The clinical findings and the necropsy reports of 5 cases of aortitis syndrome have been presented. In addition to the typical arterial changes, diffuse myocardial fibrosis with marked left ventricular hypertrophy was seen at necropsy. The relationship between these cardiac lesions and aortitis syndrome was discussed. The development of aortic valvular insufficiency in this disease was not infrequently found, and was thought to be due to the dilatation of valvular ring and/or the extension of the inflammatory change of the aorta to the aortic valve itself. The prognosis of the disease seems to be dependent largely on the severity of heart failure, aortic insufficiency and hypertension.

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From the findings at entry examination and the data obtained in the 10 years of follow-up experience, the following conclusion is reached.
(1) The mortality from cerebral thrombosis and myocardial infarction has been significantly higher in Ushibuka men than in Tanushimaru men. The increase of sum of skinfold thickness due to a remarkable reduction of physical activity and prevalence of high blood pressure seemed to influence the high mortality from cerebral thrombosis and myocardial infarction.
(2) The higher trend of cerebral hemorrhage in the men with hypertension at Tanushimaru appeared to be influenced by the low serum protein concentration with A.G ratio abnormalities due to low dietary protein and by the higher elevation of blood pressure after exercise.

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Oral administration of 10mg. of Bay-a 1040, a new coronary dilator, produced a marked reduction of arterial pressure which was associated with a consistent decrease in peripheral vascular resistance and an increase in cardiac output and stroke volume. Changes in heart rate and left ventricular work were variable. In 20 hypertensive patients treated with the drug in doses of 10mg. per day, a modest antihypertensive effect was achieved. Side effects including dryness of the mouth and burning sensation in face and legs, were observed in few patients.

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Previously, the fine structure of the carotid body, the experimental sclerosis of the carotid sinus wall, circulatory effects of carotid occlusion and adrenergic blocking agents effects for the carotid baroreceptor, were studied in this clinic. This time, circulatory changes due to carotid sinus reflex by electrical stimulation (square wave; 8v., 20-50cps) of the carotid sinus wall in situ canine carotid artery were investigated
(1) Systolic arterial blood pressure was lowered by 33.7mm.Hg from average 143mm.Hg. Diastolic arterial pressure was decreased by 21.0mm.Hg from the level of 74.8mm.Hg. P-value was less than 0.001. Coronary blood flow was also decreased 5.5ml./min. from average mean flow 30.4ml./min. (P less than 0.001). Coronary resistance was decreased 0.27mm.Hg/ml./min. from average 3.22mm.Hg/ml./min. (P less than 0.001). Cardiac output was decreased insignificantly. Left intracardiac pressure was reduced by 8.9mm.Hg (P less than 0.01). Its max dp/dt was decreased (P less than 0.01). The dp/dt/IIT was reduced by 0.06 (per cent change, 18.18%) from average 0.33. The change of the left ventricular tension measured by the straingauge arch was insignificant. The R-R and P-R intervals were slightly prolonged in the second lead of the electrocardiogram (P less than 0.001). The myocardial oxygen consumption was altered to decrease. Arterial blood catecholamine was apt to decrease.
(2) After the administration of propranolol (0.2mg./Kg.), carotid sinus reflex by the electrical stimulation did not cause the changes of intracardiac pressure and max dp/dt but those of arterial blood pressure and coronary blood flow. Cervical vagotomy inhibited these changes.
(3) It should be noted here that these decreases of cardiac work, myocardial oxygen requirement and diastolic coronary resistance are effective for the angina pectoris through the adrenergic and the cholinergic nerves with catecholamine change.

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The pattern of myocardial segment length change in an ischemic and nonischemic area of the left ventricle was studied acutely following ligation of the LADA in the dog. Results were interpreted in relation to other hemodynamic findings obtained in the same experiments. Paradoxical bulging during systole was found in the ischemic area, whereas increased shortening during systole was found in the nonischemic area. Since there was no increase in cardiac output or aortic pressure, it was assumed that the increased energy released by the nonischemic area of the ventricle was expended in stretching myocardial fiber in the ischemic area. Under the condition of ventricular afterloading, increased systolic bulging of the ischemic area and increased systolic shortening of the non ischemic area were noted. With maximum afterloading, systolic bulging of the ischemic area was diminished and ventricular systolic pressure increased. This suggested that a reduction in ventricular wall compliance might improve the function of the partially ischemic ventricle by diminishing the amount of energy expended during systole in stretching muscle fiber in the ischemic area.

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The ligature of right coronary artery near its origin produced low distal right coronary artery pressure, which showed gradual increase day by day, reaching maximum level (70% of the aortic pressure) in 8 postoperative days.
The trial to produce rapid increase of the distal right coronary pressure by augmenting the left circumflex coronary pressure by means of roller pump was carried out in normal dogs. But the increase of the distal right coronary artery pressure was only several millimeters mercury. The pressure augmentation of 2 hours in the left side, therefore, could not produce sufficient collaterals from left to right.

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A fine structural investigation was performed on the myocardial lesion induced by high doses of isoproterenol in rats. The findings in the myocardial cells at the early stage consisted of swelling of endoplasmic reticulum and mitochondria and depletion of glycogen granules. The results suggest that isoproterenol primarily affects endoplasmic reticulum and mitochondria, leading to the impairment of their membranes and metabolism, About 8min. after isoproterenol, electron dense bodies were found in mitochondria, suggesting an accumulation of calcium. Fibroblastic infiltration was noted in damaged myocardial area 6 hours after isoproterenol, and after 24 hours in some cases there occasionally appeared young myocytes which were possibly originated in surviving myocardial cells. Propranolol significantly delayed an appearance of abnormalities in endoplasmic reticulum and mitochondria at the early stage, but it had little influence on the improvement of isoproterenol-induced myocardial damages at the later stage.

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Attempts were made to clarify the mechanism with which the pulmonary infarction occurs, from coagulation-fibrinolytic point of view.
Pulmonary infarction was produced in 77.8% of the rabbits by infusion of human blood clots 2 days after intravenous injection of Lycopodium spores, in 28.6% or 55.6% of those by infusion of human blood clots on the 2nd or 3rd day after intravenous injection of minced human thrombi, and in 50.0% of those by infusion of rabbit blood clots on the 3rd day after intravenous injection of minced rabbit thrombi.
The group of rabbits with the pulmonary infarction showed more marked increase in the coagulative activity and reduction in the fibrinolytic activity on the 2nd or 3rd day after the 1st injection of Lycopodium spores or minced thrombi of either human or rabbits origin, than that in the animals without it, and in the former group a more pronounced consumption of the coagulation factors 3 hours after the 2nd injection of the clots, and increases of fibrinogen and FDP were recognized from the 1st day afterwards. A plateau type pattern of changes in the fibrinolytic activity was frequently observed during the course of the pulmonary infarction.

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