Sixteen cases (10 men and 6 women of 71 to 88 years of age) of complete right bundle branch block (RBBB) with right axis deviation (RAD) were examined for the conduction system. There were 7 cases of hypertension, 2 myocardial infarction and 6 pulmonary disease. The electrical axis was from +90°to +150°with an average of +113°, and small q waves in leads II, III, and aV_F were present in 11 cases. Duration of RBBB with RAD was within 2 months in 4 cases and over 1 year in 12. There was only 1 case who developed complete atrioventricular (AV) block.
Heart weight was from 220 to 445Gm with an average of 306Gm. Severe coronary sclerosis was found in 6 cases and myocardial infarction in 2. The AV node and the penetrating portion of the AV bundle showed only slight fibrosis, but the branching portion of the AV bundle showed moderate degeneration and fibrosis. Right bundle branch (RBB) was interrupted with fibrosis at the 1st portion in 7, 2nd portion in 8 and 3rd portion in 1. Complete interruption was found in 57 to 100% (average 87%) of the left posterior fascicles (LPF) and in 0 to 100% (average 28%) of the left anterior fascicles (LAF). It was concluded that the RBBB with RAD was produced by interruption of RBB and LPF.

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The cardiohemodynamic effects of antianginal drugs and typical vasodilators, namely nitroglycerin, N-nitroso-morpholino-aminoacetonitrile (SIN-1A), aminophylline, papaverine, trapymin, dipyridamole, carbochromene, nifedipine, etafenone, prenylamine and iproveratril, were comparatively studied in anesthetized open-chest dogs. These drugs all decreased the systemic blood pressure, although aminophylline, papaverine and trapymin induced a marked increase after an initial transient fall. Changes in the total cardiac output represented by the blood flow in the pulmonary artery were quite similar to those in the venous return (VR), sum of the inferior and superior caval flow. The contribution of the superior caval flow to the change in VR was less than that of the inferior caval flow. Changes in the right atrial pressure (RAP) were far less than those in VR, but both the RAP and VR were dose-dependently modified by these drugs. I) Nitroglycerin and SIN-1A caused decreases in both the VR and the RAP and transient increases in the heart rate (HR). IIa) Aminophylline, papaverine and trapymin increased the VR, decreased the RAP and produced a long-lasting tachycardia. IIb) Dipyridamole increased the VR and induced a barely recognizable change in the RAP and the HR. Carbochromene induced similar changes but bradycardia was more evident. IIc) Nifedipine, etafenone and prenylamine increased the VR but simultaneously raised the RAP and induced bradycardia. A large dose over the therapeutic range turned the increase of VR into a marked decrease. IId) Iproveratril decreased the VR but markedly increased the RAP and caused bradycardia. It is concluded that antianginal drugs are clearly differentiated from the other vasodilators and that the latter agents can be classified into 4 groups, judging from the drug effects on the relations between the VR and RAP.

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The sinus node artery of 10 dog hearts was auto-perfused with blood led from the femoral artery under constant pressure at 100mmHg by the aid of a perfusion pump. Acetylcholine and carbachol given into the sinus node artery induced atrial fibrillation following sinus arrest. Electric pacing with a frequency from 1 to 5Hz was applied to the middle part of the free wall of the right atrium. Electric pacing at a rate below the sinus rate caused some extrasystoles, but pacing at a rate above the sinus rate did not cause any extrasystoles; by pacing at a higher rate than 4.5Hz, AV block was induced. The induction of atrial fibrillation by acetylcholine or carbachol was prevented by various frequencies of electric pacing at a rate either below or above the control sinus rate. But higher frequencies of pacing, 4 to 4.5Hz, occasionally could not prevent atrial fibrillation induced by acetylcholine or carbachol. The sustained atrial fibrillation induced by carbachol was not blocked by artificial pacing of the free wall of the right atrium at any rate of electric pacing.

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The effect of nitroglycerin on excitation of afferent cardiac sympathetic nerve fibers has been examined. Using anesthetized dogs, action potentials of the fibers were derived from either the 2nd or 3rd thoracic communicating ramus of the left side.
Occlusion of the anterior descending branch of the left coronary artery resulted in development of systolic bulge of the anterior wall of the left ventricle and in excitation of myelinated Aδ and unmyelinated fibers. Systemic administrations of nitroglycerin in a dose of over 30μg/Kg reduced or eliminated systolic bulge and suppressed excitation of the afferent nerve fibers. The maximum duration of its inhibitory effect on afferent discharge was 240sec and it was produced with 60μg/Kg. The inhibitory effect of nitroglycerin was not observed during hypotension produced by the injections of regitine. The systemic administrations of regitine in a dose of over 100μg/Kg and a fall in systemic blood pressure produced by occlusion of the caval veins also eliminated systolic bulge and suppressed the afferent discharge.
It is concluded that the inhibitory action on excitation of afferent cardiac sympathetic nerve fibers during myocardial ischemia is not specific for nitroglycerin and that the inhibitory action of nitroglycerin is dependent on the level of systemic blood pressure.

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Relationships of doses of α- and β-adrenergic receptor blockers to arterial pressure, cardiac output, total peripheral resistance, and heart rate were observed in SHR (spontaneously hypertensive rat) and NCR (normotensive control rat) under pentobarbital anesthesia and positive pressure respiration. The decreases in arterial pressure and total peripheral resistance by phenoxybenzamine were greater in SHR than in NCR. By increasing dose of this drug, the differences in these parameters between SHR and NCR were gradually diminished and finally disappeared. Propranolol induced a similar equalization of heart rate between SHR and NCR. These findings are consistent with that the hypertensive state in SHR is maintained by an elevation of the sympathetic tone. Sympathetic vasoconstrictors seem to play a major role over cardiac sympathetics in the hypertension of SHR, since propranolol alone could not markedly diminish the arterial pressure in SHR.

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Results obtained in (1) and (2) indicated there was a cardiac hyperfunction associated with increased NE metabolism in the incipient stage of hypertension of SHR. However, relative ineffectiveness of β-blocker in arresting the development of hypertension (3) showed that cardiac hyperfunction was not the sole mechanism for the development of hypertension but rather an index of increased outflow of autonomic nervous system to the cardiovascular system as a whole. Enhancement of mesenchymal metabolism of vasculature, probably in response to the increased load to the vascular wall, was detectable even in the incipient stage of hypertension (4), and such a rapid mesenchymal response of vasculature, closely cooperating with the increased autonomic nervous outflow, seems to be important for the development and maintenance of hypertension in SHR.

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KRA in 1.7-month-old SHR was slightly larger than that of the control, but it was not significant. After the age of 3 months, KRA of SHR decreased. Both DNase and RNase activities in SHR were higher than in the control. β-GPase activity was slightly higher in 1.7-month-old SHR than in the control. Cathepsin showed increased activity in 13 to 15-month-old SHR.

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1. The daily urinary volume of SHR with common diet (C₂) is larger than that of normal control Wistar rat (C₁) and the osmotic pressure of the urine in SHR (C₂) is lower than the control rat (C₁) (Table).
2. The kidney weight in SHR (C₂) is larger than the normal control.
3. The kidney weight in SHR receiving high salt, low protein and Tokyo.high carbohydrate diet (S₃) was smaller than SHR on normal diet (C₂).
4. The kidney of SHR receiving a high salt and high protein diet (S₂) was twice as heavy as the kidney of normal rat.
5. The serum potassium and BUN of SHR on high salt, low protein and high carbohydrate diet (S₃) were slightly lower than the SHR on normal diet and the normal control of Wistar rat.

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The present study on the developmental course of hypertension in some substrains of SHR with marked differences in the incidence of cerebrovascular lesions clarified that rapidly developed and augmented hypertension was probably related to the higher incidence of cerebrovascular lesions. Accelerated development of severe hypertension in young stage seems to cause greater damage in relatively immature vascular wall and initiate the vicious sequence finally ensuing in cerebrovascular lesions. However, possible involvement of other factors than severe hypertension in the difference of vascular vulnerability in the substrain can not be eliminated and is still under investigation.

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The present study showed a clear difference in the vulnerability to hypoxia in SHR, especially in A₁-sb compared with NR. The increased vulnerability to hypoxia in SHR might be partly related to their increased cerebrovascular permeability preexisting under non-hypoxic state which was supposed to be augmented under hypoxia as proved in NR.

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Frequent tracings of ECG during attacks of the nocturnal angina pectoris of a 69-year-old man failed to show any evidence of angina pectoris electrocardiographically. Angina pectoris was, however, induced by an intravenous administration of 50% glucose unexpectedly, and relieved by sublingual nitroglycerin and oxygen inhalation. The mechanism of this unusual phenomenon was discussed in relation to the serum-potassium, plasma-insulin, and the spasm of the coronary artery.

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