Anew technique of precordial counting with ¹³¹IMAA for measurement ofright ventricular residual ratio (RVRR) was described. ¹³¹IMAA was rapidly injected into the right ventricle at the time of right heart catheterization. The fraction of isotope discharged from this chamber per beat was determined with a crystal detector with tapered collimator which was pointed to the center of right ventricle. The radioisotope dilution curve was corrected by using the lung built up curve recorded by the other detector pointed to the lung field. Then, the right ventricular endsystolic volume (ESV) and the right ventricular enddiastolic volume (EDV) were calculated from the RVRR and stroke volume.
In 6 patients with normal hemodynamics, the RVRR averaged 57.8±4.9%, the ESV 52.2±13.6ml/M² and the EDV 89.4±15.1ml/M². In 16 patients with heart diseases, the RVRR averaged 60.6±7.1%, the ESV 80.6±34.0ml/M² and the EDV 127.2±43.6ml/M². In 11 patients with chronic pulmonary diseases, the RVRR averaged 70.7±9.9%, the ESV 94.7±42.4ml/M² and the EDV 133.0±46.5ml/M². The RVRR in the last group increased significantly.

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Arterial embolus is usually a serious complication of rheumatic or atherosclerotic heart disease. One hundredfifteen surgical procedures performed in 86 patients with arterial emboli in a 10 years' period in the Department of Adult Thoracic and Cardiovascular Surgery of our university are analyzed regarding the etiology, the treatment, and the results of this complication. Most of the patients were delayed cases showing mild to severe degrees of trophic, sensory and motor disturbances in the limbs without gangrene. These cases are also subjected to vascular surgery (removal of the embolus) as a chance to enable them to use their extremities in lieu of prostheses even when motor and sensory changes persist.

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Isopotential map was obtained every 3 msec after the onset of ventricular activation from 85 unipolar lead ECGs of a normal subject (Measured map) and similar map at the corresponding instant (Simulated map) was also obtained by means of mathematical calculation under the assumption that the cardiac electromotive force can be represented by a single electric dipole fixed at the heart center. These 2 maps were quantitatively compared and difference was delineated on a map (Difference map).
Although, in major aspect, there was a fairly good agreement between Measured and Simulated maps during early stage of ventricular activation, a remarkable difference of potential distribution began to appear between them around the time of occurrence of epicardial breakthrough of the ventricular activation front.
From that time on, it became impossible to represent the cardiac electromotive force by a single electric dipole fixed to the anatomical heart center and there appeared a map pattern suggestive of the separation of electromotive force into 2 or more electric dipoles in Difference map.
Difference maps around the instant of epicardial breakthrough of the ventricular activation were supposed to be helpful for the estimation of the spread of ventricular activation.

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As reported previously, oxidative phosphorylation was uncoupled in the infarcted canine heart muscle. In this study, it was revealed that the heart rate increased and the left ventricular isometric time tension index was deteriorated in experimental coronary ligation in dogs. Isoproterenol infusion before and after coronary ligation modified hemodynamic changes due to coronary occlusion. Mitochondria from the infarcted myocardium of the isoproterenol treated dog showed uncoupling of oxidative phosphorylation as same as cases of coronary ligation without isoproterenol treatment. By injection of propranolol prior to coronary ligation, however, hemodynamics were more depressed and uncoupling of oxidative phosphorylation in the infarcted myocardium was mitigated, followed by decreased mitochondrial oxygen consumption rates. With artificial pacing before and after coronary ligation, oxidative phosphorylation was still uncoupled when the pacing rate was made frequent while it was less uncoupled when the contraction rate was decreased.
It might be considered that uncoupling of oxidative phosphorylation in the infarcted myocardium was enhanced in the state of enforced increment of chronotropism and inotropism while it was rather protected in the state of moderate cardiac suppression. Energy liberation in the infarcted heart may be affected by changes of hemodynamics.

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The propagation process of the atrial excitation was investigated during ectopic atrial rhythms evoked by electrical pacing through stimulation at several sites in 35 isolated rabbit atria using intracellular microelectrodes. Excitation sequence was correlated with the atrial deflections in a distant bipolar electrogram representing a craniocaudal atrial activation. The conduction velocity was faster along the crista terminalis but slower across the coronary sinus ostium than in the ordinary atrial muscle. These differences in conduction velocity resulted in the upward atrial deflection on the distant bipolar electrogram in the rhythm which was produced by stimulation at the right side of the lower interatrial septum. On stimulation of the left atrial appendage, Bachmann's bundle displayed a function as a preferential conduction pathway in the case of left to right direction of excitation, as in left atrial rhythm. On stimulation of the posteroinferior region of the left atrium, the region around the coronary sinus ostium was the first area in the right atrium to be activated. Inversely, the impulse originating from the coronary sinus ostium was conducted relatively fast to the posteroinferior region of the left atrium. These findings suggested that there might be a preferential conduction pathway along the coronary sinus vein or its neighbouring tissues.

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Direct perfusion of the sinus node artery at constant pressure of 100mm Hg was arranged in 6 canine hearts in situ. The injection of phentolamine into the sinus node artery usually induced dosedependent positive chronotropic effect. However, at a larger dose of 300μg, phentolamine frequently induced a biphasic chronotropic response, i.e., sinus deceleration followed by sinus acceleration. Phentolamine at a large dose of 1mg usually induced a negative chronotropic effect. The threshold dose for inducing sinus acceleration was about 1 to 10μg. The positive chronotropic response to phentolamine was blocked either by propranolol or by tetrodotoxin. That to norepinephrine was blocked by propranolol but not suppressed by tetrodotoxin. These results suggest that the phentolamineinduced sinus acceleration is due to catecholamine which is released by excitation of local adrenergic fibers. The sinus deceleration to higher doses of phentolamine was not blocked either by atropine or by tetrodotoxin. It suggests that phentolamine has a direct depressive effect on the SA node at extremely high dose levels.

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Constriction of one renal artery in the presence of the opposite kidney can produce persistent hypertension which is often associated with increase in plasma renin activity, decrease in serum potassium and increase in water intake. In the present study the clipped kidney was removed in 15 hypertensive rabbits 12 to 54 weeks after the constriction. Blood pressure showed a prompt and transient fall which was followed by a slight rebound and subsequently a gradual decline. However, it still remained above the normal 5 weeks after the removal. Removal of the clipped kindney resulted in return to normal of increased plasma renin activity, decreased serum potassium and increased water intake at the end of the postoperative first week.

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An autopsy was performed on a female stillborn infant with generalized edema associated with ascites. On gross examination of the heart the pulmonary trunk was atretic from its origin of the heart to the bifurcation. The ductus arteriosus was abnormally wide. The right ventricle was hypoplastic and its endocardium was diffusely thickened. The inner surface of right ventricle appeared pale, obscuring the identification of trabeculae carneae and papillary muscles. At the posterior wall there was an extremely thin lesion where no apparent cardiac muscle was contained. The tricuspid orifice was stenotic and the valve was hypoplastic. The right atrium was markedly enlarged and its wall was thickened. The foramen ovale had patency of the valvular competent type. Atrial septal defect (ASD) was not present. The left ventricle was remarkably dilated with markedly thick wall. Ventricular septal defect (VSD) was present immediately beneath the right coronary cusp of the aortic valve.
Light microscopic examination of the right ventricle revealed a marked increase of collagen and elastic fibers with extensive deposits of calcium not only in the endocardium but also in the deep portion of myocardium. Fibroelastosis appeared particularly prominent in the subendocardial layer. The muscle fibers surrounded by these penetrating fibers and deposits of calcium showed degeneration. The entire myocardial layer of the specific area in the right ventricle where the wall was paperthin was fully replaced by fibers and calcium. Inflammatory cell infiltration was found only at some places of the pericardium. The left ventricular wall also showed fibroelastosis, although the degree of involvement was much less as compared to that seen in the right ventricle. There were no significant pathological changes in both atria.

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