The patterns of hypertension in 26 patients with pheochromocytoma were related to the content and turnover rate of catecholamines in the tumor, and to the patterns of urinary excretion of catecholamines and their metabolites. The patients with paroxysmal hypertension were older, and had longer clinical course, larger tumor with an increased catecholamine content, a slower rate of catecholamine turnover and a metabolite dominant pattern of excretion when compared with those in patients with sustained hypertension.

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The effect of pyridinolcarbamate treatment in atherosclerosis obliterans was evaluated in 47 patients during a double-blind crossover trial using the mean of crest time from toe plethysmography.
After the initial 3 weeks of placebo washout a 10 week regimen of placebo or pyridinolcarbamate (1.5Gm. daily) and another 10 week of alternative regimen were given successively.
1) Twenty-two cases completed the trial and after the pyridinolcarbamate regimen the prolonged crest time was improved in 8 out of total 44 legs (18.2%), no change in 36 (81.8%) and worsening in none. After the placebo regimen, there was improvement in none, no change in 37 out of 44 legs (84.1%) and worsening in 7 (15.9%). This difference was statistically significant (p<0.005).
2) The crest time before treatment was tabulated by the location of arterial obstruction; aorto-iliac 0.39±0.033sec., femoropopliteal 0.35±023sec. and arteries in lower leg 0.31±0.026sec. Crest time in patients with aorto-iliac obstruction was more prolonged than in femoro-popliteal, which in turn was more prolonged than in more distal leg obstruction, but these differences were not statistically significant (p<0.10).
3) Pyridinolcarbamate treatment reduced the prolonged crest time more than placebo treatment even in dropout patients (p<0.005).
4) There was no difference in side effects among pyridinolcar-bamate and placebo trial except the one case which showed transient SGOT and SGPT elevation during pyridinolcarbamate treatment.
Our observations show that pyridinolcarbamate exerts a favorable effect in patients suffering from atherosclerosis obliterans.

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(1) Changes in platelet count, platelet adhesiveness, activated partial thromboplastin time, one-stage prothrombin time, plasma coagulation factors VIII, VII-X, X, V, II (prothrombin), and I (fibrinogen), euglobulin lysis time, plasminogen level, antiplasmin and trypsin inhibitor activity of plasma were determined before and after the development of myocardial infarction in 3 cases.
(2) Before the onset of the infarction, platelet adhesiveness was increased, but fibrinolysis was not decreased. Factor VIII activity was increased in 1 case in which it was measured.
(3) Immediately after the onset of myocardial infarction, platelet adhesiveness was transitorily decreased in 2 cases, factor VIII activity was rapidly enhanced to an extraordinarily high level in I case. Levels of the other clotting factors varied, but a trend was for elevation of these factors. Regarding fibrinolysis, hyperfibrinolysis was present at that time, as indicated by shortened euglobulin lysis time and decreased antiplasmin activity. Subsequently, a marked increase in platelet adhesiveness and fibrinogen, normalization of factor VIII activity, a prolongation of euglobulin lysis time, and a significant increase in plasma trypsin inhibitor activity were found.
(4) The results obtained in the present investigation strongly suggest that increased platelet adhesiveness is of great importance concerning the etiology of coronary thrombosis. Decreased fibrinolysis was not demonstrated in our 3 cases just before the development of myocardial infarction.

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Clinicopathological correlation was made in 8 cases of various A-V conduction disturbances, which consisted of 2 cases of complete, 4 of advanced, I of 2: 1 A-V block and 1 of A-V nodal rhythm. Serial sections of the conduction system revealed 4 types in location of main lesions. Type I (necrosis and/or fibrosis of A-V node) was found in 2 cases with syphilitic endoarteritis and acute myocardial infarction, respectively. Type II (fibrosis and fatty metamorphosis of the penetrating portion of A-V bundle) was found in 1 case. Type III (fibrosis with increased acid mucopolysaccharide of the branching portion of A-V bundle) was found in 4 cases with special relation to aging and degeneration of the central fibrous body. Type IV (necrosis of bilateral bundle branches) as found in 2 cases with fresh myocardial infarction. In general, degrees of histological damage and A-V conduction disturbances were fairly correlated. Etiological analysis showed ischemic necrosis (Type I, II and IV) in 4 cases, and degenerative changes (Type III) in the remaining 4. Degeneration of the branching portion of the bundle of His strongly suggested the similar etiological background with the "right bundle branch block with left axis deviation".

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Nine mongrel dogs were sacrificed to know hemodynamic effect of nitroglycerin, dipyridamole and theophylline ethylendiamine on coronary circulation.
Coronary blood flow (CBF) was measured by electromagnetic flowmeter. Aortic and left ventricular pressure were measured at the same time. Arterial and coronary sinus oxygen tension were measured.
Dipyridamole gave effect of marked and continuous increase in CBF, decrease in coronary vascular resistance (CVR) and raised coronary sinus oxygen tension.
Nitroglycerin gave effect of increase in heart rate immediately after the injection, followed by decreased heart rate and decrease in TTI 3min. later.
Theophylline ethylendiamine gave effect of decreased CVR and TTI immediately after the injection, however, noteworthy change could not be seen 3min. later.
The types of change in coronary vascular resistance induced by coronary vasodilators were divided into 3 groups.
In group A, decrease in systolic CVR without decrease in enddiastolic CVR (EDCVR) was seen. Here, decrease in TTI with increased heart rate was seen.
In group B, coronary vasodilation in enddiastole without decrease in mean CVR was seen. Probably, extravascular compression played an important role here.
In group C, reduction of CVR in systole and enddiastole was seen with decrease in TTI/CBF ratio and lowered aortic pressure, suggesting extravascular compression was rather indifferent.

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Surface and intracellular electrograms and ventricular pressures were used to study the effects of epinephrine and propranolol on electrophysiological properties in the in situ heart of 21 anesthetized dogs. Five sec. after the infusion of epinephrine, the ST segment became slightly depressed. About 10 to 20sec. after epinephrine, the ST segment became elevated and the negative T wave became more inverted. Initially, the upward convexity of phase III of the membrane action potential deepened slightly. Phase II of the membrane action potential gradually decreased in amplitude and became prolonged in duration. Phase III of the membrane action potential increased slightly. The membrane resting potential remained almost unchanged. Intracellular electrographic changes due to epinephrine were of abnormal configuration. That epinephrine may cause anginal pain is well known. Propranolol inhibits epinephrine's effects on the electrophysiologic properties of the heart. It is thought that propranolol helps to relieve the pain of angina pectoris by decreasing cardiac work and by increasing coronary blood flow.

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As one of the tissues possessing profound influence on body surface ECG, the lung was especially studied through placing dog lungs or a lung model in the human torso model. As the electrical source, an artificial current dipole or dog heart perfused according to Langendorf's technique was used to study the influence of the lungs on the transfer impedance vector and body surface ECG.
The image surface of the inhomogeneous model (with the lung model) showed shrinkage on the dorsal side with interpolation of the lung as compared with the homogeneous model. In the portion without interpolation of the lung, it enlarged under the influence of the lung.
On the homogeneous model, the orthogonal systems of Frank and Polyograph III demonstrated very good performance in normality and orthogonality. But the emplacement of lungs caused considerable deterioration of these VCG systems. A very good correlation was noted between the changes of body surface ECG and those of the transfer impedance vector in the homogeneous and inhomogeneous model.
The lead field-potential distributions within the human torso were measured. From this result, it was concluded that an electric current tended to flow towards the regions where the lungs did not intervene.

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