In patient with chronic cor pulmonale which was caused by pul-monary emphysema, circulating autoantibodies against the heart tissue were investigated by hemagglutination and hemagglutination-inhibition techniques using normal rabbit's myocardium as antigen. Quantitative analysis of serum IgG, IgA and IgM were carried out by use of the radial immunodiffusion method. These results were compared with clinical findings, specifically cardiopulmonary hemodynamics and patho-physiological changes.
Circulating anti-heart antibodies were found in 13 out of 25 (52 per cent) patients with a definite complication of chronic cor pulmonale. The titers of circulating anti-heart antibodies indicated a good correla-tion with hypoxia and pulmonary hypertension and/or pulmonary circu-latory disturbance. Furthermore, a good correlation was noted between anti-heart antibody titers and the serum IgG levels.
These data could be utilized in evaluation and discussion of the pathophysiological findings of the patients with chronic cor pulmonale.

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(1) Autopsy data obtained personally at the University of Glasgow on 100 cases of lung cancer were analyzed with reference to spread to the great vessels, pericardium and heart.
(2) These 3 sites were found to be invaded in 38, 27, and 7 cases respectively.
(3) This centrifugal order of spread and the other observed patterns of spread suggest the conclusion that these sites are usually invaded through lymphatic spread.
(4) It is emphasized (a) that lymph-borne mediastinal deposits are intially formed discretely in the classical manner of metastasis, (b) that these metastatic deposits subsequently coalesce with one another, and (c) that it is this coalescence which makes them to look deceptively like deposits formed in continuity through direct spread.

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Clinical and experimental studies were performed to examine the meaning and implication of the "His bundle spike" recorded with the current techniques.
Tracings obtained with various locations of electrodes along the A-V conducting system revealed that the more ventricularly the sensing electrode(s) was (were) introduced, the shorter the interval between the "His bundle spike" and the onset of ventricular deflections (spike-Q interval) on the electrogram.
The His bundle and bundle branch potentials should be understood not as the discrete phenomena but as the local manifestations of the suc-cessive depolarization of the A-V conducting system.
The His potential observed in a bipolar lead with 2 catheter electrodes was occasionally not seen in a unipolar lead with one of the 2 electrodes, therefore, the measurement of the intervals of the deflections would be of clearer meaning with unipolar lead which is more suitable for detailed study of the A-V conduction. Calculated condution velocity in human His bundle approximated to 1.25M/sec.

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In the isolated rabbit hearts the presence of an electrical longitudinal dissociation in the atrial portion of the His bundle was examined by the microelectrode method. Under the normal condition no marked differ-ence was found in the duration of the action potential of the cells at the same transverse level of the His bundle. However, the possibility of separation to at least dual pathways of the His bundle was disclosed, when the arrival time of excitation was observed or when, in addition, the site of stimulation was changed or intracellular stimulation was applied.
By passing the current intracellularly into the His bundle the elec-trotonic potential was found to be large in a direction parallel to the running of the His bundle while it was found to be almost zero in a direc-tion perpendicular to it. The longitudinal electrical separation was pre-sumed, however, not to be complete under the normal condition, because the intracellular stimulation of one tract was found to be transmitted to the other tract and the spontaneous activity of one tract was found to be conducted to the other tract. A high potassium content or low sodium content did not increase the longitudinal separation markedly in most cases. But in 1 experiment a high potassium content increased it, showing a possibility that under abnormal conditions a complete longitudinal electrical dissociation may occur.

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It was said that hemolysis could take place in the artificial heart pumping, so that some changes in the red blood cells would be expected as a cause of hemolysis. These changes were caused by the trauma to the erythrocytes. In order to elucidate the energy metabolism of the red blood cells, 4 calves, which survived for 408, 150, 64, and 41 hours after the total replacement by the artificial hearts, were subjected to the analysis of the erythrocyte's adenine nucleotides (adenosine-tri-phosphate; ATP, adenosine-di-phosphate; ADP, and adenosine-mono-phosphate; AMP).
Analysis of adenine nucleotides were performed by the enzymatic method. Peripheral blood smear was made and stained with Wright's solution. % crenocytes was obtained by this preparation.
It was demonstrated that ATP was decreasing and ADP was increasing toward the end of pumping. ATP: ADP ratio went down. AMP showed fluctuation. Close relationship between ATP level and crenocytes was observed.
It was considered that glycolytic activities in the red blood cells during the artificial heart pumping were much influenced by its mechanical and physical trauma, so that their ATP contents went down and the crenocytes increased in number.
This led to the intravascular and extravascular hemolysis in the artificial hearts pumping.

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Using a total number of 30 anesthetized dogs, embolism was produced by injecting air into the right vertebral artery. The efferent impulses from left renal nerve were recorded simultaneously with the arterial pressure. The renin activity in the renal venous blood and aortic blood was measured by the Helmer's method.
A slight initial step up in blood pressure and transient increase in renal sympathetic discharge were observed immediately after the embolism. Then the blood pressure rose up markedly and the nerve activity was depressed, which was considered that the phase of reduced sympathetic nerve activity was produced by excitation of the buffer nerves caused by the second rise in pressure. Thereafter, with the falling of the pressure to the control level, bursts of sympathetic discharge started again.
Renin release following vertebral embolism was estimated by a percent change of circulating renin activity of the left renal vein from each animal's control level, by multiplying the activity of renal venous blood with the left renal plasma flow. The circulating renin activity thus ob-tained in the control phase was 363±238ng angiotensin/min. It starts to increase during 6-10min after embolism, then within 20-30min it attained its peak of 217±104% in average compared with control values.The latter increase was highly significant (p<0.01). It is most likely that the first increase in renal sympathetic nerve activity caused the increase in renin release and the second rise in blood pressure was caused not by the increase in renin activity but by the increase in catecholamines.

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The effect of propranolol on excitation of afferent cardiac sympathetic nerve fibers during myocardial ischemia has been examined. Using anesthetized dogs, the action potentials of the fibers were derived from either the 2nd or 3rd thoracic communicating ramus of the left side. Coronary artery occlusion resulted in excitation of the myelinated Aδfibers and unmyelinated C fibers, and in development of systolic bulge of the occluded area of the left ventricular wall. Eight to 16min after the systemic administrations of 0.5-5mg/Kg propranolol, development of systolic bulge was suppressed and the latency for excitation of the afferent nerve fibers became longer than that of the control occlusion experiments. The number of the action potentials per second during occlusion was significantly smaller than that of the control occlusion and percent change in number per second was close to that of heart rate. Resultantly, the num-ber of the action potentials per cardiac beat was not different from that of the control occlusion experiments. It is considered that propranolol suppressed excitation of the afferent cardiac sympathetic nerve fibers through reduction in heart rate.

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Myocardial tissue blood flow of the left ventricle was measured by means of the heat clearance technique in open chest dogs under chloralose. The myocardial segment chosen for the flow measurement was rendered ischemic by occlusion of the left anterior descending (LAD) artery. In the ischemic state the area explored was supplied exclusively by the collateral vessels. Local vascular responses to various forms of adrenergic excitation (stellate stimulation, administration of noradrenaline and isoproterenol) were registered both before and after coronary occlusion. Coronary reactions were expressed as per cent local vascular conductance changes.
In the normal state all forms of the adrenergic activation elicited significant coronary dilatation (increase in vascular conductance). After coronary occlusion the average value of this coronary dilatation considerably decreased. At the same time, a systematic inverse relationship was found between the resting level of the collateral vascular conductance and its chance for an increase during adrenergic activation; in cases of high resting collateral conductance values, instead of an increase, a decrease was observed during stellate stimulation and noradrenaline administration. Pure beta-adrenergic activation induced by isoproterenol did not elicit similar decreases in the collateral conductance. The results suggest that adrenergic activation is able to upset an uncertain intrinsic vascular balance in the ischemic myocardium.

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Pericardial distensibility curves and chronotropic changes accompanying pericardial distension were investigated in 24 isolated perfused frog hearts. The distensibility curve had a slow phase and a steep phase attributable to elastic and collagen components of the pericardium. Changes in pericardial pressure were accompained with reversible changes in the heart rate. The mean control rate rose from 33/min to a peak of 44/min (33% acceleration) as the pericardial pressure was raised from 0 to 4mmHg. Further increase in pericardial pressure resulted in progressive bradycardia, the mean heart rate declining to 13/min (60% declination) at 20mmHg. The acceleration response (p<.01) was observed in 8 out of 14 (57%) hearts but bradycardia (p<.001) occurred in all hearts. Atropine and propranolol did not influence these chronotropic changes. With increase in temperature and in summer the initial heart rate was high and bradycardia was a dominant feature, The chronotropic effects could only be attributed to alterations in the mechanical stretch of the pacemaker cells. The positive and negative chronotropic changes corresponded with slow and steep phases of the pericardial distensibility curve and may be due to increased stretch and relaxation of pacemaker, respectively.

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The sinus node artery of 11 anesthetized mongrel dogs was perfused at a constant pressure of 100mmHg. A relatively small dose of norepinephrine, 0.01 to 1.0μg, usually induced a positive chronotropic response when injected directly into the sinus node artery. Occasionally, however, a combination of a positive and a negative chronotropic response or only a negative chronotropic response was apparent. A larger dose of norepinephrine, 10 to 30μg, consistently induced a triphasic response: there was a brief positive chronotropic response, followed by a longer negative chronotropic response, and finally a sustained positive chronotropic response. The negative chronotropic response usually began before the systemic blood pressure became elevated as a consequence of the systemic effects of the norepinephrine. The negative chronotropic response was not influenced appreciably by bilateral vagotomy. However, it was completely blocked by a small dose of atropine, 1μg. These results suggest that norepinephrine releases acetylcholine from parasympathetic nerve terminals.

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A histological study by serial sections of the conduction system was performed in a case of 84-year-old female with a diagnosis of hypertension and complete atrioventricular (AV) block. The course of her electrocardiogram was divided into 6 stages as follows: 1) left ventricular hypertrophy (11 years before), 2) complete right bundle branch block (CRBBB) and no axis deviation with PQ interval of 0.20sec (10 years before), 3) C-RBBB with right axis deviation (2 years before), 4) advanced AV block with occasional ventricular capture, 5) C-RBBB with left axis deviation for 10 days' duration (1 year and 3 months before), and 6) complete AV block with the idioventricular rhythm with RBBB type (terminal 1 year).
There were moderate fibrosis in the AV node with partial destruction of conduction cells and the same fibrotic changes in the proximal portion of the AV bundle. The proximal portions of posterior and anterior fascicles of the left bundle branch were completely interrupted by the marked endocardial fibrosis. The right bundle branch showed sporadic fibrosis in the first portion, but in the second portion the conducting cells were thoroughly destroyed. The above-mentioned findings were compatible with the trifascicular block reported by Rosenbaum in 1969, in both the electrocardiographic and histological findings.

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