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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Numerous studies have been reported on the effects of temperature on the electrical and mechanical properties of myocardium, and the augmentation of tension in low temperature has been generally considered to be simply due to a marked prolongation of the membrane action potential. In recent years, however, several kinds of the membrane currents such as I_Na1, I_Na2, I_Ca, I_K1, I_K2, I_X1, I_X2, and I_C1 were discovered on the myocardium and the complicated processes of membrane excitation-contraction coupling (E-C coupling) were greatly analized in relation with the roles of these membrane currents and sarcoplasmic reticulum. Accordingly, the mechanisms of the inotropic effect of low temperature must also be re-examined on the basis of these lately developed knowledges. The present study, therefore, undertaken to elucidate fundamental mechanisms of the action of temperature upon the membrane currents and E-C coupling processes, by examining the frog heart muscle with voltage clamp technique. The preparation used in the present experiments was the atrial muscle bundle isolated from the bullfrog (Rana cathesbiana). The thin muscle bundle was about 7mm in length and 0.6-0.8mm in diameter. The membrane potential, current and contractile tension were measured by means of the double glycerol-gap technique in voltage clamped conditions. The muscle chamber consisted of five compartments (1, 2, 3, 4 and 5). The large terminal compartments (1 and 5) were flowed with 200mM KCI solution, the intermediate compartments (2 and 4) with isotonic glycerol solution, and the central compartment with Ringer or test solutions. The width of glycerol gap was 1mm, and that of the central compartment ranged from 0.3 to 0.6mm. The membrane potential was obtained as the potential difference between the central and terminal compartments (3 and 5), and the cur-rent, from the central compartment (3) which was kept at nearly earth potential by the aid of an operational amplifier (Philbrick, P65AU). The muscle tension was measured by the aid of a strain gauge (Nihon Kohden, SB-1T), the sensitive arm of which was connected to the end of muscle bundle in the terminal compartment (5). These potential, current and tension were recorded simultaneously utilizing by a triad-beam oscilloscope (Nihon Kohden, VC-7) and a inkwriting oscilloscope (Nihon Kohden, WI-180).

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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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