In order to study the distribution of blood flow in diseased human kidneys, Xe¹³³ washout curves were obtained from 34 patients with chronic renal disease or hypertension.
The curves recorded for over 45min. were resolved into 4 components, while the curves recorded for 30min. showed 3 components. The values of components I, II and III in the 30min. record coincided with those of the components I, the average of II and III, and IV in the 45min. record, respectively.
The percentage of the total renal blood flow (flow ratio) distributed to the component I of the 30min. record was correlated with that due to cortical blood flow as determined by the dye-dilution method. It is suggested that the component I of the Xe¹³³ washout curve from the human kidney represents the cortical blood flow.
The results obtained from the Xe¹³³ washout curves recorded for 30min. were compared with the renal function of the patients. The flow for unit mass of tissue (flow rate) and the flow ratio of the fastest component (component I) were decreased in the azotemics. The flow rate of component I was also decreased in proportion to the reduction of the RBF calculated from C_PAH (RBF_PAH), GFR from C_Thio and maximal urinary osmolality, while the flow rate of component II did not change significantly. As the renal function became impaired to the level of RBFPAH less than 500ml./min., GFR 50ml./min. and maximal urinary osmolality 700mOsm, the flow ratio of component I decreased and that of component II increased progressively.

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Cardiac output and ST-T change of electrocardiogram were studied before and after exercise in 64 patients with ischemic or hypertensive heart disease or without heart disease. When ST depression was arised or increased more than 1mm. after exercise, cardiac output was increased in 47%, stroke volume was decreased in 82% and heart rate was increased in 94%. When peak of T was changed to upward more than 2mm. without ST depression or elevation more than 1mm. after excercise, cardiac output was increased in 91%, stroke volume was increased in 87% and heart rate was increased in 91%. Electrocardiographic change after exercise might be good index of exercise capacity in patients with ischemic or hypertensive heart disease.

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The second heart sounds in 29 cases with right bundle branch block, mainly surgically induced, were studied.
Three general types of the second sound were classified.
Eleven cases revealed wide splitting of the second sound (0.05sec. or more), and 14 cases showed narrow splitting less than 0.05sec.), while 4 cases showed a single 2nd heart sound throughout the respiratory cycle.
Ten cases revealed a respiratory change in the splitting, and 14 cases showed fixed splitting.
The cases with a widely split 2nd sound revealed fixed splitting except in 2 cases. Among the cases with narrow splitting, 8 cases (57%) showed respiratory change.
All cases with a QRS duration of 0.14sec. or more revealed fixed splitting.
A Valsalva maneuver was performed in 18 cases with RBBB. Five cases showed a widening of the split 2nd sound immediately following the release of Valsalva maneuver and then the IIA-IIP interval decreased, but in only 2 cases did the IIA-IIP interval merge into single sound. In 13 cases the IIA-IIP interval remained unchanged throughout the Valsalva maneuver.
No correlation was found between splitting of the second heart sound and the type of vectorcardiogram in RBBB.
The mechanism of these observations was discussed.

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A new approach to the measurement of pulmonary function was attempted by the use of catheter-type semiconductor radiation detector (CASRAD). When Kr⁸⁵ dissolved in normal saline solution is injected as a bolus intravenously, the maximum counting rate obtained in a particular bronchus is a reflection of the amount of pulmonary blood flow and the subsequent washout rate, that of ventilatory efficiency of that lobe. From the basic and model experiments, it is concluded that the ratio of Kr85 counting rates in different bronchi measured by CASRAD can be compared as the concentration ratio of Kr⁸⁵ if these bronchi are similar in size. Three dogs were used for animal experiments. Kr⁸⁵ solution was injected as a bolus into the right side of the heart and the counting rate was measured in the upper and the lower lobe bronchus where CASRAD was placed respectively. The maximum counting rates were essentially the same in the upper and the lower lobe bronchus for the supine position, while they tended to get higher in the lower lobe for the head-up position. This phenomenon was explained by the increase of perfusion to the dependent zone of the lung due to the gravity. The approximation of the perfusion ratio between the upper and the lower lobe by the ratio of the maximum counting rate was also attempted. When washout rates of Kr⁸⁵ in the upper and the lower lobe were compared, there was no significant difference between them whether the dogs were placed supine or head-up. As a preliminary study for the clinical application, CASRAD was used for the measurement of ventilatory efficiency, lobar function, and for the bronchospirometry. The clinical applicability was confirmed. The advantages and limitations were discussed comparing CASRAD with the external counting method.

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The effect of withdrawing dietary sodium was determined in 10 rats with marked hypertension induced by ligation of a branch of the renal artery and contralateral nephrectomy and in 10 normal control animals. No significant change occurred in the systolic blood pressure of either group of animals during 5 days of sodium withdrawal. Throughout the period of observation, the urinary output was greater in the hypertensive than in the normotensive group. Reduction of urinary output and water intake was observed in both groups during sodium depletion. The reduction in the urinary excretion of sodium was greater in the hypertensives than in the normal animals for several days after sodium was withdrawn. Hypertensive rats, accordingly, retain sodium more efficiently than do normotensives after sodium withdrawal.

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The author has reported that a variable, e(t)=p(t)/v(t), is approximately unchanged in the areflexive heart of the dog over a wide range of end-diastolic volume of the left ventricle, where p(t) is systolic left intraventricular pressure, v(t) is systolic left intraventricular volume, and t is time from the beginning of systole in each cardiac cycle. e(t) is studied further under various extents of an aortic occlusion, without the change in left intraventricular end-diastolic volume, monitored on left intraventricular end-diastolic pressure of the areflexive heart of the dog. For actual computation,
e(t)=p(t)/{(1-ρ)^-1•v_s-∫^t_oi(t)dt},
where p(t) is measured by a straingauge electromanometer, ρ is residual volume ratio measured by a thermodilution method, v_s is stroke volume as time-integral of ascending aortic flow velocity i(t) in a given cardiac cycle, and i(t) is measured by an electromagnetic flowmeter. End-diastolic volumes of the left ventricle are kept approximately constant by controlling venous return to the heart with a balloon-catheter in the inferior vena cava. The results show that e(t) is approximately unchanged by an ascending aortic occlusion, in spite of the conspicuous changes in p(t), i(t) and v(t) in each dog. Therefore, e(t) is considered to be a steady and characteristic variable of the pumping properties of the areflexive left ventricle.

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The effects of propranolol on the electrical behavior of ventricular muscle fibers were investigated in the anesthetized dog by simultaneously recording surface and intracellular electrograms. After administration of propranolol during sinus rhythm, the RR, PQ and QT intervals were significantly prolonged, while the QRS duration remained unchanged. During electrically driven rhythm, propranolol caused a slight but insignificant prolongation of the QT interval. There were no changes in the QRS duration. Significant delay of the interatrial and atrioventricular conduction times was observed. There were no significant changes in the intraventricular conduction time. Propranolol principally affects the sinoatrial node, the atrioventricular node and the conduction time of the atria. Effects of propranolol on the intracellular electrograms from the ventricle were as follows. The duration of the membrane action potential was significantly prolonged. No changes were observed in the amplitudes of the membrane action potential, membrane resting potential and overshoot. The maximum upstroke velocity of the membrane action potential did not change. Propranolol has a quinidine-like action as well as a beta adrenergic blocking action. Both actions contribute to the effectiveness of the drug in the treatment of cardiac arrhythmias.

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(1) The effects of chlorpromazine (CP) on the action potentials (AP's) and contractions of the isolated guinea pig heart were investigated by means of a microelectrode and a strain gauge transducer.
(2) CP at concentrations of 2×10^-6 to 5×10^-1Gm./ml. decreased markedly the pacemaker activity of the sino-atrial node. By the repeated application of the drug to the tissue, however, a considerable tolerance to the drug was developed, and in some preparations the acceleration of the beat rate occurred rather than the deceleration.
(3) CP shortened AP-duration of the left atrial muscle and the left ventricular papillary muscle by 10 to 20%, but slight prolongation occurred for a longer treatment with the drug in some preparations.
(4) CP definitely decreased the maximum rate of rise of AP's of both atrial and ventricular muscles without significant change in the resting potential.
(5) The excitability assumed by the strength-duration curve of the atrium was decreased by the application of CP, and the full-recovery time of the atrium was delayed.
(6) Contractile tension of both the atrium and the ventricle was strikingly reduced by the application of CP, but recovery was almost complete.
(7) Clinical electrocardiographic abnormalities induced by fairly high dosage of the phenothiazine drugs and antiarrhythmic actions of these drugs were discussed in relation to the results obtained.

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Spatial changes of ST and T induced by exercise were studied in 15 control subjects, 19 patients with hypertension, 15 patients with angina pectoris and 10 patients with myocardial infarction. ST vector, the maximal T vector, the half maximal T vector (hm1 and hm2) and the angular range in horizontal plane were determined before, during and after exercise, using Frank's lead system. The vectorial difference between 2 vectors before exercise and at the point of the maximal ST change during or after exercise was obtained for ST vector, the maximal T vector, hm1 and hm2 (ST, T, hm1 and hm2 exercise vector, respectively).
(1) The mean values and standard deviations of the spatial magnitude of ST exercise vector were 0.6±0.4mm. in the control group, 0.6±0.5mm. in the hypertensive group, 1.5±0.7mm. in the group of angina pectoris and 1.8±0.6mm. in the group of myocardial infarction.
(2) ST exercise vector was directed to the right and posteriorly in the control and the hypertensive group, mainly to the right and posteriorly in the group of angina pectoris, to the right and anteriorly, to the anterior or to the left and anteriorly in the anterior infarction group, and to the right and posteriorly or to the posterior in the inferior infarction group.
(3) T exercise vector was directed to the right and posteriorly in the control group, the group of angina pectoris without hypertension and the inferior infarction group, and to the left and anteriorly in the hypertensive group, the group of angina pectoris with hypertension and the anterior infarction group.
(4) Both hm1 and hm2 exercise vectors were directed to the right and posteriorly in the control group, the group of angina pectoris without hypertension and the inferior infarction group, and to the left and anteriorly in the hypertensive group. In the group of angina pectoris with hypertension, hm1 exercise vector was directed to the right and posteriorly and hm2 exercise vector to the left and anteriorly. In the group of the anterior infarction group, hm1 exercise vector was directed to the right and anteriorly and hm2 exercise vector to the left and anteriorly.
(5) The mean values and standard deviations of the difference of the angular range before exercise and at the point of the maximal ST change (|φ2-φ1|) were 9.2±7.6 degrees in the control group, 11.0±7.9 degrees in the hypertensive group, 42.5±28.4 degrees in the group of angina pectoris and 50.8±29.4 degrees in the group of myocardial infarction.
(6) There was a linear relationship between the magnitude of T exercise vector and φ2-φ1 for the control group, but not for other groups.
(7) ST exercise vector of 1.0mm. and |φ2-φ1| of 20.0 degrees would be appropriate as criteria of exercise vectorcardiogram for the diagnosis of ischemic heart disease.

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Pacemaking was used on a 46-hour-old infant suffering from congenital complete heart block and it was followed by rapid improvement in the cardiac failure. This appears to be the 5th effective attempt at neonatal pacemaking in the available medical literature.
Along with electrocardiographic tracing, blood gas and acid base analysis were repeatedly carried out before and after pacemaking. PaO₂ represented the clinical state of the cardiac failure more accurately than any other data: hence it appears to be one of the important indices in determining an indication for pacemaking.

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