Echocardiography and cross-sectional echocardiography have proved to be valuable in the study of the left ventricular wall motion and the assessment of left ventricular function. Recently, echocardiography has revealed a characteristic ventricular septal motion in patients with left bundle branch block. It has been postulated that abnormal septal motion is related to altered sequence of activation and contraction. The purpose of this study was (1) to analyze motions of interventricular septum and the left ventricular posterior wall in patients with complete left bundle branch block by echocardiography and cross sectional echocardiography; (2) to relate septal motion during the right ventricular endocardial pacing to that in LBBB; (3) to compare septal motion in LBBB with that in septal infarction. Materials and Methods: Echocardiogram and cross-sectional echocardiogram of thirty patients with complete left bundle branch block (LBBB) were compared with those of five patients with complete A-V block during right ventricular endocardial pacing, twenty patient with anteroseptal infarction, and twenty normal subjects. Echocardiogram and cross-sectional echocardiogram were recorded simultaneously with electrocardiogram (ECG) and phonocardiogram (PCG), using an ALOKA SSD-33 instrument utilizing a 2.25 MHZ unfocused transducer of 10mm diameter with a repetition rate of 1000 inpulses per second. Ultrasonic cross-section (stop-action B-scan) were made along the long axis of the left ventricle, with the transducer tilting in an arc setor from the base of the heart to the apex, at end-diastole (the peak of R-wave in ECG), early systole (pre-ejection period) and end-systole (aortic component of the second heart sound in PCG), respectively.

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The effect of digitalis preparation on the normal heart has been the subject of controversy. Most of the studies using acute intravenous administration of digitalis or oral administration of its full dose demonstrated no positive effect on the normal heart. In subjects without congestive heart failure the positive inotropic action was probably masked by the increased peripheral vasoconstriction. In this study left ventricular performance was assessed mechanocardiographically and echocardiographically in ten normal non-trained subjects before and after oral administration of small dose of digoxin. Subjects and Methods Out of 100 non-trained healthy young males, ten subjects aged from 22 to 33 years were selected in whom a clear left ventricular echocardiograms could be contineously recorded at rest and during exercise. Echocardiogram (UCG), electrocardiogram (ECG), phonocardiogram (PCG) and blood pressure readings were obtained in the basal state and every one minute during 120 Watt steady state exercise of three minutes' duration in recumbent position before and after oral administration of digoxin, 0.5 mg on the first day and 1.0 mg on the subsequent day. The experimental procedures after digoxin treatment were done 4 hours after the second administration of digoxin. Blood pressure, the ratio of preejection period to ejection time (PEP/ET), percent shortening of left ventricular minor dimension (ΔD), ejection fraction (EF) and mean velocity of circumferential fiber shortening of the left ventricle (mVcf) were analyzed by the paired student's test comparing the control measures to the digoxin measures in the basal state, during and after exercise. Results Systolic and diastolic pressures were not affected by digoxin treatment. After digoxin administration, despite a decrease in heart rate from 67 ± 4 to 60 ± 5 in the basal state, PEP/ET decreased from 0.42 ± 0.05 to 0.38 ± 0.03 (p < 0.01), ΔD increased from 33 ± 4 to 38 ± 3% (p < 0.001), EF increased from 69 ± 6 to 76 ± 4% (p < 0.001) and mVcf increased from 1.20 ± 0.13 to 1.35 ± 0.11 (p < 0.01). During exercise, while a decrease in mean heart rate by digoxin treatment was as much as that of basal state, effects of digoxin therapy on ΔD and EF were augmented during exercise: ΔD increased from 34 ±4 to 44 ± 4% and EF increased form 71 ± 5 to 83 ± 4% at three minutes after initation of exercise. An increase in ΔD after digoxin treatment was mainly caused by a change in endsystolic dimension.

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Since Mirowski et al. have published a series of papers on the left atrial rhythm, a number of studies have been carried out clinically or experimentally without clear differentiation of the left atrial rhythm from the other supraventricular ectopic rhythms, especially the A-V junctional rhythm and the coronary sinus rhythm. In order to clarify the differences among these ectopic rhythms and to establish criteria in the diagnosis of these ectopic rhythms including the left atrial rhythm, electrical stimulation was given at various of the left and right atria of isolated perfused hearts of adult mongrel dogs and P wave polarity, morphology and P-R interval in leads V_F, V₁ and V₆ were examined during electrical stimulation. Effects of heart position and conduction disturbance on the P waves were also examined. Methods: Forty adult mongrel dogs weighing 9 to 14 kg were used. An isolate heart was perfused with Tyrode's solution kept at about 35°C by means of Langendorff's methofs in a cylindrical torso model simulated human thorax. The isolated heart was placed anatomically and electrocardiographically most similar to the normal heart in the human body, as described in a previous report. This position was used for the control experiment. Experiment 1. Thirty isolated perfused hearts placed in the control position were stimulated electrically at several sites of the left and right atria and P wave polarity and morphology in leads V_F, V₁ and V₆ were examined. A region, in which electrical stimulation produced negative P wave in lead V_F, "dome and dart" in lead V₁ and negative in lead V₆, was determined in each heart and conduction times from electrical stimulus to Q wave, i. e. St-Q time, were measured from the records to study intra-atrial and atrioventricular conduction velocity. P wave changes during atrial stimulation were examined with the heart turned clockwise around the ventrical axis by 45° and then counterclockwise from control position, and also lying horizontally. Experiment 2. P waves produced by the atrial stimulation at various sites were examined in the isolated perfused hearts with conduction disturbances of the atria and the atrial septum. The conduction disturbances were produced by an extensive incision to separate the lower part of the right atrium including the internodal tract (incision (I)) and a incision to separate the atrial septum including the anterior and middle internodal tract (incision (II)). Conduction times to various sites of both were measured using stimulating electrodes fixed at the right caudal atrium (the lower part of the incision (I)). Bipolar platinum electrodes with an inter-electrode distance of 1 mm were used for atrial stimulation in connection with the battery-powered pacemaker, Medtronic 5880A, both in Experiments 1 and 2. The intensity of the stimulation was twice as much as the threshold value. ECG's amplified with a main amplifier ( Yokokawa Electric Type 3122) via preamplifier were recorded on a photorecorder at a paper speed of 100mm/sec. The sensitivity was 1.5 cm/20 μv.

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It has been suggested that cyclic AMP (c-AMP) and cyclic GMP (c-GMP) are biologic effectors involved in regulating cellular functions that are controlled bidirectionally. In the control of vascular smooth muscle tone, cyclic nucleotides may act in a reciprocal manner with increases in c-AMP promoting relaxation and increases in c-GMP promoting contraction. But most of studies have been carried out in vitro. In order to elucidate the role of c-AMP and c-GMP in coronary vasodilation in vivo, the concentration of c-AMP and c-GMP in the conary artery and left ventricular muscle of anesthetized dogs were measured after the administration of various coronary vasodilators. Materials and Methods Seventy mongrel dogs weighing 9 to 11 kg were anesthetized with sodium thiamylal (25 to 30 mg/kg I.V), intubated and ventilated with a Harvard respirator. The chest was opened on the left side between the 4th and 5th ribs and the pericardium was opened. After 30 min control period, coronary vasodilators, which were papaverine (4 mg/kg), dipyridamole (0.5 mg/kg), nitroglycerin (0.02 mg/kg), isosorbide dinitrate (0.3 mg/kg), amyl nitrite (0.25 ml), nifedipine (5 μg/kg), and diltiazem (0.2 mg/kg) were administered intravenously except for amyl nitrite. We performed a method of catheterization of the coronary sinus as means of measurement of coronary blood flow. The blood flow. The blood from the coronary sinus was returned to the external jugular vein and a electromagnetic flowmeter (Nihon-Koden MF-2) was setted between the coronary sinus and the external jugular vein. When coronary blood flow was at its maximum, the heart was removed and immediately irradiated for 2 min with microwave (2450 MHz, 600W) for inactivation of the enzymes. The coronary artery and the left ventricular muscle were removed from the heart and weighed in cold room at 4°C. Tissue samples were homogenized in 1 ml of 6% trichloroacetic acid. C-AMP and c-GMP were measured by a modified radioimmunoassay of Cailla. Ethyl alcohol was administered in control group of nitroglycerin and nifedipine and distilled water was administered in the other control group. Mean and standard error of the mean were calculated and the data were compared by Student's unpaired t test. P values of less than 0.05 were considered significant.

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It has become apparent that the lung has many functions other than respiration within recent years. Among them, the metabolism of vasoactive substances in pulmonary circulation has been interested in by many investigators because of its influence upon the pathophysiology of the systemic circulation. Angiotensin I-converting enzyme (ACE) converts inactive angiotensin I(AI) to angiotensin II(AII), a potent vasopressor octapeptide, by releasing the C-terminal dipeptide of AI. Recently the enzyme is also thought to be capable of inactivating bradykinin (BK) and to be identical with kininase II. The lung has been pointed out as an organ which is rich of this enzyme by many investigators. So, if the enzyme acts on both renin-angiotensin and kallikrein-kinin system in the pulmonary circulation, the change of this enzymic activity in the pathological lung is considered to have very important influence on the metabolism of those both systems, resulting in the change of systemic circulation. To elucidate the physiological roles of ACE in lung, the following three experiments were performed. 1) Purification of ACE from rabbits lung and determination of properties and characteristics of the purified enzyme. 2) Estimation of ACE activity in pulmonary tissue and in plasma of normal rabbits and rabbits with chemically induced pneumonitis. 3) Perfusion experiment with isolated lung of normal rabbits and of rabbits with chemically induced pneumonitis for determining metabolic activity of AI and BK. Materials and Methods: Purification and determination of properties of ACE from rabbit lung: The membrane fraction of the lung was precipitated from lung homogenate by acid treatment (pH 5.2). ACE was solubilized from the membrane fraction using trypsin treatment and purified using columns of DE-52 cellulose, hydroxylapatite and Sephadex G-200. The analytical disc gel electrophoresis was performed. The activity of ACE was assayed by the spectrophotometric method using Hip-His-Leu as the substrate. Biological assay of the enzymic activity was also performed in the isolated rat uterus using AI, AII and BK as the substrate. The products of the reaction were identified by high voltage paper electrophoresis. The molecular weight of the enzyme was determined by gel filtration of Sephadex G-200. Km value, optimal pH, Cl^- dependency and inhibition by Arg-Pro-Pro, SQ 20, 881 and SQ 14, 225 were also examined. Production of chemically induced pneumonitis: Rabbits were treated with intravenous injection of complete Frund's adjuvant (FA) for the acute experiment or N-nitroso-N-methylurethane (NMU) for the chronic experiment. Measurement of ACE activity in pulmonary tissue and in plasma: Lungs were homogenized and sonicated by Polytron^R. ACE activity was measured spectrophotometrically and expressed as nmol/mg prot./min for the lung and nmol/ml/min for the plasma. Perfusion of isolated lung: Lungs were perfused with constant volume of Tyrode's solution from a cannula placed in the pulmonary artery without taking out of the thorax, AI, AII or BK were injected via the canula and the perfusate was collected respectively from left ventricle. AI and AII were assayed radioimmunologically. Rate of conversion of AI and of inactivation of BK were calculated. Mesurment of systemic blood pressure: A catheter was placed in femoral artery of unanesthetized rabbits and connected to mercurial manometer.

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