Five patients of prolapsing mitral leaflet syndrome, clinically identified, are discussed. Relevant literature is reviewed.

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Investigations on the influence of nicotine and acetylcholine on isolated 30 frog and 10 rabbit hearts stopped with 0.5ml of 50% alcohol and 0.1 to 0.5ml of 0.5 to 1% cortisone, hydrocortisone and prednisolone indicated that 0.1 to 3ml of 10^-4Gm/ml of nicotine restarted the stopped hearts. Acetylcholine in a dose of 0.1 to 3ml of 10^-7 to 10^-4Gm/ml was less effective in restarting the stopped hearts. Prior or simultaneous administration of nicotine or acetylcholine prevented occurrence of cardiac asystole with alcohol and glucocorticoids or cut short its duration. Prior administration of alcohol modified the action of nicotine. Catecholamine release from cardiac neural elements does not appear to be involved in antiasystolic action of nicotine and acetylcholine. It has been suggested that asystolic and antiasystolic actions may be coupled with a common receptor or enzyme system through which drugs produce biphasic and opposite effects depending upon concentration.

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(1) The forward triangle method vs. the semilogarithmic method showed the regression equation of Y=0.211X-171(mm²) (r=0.897).
(2) The integral method vs. the semilogarithmic method showed the regression equation of Y=1.021X-104 (r=0.994).
(3) The tangential method vs. the semilogarithmic method showed the regression equation of Y=1.006X-210 (r=0.992).
These data showed that these 3 methods for the rapid estimation of the area under the thermodilution curve were applicable practically, with the reasonable accuracy, the simplicity and the cost.

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The coronary hemodynamics after the administration of sublingual nitroglycerin were examined by the continuous local thermodilution method in 17 patients. The patients were divided into the myocardial ischemic and non-ischemic groups considering the functional state of the myocardium clinically.
The coronary sinus ostial and the great cardiac vein flows increased even in some of the patients in the myocardial ischemic group. Either the increase or the decrease of the flows occurred regardless the functional state of the myocardium according to the criteria of this study.
The cardiac work, however, decreased in both the myocardial ischemic and non-ischemic groups in a similar manner.

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In order to make accurate diagnosis of cardiac attacks, such as angina pectoris or transient arrhythmia, it is necessary to obtain electrocardiograms during the episodes. To make this possible, we have developed a pocket electrocardiograph that is small, light, easy-to-operate, features minimal recording distortion and is inexpensive.
The efficiency of this system in making clinical diagnosis has been proved by its application to 100 cases of varying cardiac attacks. There were several interesting cases among these in which the findings obtained by application of our system were unexpected.

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Pulmonary infarction was produced by the infusion of rabbit blood clots on the 3rd day after the injection of minced rabbit thrombi, and, concurrently, UK, heparin, t-AMCHA, or ellagic acid was injected to evaluate the influences of these agents upon the frequency of production of pulmonary infarction. In addition, the coagulation-fibrinolytic observations were made during the course of these experiments.
(1) The frequency of production of pulmonary infarction was 50% in the control group, while those in the UK-treated group, heparin-treated group, t-AMCHA-treated group, or ellagic acid treated group was 20%, 40%, 80%, and 60% respectively. UK and heparin seemed to be applicable drugs for clinical practice.
(2) The prerequisites for production of pulmonary infarction from the results of venous blood examinations seemed to be formation of advanced secondary thrombosis under persistence of hypercoagulability and activa tion of secondary fibrinolysis which was not so intense as to fibrinolyze the secondary thrombi.
(3) In the clinical application of UK, the dose should be determined theoretically in consideration of factors at the side of a patient and by fibrinolytic time from a patient plasma with TEG.

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In spontaneously hypertensive rats (SHR) and normotensive control rats (NCR) anesthetized with pentobarbital sodium, first the right and then the left splanchnic nerves were cut. After arterial pressure had stabilized at a new lower level following each cut, the peripheral cut end of the nerve was stimulated electrically with a train of square pulses of 10V-5 msec, to determine the frequency needed to restore the level of arterial pressure before the severance (equivalent stimulation frequency, ESF). ESF is assumed to represent the average discharge rate of sympathetic vasoconstrictor fibers in the splanchnic nerve. ESF's were significantly higher in SHR than in NCR, being 3.4±2.5/sec vs. 0.67±1.63 for the right splanchnic nerve and 3.7±1.1/sec vs. 0.86±0.52 for the left splanchnic nerve (each mean with SD, n=9). Thus SHR is characterized by an elevated sympathetic tone. After severance of the right or bilateral splanchnic nerves the difference in arterial pressure between SHR and NCR was no longer significant.

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The relationship between the initial heart rate and the cardiotoxic dose of ouabain was investigated in the dog heart-lung preparation. It was observed that with a relatively slower heart rate, the dose of ouabain necessary to produce ventricular tachycardia as well as ventricular fibrillation or cardiac arrest was increased significantly (p<0.05). When the heart was paced at either 150 or 180 beats/min, the dose of ouabain needed to produce ventricular tachycardia was significantly greater than that in the control group (heart rate 128±4 beats/min). However, in these groups, there was no difference in the dose of ouabain necessary to produce lethal effects. Thus to some extent, an inverse relationship between the heart rate and the cardiotoxic dose of ouabain was observed. The significance of these findings is discussed.

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Electrical and mechanical response of bullfrog's heart muscle affected by hydrazine was investigated in the high K⁺ solution. Hydrazine as well as adrenaline in the excess K⁺ solution enhances the overshoot, whereas ouabain suppresses the overshoot. The increased contraction by hydrazine under the influence of excess K⁺ ions is more persistent than that by adrenaline. A complete loss of excitability of membrane due to excess K⁺ ions is also recovered by hydrazine as well as adrenaline.
In conclusion, the mode of a positive inotropic action of hydrazine would be essentially similar to that of adrenaline. Presumably, hydrazine increases the permeability of membrane to calcium ions.

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Two aged cases of atrial septal defect were presented. A correct diagnosis could not be made until the old age, because of various complications which might modify the characteristic findings on auscultation. These cases were complicated by a mild or moderate pulmonary hypertension, and, maybe, tricuspid incompetence. Pericarditis was observed in one case.

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