rat (SHR). Plasma renin levels and pathological findings were studied in stroke-prone and -resistant strains of SHR at various ages. The stroke-prone strain showed significantly higher plasma renin levels at and after seven months of age, while the stroke-resistant strain showed no significant differences from the control at any age. High plasma renin levels were always associated with evident vascular complications in the kidney and the brain, indicating underlying angionecrosis and malignant transformation of hypertension. However, no evidence indicated that a higher plasma renin preceded the development of vascular lesions. Thus the high plasma renin would be a result rather than the cause of hypertensive vascular lesions.

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Relationship between cardiac dynamics and myocardial energy metabolism was studied using dogs treated by isoproterenol, dinitrophenol, propranolol or amobarbital. Isoproterenol changed cardiac dynamic state to positive chronotropism with positive inotropism and myocardial energy liberation to uncoupling of oxidative phosphorylation. Dinitrophenol inducing uncoupling of oxidative phosphorylation, revealed also positive chronotropic and positive inotropic state. Propranolol changed cardiac dynamic state to negative chronotropism with negative inotropism, and myocardial energy liberation to suppression of oxidation. Amobarbital inducing inhibition of intracellular terminal oxidation, revealed also negative chronotropic and negative intropic state. From the above-mentioned results, it might be clear that the positive chronotropism with positive inotropism appears to be relating to the uncoupling of oxidative phosphorylation, as well as the negative chronotropism with negative inotropism to the suppression of mitochondrial respiration.

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The fine surface structural appearance of the cardiac intercellular connection was studied scanning electron microscopically in culture. When individual heart cells contact each other, they start to beat synchronically. On the base of scanning electron microscopic observation, the early pattern of the formation of it could be suggested as follows: five ramified processes extend from the edge of the cells, and the ends of these processes bridge each other to form the intercellular connection.

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1) Three cases of false atrial dissociation (the Deitz-Marques phenomenon) were presented to show the dependence of this phenomenon on dyspnea. 2) The pseudo-P wave of the Deitz-Marques phenomenon coincided with the beginning of inspiration. 3) In a case of silicotuberculosis, the length of the pseudo-fibrillation was nearly equal to that of laborious inspiration. 4) In a case of aspiration pneumonia, every second cardiac contraction was synchronized with the beginning of inspiration two hours before death. 5) In a case of hyperpotassemia, the pseudo-P wave persisted even after the disappearance of the sinus P wave. 6) The pseudo-P wave was not affected by retrograde activation of the atria by the A-V junctional impulse.

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An autopsy case of congenital interruption of the aortic arch in a four months old male with PDA and VSD is reported and a review of the pertinent literature is presented.

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1.食用ガエル心房筋の摘出標本について,膜興奮から張力発生に至る過程への温度1の効果を2重隔絶膜電位固定法を用いて検討した.2.心房筋を高温(3℃)から(4℃)に冷却するとき,膜のわずかな脱分極,活動電位の振巾の増大とその持続時間の顕著な延一長にともない,静止張力の減少と,単収縮張力の著しい増大が出現し,加温すればいずれにおいても可逆的な復元が認められた.3.膜電位を静止電位レベルに維持し,数秒おきに1秒間の矩形波脱分極固定を行った場合にも,冷却により単収縮張力は増大し,静止張力は減少した.この所見は低温による単収縮張力の増強が活動電位の.単なる延長のみによるものでない事を示す.4.このさい,矩形波脱分極固定に対する終末電流ならびに容量性電流は減少し,また,活性内向き電流の経過は遅延し,外向き遅延電流は著しく抑制された.5.TTX(10^-7g/ml)存在下でも低温により単収縮は増大し,静.上張力は減少した.また遅い内向き電流の増強ないし遅延電流の抑制も認められた.6.正常リンゲル液中の膜電位一電流特性から,冷却による遅い内向き電流の増強と,遅延電流の抑制は別個に出現する現象であることが推測された.また冷却により活動電位の振巾は増大し,内向き電流の逆転電位は上昇するが,さらに収縮の立上り速度の上昇,頂点時間の延長などの変化の所見から低一温ではI_Caによる張力発生が主役を果すと考えられた.7.また矩形波脱分極と発生張力の関係から,冷却は膜電位一張力曲線を過分極側に移行せしめるとともに.収縮張力発生の閾値,張力飽和の飽和電位も過分極側へ移行することが認められた.8.以上の所見から,低温はおそらく膜結合のCaを増加し,これが膜抵抗, I_Caの増大をもたらし, I_Caの増大は単収縮張力を増強するという変力機構の存在に加えて,他方,膜抵枕の増大,外向きのI_K1,I_X1電流の抑制はいずれも活動電位の持続を延一長し,さらに収縮張力の増強をもたらすという2重の変力機構があることが結論された.

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In order to study the therapeutic implication of controlling heart rate in the treatment of aortic regurgitation, the present experimental study was carried out on in situ dog heart with an aorto-ventricular shunt. Methods : A bilateral transsternal thoracotomy was per-formed in 10 dogs anesthetized with sodium pentobarbital. As illustrated in Fig. 1A, the left ventricle was connected with the aorta through a circuit which involved a flow probe and a check-ball-valve. The latter permitted flow to occur only from the aorta to the left ventricle. A flow probe was also placed around the aortic root. After crushing the sinus node, the heart was paced electrically. As the heart rate was increased in steps, total cardiac output, regurgitant flow rate, effective cardiac output, aortic pressure, left ventricular end-diastolic pressure and PO₂, PCO₂, and pH of coronary sinus blood were measured. Results: The hemodynamic effects of the change of heart rate were studied on the hearts with the shunt opened (regurgitation group) and those with the shunt closed (control group). The opening of the shunt resulted in the regurgitation with a regurgitant ratio of approximately 33% at the heart rate of 100 beats per min (Fig. 3B). In the regurgitation group, total cardiac output remained unchanged until the heart rate was increased to 180 beats per min and then tended to decrease (Fig. 2) while the regurgitant flow and regurgitant ratio continued to decrease (Fig. 3A, 3B). The effective cardiac output was maximal in the heart rate range between 120 and 160 beats per min (Fig. 4). The shortening of the duration of diastole per min and the elevation of aortic diastolic pressure due to heart rate increase were more profound in the regurgitation group than in the control group (Fig. 5, 6). No decrease of coronary sinus blood PO₂ was observed in both groups unless the heart rate was raised beyond 180 beats per min (Fig. 7).

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