The myocardial shortening velocity of 20 patients was recorded by inserting a pair of prongs with strain gauges through a cardiac catheter into the right ventricular muscle. The patients were divided into 3 groups; Group 1: 5 normal controls, Group 2: 9 patients with heart diseases but without heart failure, Group 3: 6 patients with physical and hemodynamic findings of right heart failure. All the patients of Group 3 showed lower maximal myocardial shortening velocity, higher right ventricular end-diastolic pressure and higher tension-time index compared to those of Group 1 patients. The values of Group 2 scattered between those of Groups 1 and 2. Myocardial shortening velocity thus measured is not completely free from the effects of preload and afterload, but can easily be obtained also by other methods. The applicability of the shortening velocity for the assessment of myocardial contractility was discussed.

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A case of 31-year-old woman with myotonic dystrophy who developed only slight cardiac symptoms has been reported. Light and electron microscopic study was performed on myocardium obtained with endomyocardial biopsy.
Light microscopy revealed a considerable degree of fatty infiltration in the myocardium, slight interstitial fibrosis and degenerated myocardial cells. On electron microscopy, marked mitochondriosis and a small number of vacuoles consisting of single limiting membrane and indefinite content low in electron density were observed. Peculiar intranuclear structure and myofibrils showing partial over-contraction and indistinct Z band were also present, and these findings were discussed comparing with the previous reports.
Endomyocardial biopsy seemed to be very useful to detect the myocardial changes even in the early stage of this disease, and the electron microscopic examination of the myocardium may provide the finding which is pathognomonic for the development of the cardiomyopathy in myotonic dystrophy.

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In our series of 111 cases of tetralogy of Fallot, the result revealed that cases with high Hb-content was accompanied more frequently by hypertension. However, their causes and effect relationship could not be clarified and more complicated mechanism was imagined to be acting.
From this series, these conditions of high Hb-content, hypertension and positive urinary protein will be estimated to occur in a patient at about the age of 10 years with tetralogy of Fallot, but for surgical point of view, such conditions do not contraindicate primary corrective surgery for the disease. Palliative operations are also found to be preferable to improve these conditions. In patients of an advanced age with hypertension, careful examinations including renal biopsy will be helpfu 1 to make the final decision for surgery.

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In 19 vagotomized open-chest dogs with sodium pentobarbital anesthesia, hemodynamic effects were evaluated following injection of angiotensin into either vertebral artery using a fine catheter tied into place. Doses of 5ng/Kg produced an increase in both right ventricular stroke volume and the maximum rate of right ventricular pressure rise, without an effect on the left ventricle, mean pulmonary artery pressure (MPAP) mean systemic arterial pressure (MAP) or heart rate (HR). Doses of 10ng/Kg caused an increase in both right and left ventricular stroke volume and dp/dt without an effect on MAP, MPAP, or HR. Doses from 15 to 50ng/Kg raised arterial pressure, which was accompanied by an augmented HR, stroke volume and dp/dt of both ventricles. These effects, however, could not be reproduced by similar intravenous or intracarotid artery doses which provided an equipressor response. These results may suggest that the central nervous system activity of angiotensin operates by stimulation of sympathetic, predominantly beta adrenergic sites.

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Under pentobarbital sodium anesthesia and bilateral vagotomy, studies were carried out in 2 groups of 3 dogs and another group of 4 and 7. Group 1 (4 dogs): Continuous i. v. infusion of angiotensin (5ng/Kg/10ml/min) produced no effects on LV contractility (LV dp/dt, maximum aortic flow velocity), LV stroke volume, heart rate or mean systemic BP. Group 2 (7 dogs): This concentration of angiotensin produced a greater increase in LVdp/dt following i. v. glucagon than those produced by glucagon alone. This potentiation with angiotensin, however, did not occur using epinephrine or isoproterenol, doses of which were chosen to provide a similar increase in LVdp/dt. Augmentation by angiotensin of chronotropic effects of these 3 drugs was not observed. Group 3 (3 dogs): Modification by angiotensin of inotropic effect of glucagon could be reproducible in propranolol pretreated dogs, and in 6 papillary muscle preparations (Group 4-3 dogs). The results suggest that small concentration of angiotensin (probably physiological level) may act on the cardiac contraction by indirect fashion.

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Except positive inotropic action, hydrazine has been detected to have negative chronotropic and dromotropic actions in the rabbit's atrial and bullfrog's ventricular muscles. Aconitine-induced atrial tachycardia in rabbits and spontaneously beating ventricular tachycardia in bullfrogs were promptly converted to bradycardia by hydrazine. The mechanisms of these actions of hydrazine were concluded to result from (1) a prolonged refractory period, (2) a suppression in automaticity, (3) the increase of threshold, and (4) the delayed conduction velocity.

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An investigation was carried out on isolated bullfrog's ventricular muscles so as to study the mechanism of an increasing positive inotropic effect of hydrazine, using a conventional microelectrode technique and a force-displacement transducer; membrane potentials and isometric twitch tensions were observed. A low concentration, 1.5 to 15mM, of hydrazinium ions produced an increase of isometric twitch tension, having a shorter contractile duration with an increasing velocity of contraction and relaxation. The developments of twitch contractions illustrated a typical sigmoid curve. However, the shortened contractile duration with the deeper negative deflection of dT/dt remained after the increased contraction was returned to the initial value. These increasing twitches were markedly enhanced in the Ca⁺⁺-rich solution as compared with those observed in normal Ringer's solution. The action potentials generated in the bullfrog's ventricular muscles revealed the shorter duration and the decreased maximum rate of rise of the action potential. Phase II, the late portion of the upstroke of the action potential, was augmented by hydrazine in the Na⁺-deficient and the Ca⁺⁺-rich solutions. The resting potentials were slightly reduced.
In conclusion, it is postulated that the positive inotropic actions of hydrazinium ions on this tissue are mainly due to the depolarization of cell membrane and the increasing permeability of cell membrane to calcium ions. In one respect, the mode of action of hydrazinium ions on these cells would be essentially similar to that of adrenaline.

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By means of an electromagnetic flowmeter, cardiac output was measured simultaneously with arterial pressure in spontaneously hypertensive rats (SHR, Okamoto strain) anesthetized with pentobarbital sodium under positive pressure respiration. The rats were aged 12-23 weeks and in the early stage of hypertension. Cardiac output, arterial pressure, and total peripheral resistance were 12.6±2.7ml/min/100Gm, 116±24.6mmHg, and 9.46±2.74mmHg/(ml/min/100Gm) respectively, each being the mean of 9 rats with SD. When compared with normotensive control rats (NCR), cardiac output was not different, while arterial pressure (P<0.005) and total peripheral resistance (P<0.025) were significantly higher in SHR. After ganglion blockade with hexamethonium bromide, there was no difference in the above 3 parameters between SHR and NCR. Heart rate was also significantly higher in SHR before ganglion blockade and not so after blockade.

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The pacemaker site of the so-called "nodal" rhythm was examined by the His bundle electrogram with the in situ heart and also by the microelectrode technique with the isolated cardiac muscle preparation of dogs. The His deflection showed a decrease and an alteration in shape in this subsidiary pacemaker beat or rhythm and was found to originate from the area which was not affected by vagal stimulation and acetylcholine administration. In a similar condition the same deformation of the His deflection and slow diastolic depolarization with slow rise of the action potential appeared in the intracellular recording of the His bundle in the isolated muscle preparation. Therefore, more confirmatory evidence was obtained that the pacemaker site was the His bundle, especially when deformed His deflection was found.

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A 63-year-old male, who had systemic arterial hypertension, left ventricular hypertrophy and probable atherosclerotic heart disease, was admitted with dizziness and an episode of syncope. It was revealed that the patient had accrochage at a rate of 41 per minute. There were occasional sinus premature beats, which were all conducted to the ventricles. This arrhythmia was promptly abolished by the administration of atropine, which increased sinus rate. During the 8 months follow-up after discharge from the hospital the patient has remained asymptomatic with normal sinus rhythm.

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