Direct cause of hypertensive cerebral hemorrhage was not arteriosclerosis but arterionecrosis of the intracerebral arteries, which formed microaneurysms leading to their rupture.
The earliest change of the arterionecrosis was muscle cell necrosis in the tunica media of the intracerebral arteries, in which subsequently occurred blood plasma insudation. The blood plasma infiltration induced histolysis of the arterial wall and then caused intimal deposition of fibrinoid substance consisting mainly of fibrin.
The arterionecrosis was frequently found in the brains of hypertensive autopsy cases, but not in those of normotensives. The arterionecrosis and microaneurysms were frequently found in the putamen, thalamus, caudate nucleus, and cerebral cortex, and predominantly in arteries of approximately 150μ, in diameter, but seldom in the palliduin.
The medial muscle cell necrosis, that is, the primary lesion of the arterionecrosis, was considered to be caused by hypertension, aging, and poor nutrition (low lipid diet), all of them bringing injurious effects on the tunica media which was primarily poor in structure.
As-for the cause of the histolysis of elastic and collagenous fibers, which was the characteristic finding of the arterionecrosis, blood plasma insudation was considered important. So that the arterial lesion was designated as “plasmatic arterionecrosis”.
Intracerebral microaneurysms were studied by the method combining postmortem cerebral arteriography, brain tissue clearing in tetralin, and serial paraffin sectioning. The microaneurysms were found frequently and in multiple occurrence in cases of cerebral hemorrhage and hypertension, but usually not in normotensive cases. Most of the aneurysms were 300-700μ in diameter, and all of them were caused by the arterionecrosis. Twenty-one % of the aneurysms were occluded by thrombi.
The process of large hematoma formation was supposed to be the following three stages : 1) Single or multiple rupture of the microaneurysms; 2) multiple capillary bleeding due to disturbed blood circulation in the distal areas of the ruptured arteries; and 3) venous hemorrhage caused by disturbed return flow in veins compressed by hematoma and brain edema.
In the cerebral arteries of hypertensive rats with the bilaterally constricted renal arteries were seen arterionecrosis-like lesions, which were also preceded by medial muscle cell necrosis. The medial muscle cell necrosis was significantly inhibited by a high lipid diet.
The arterionecrosis-like lesions of hypertensive rats with the bilaterally constricted renal arteries were healed when the bilateral constricting clamps, namely, the causes of hypertension, were removed.
Microaneurysms caused by arterionecrosis were sometimes occluded by thrombi and saved from rupture. The occluded lesions, however, were one of the causes of small infarction in the basal ganglia. Autopsy study gave us an impression that the ratio of the microaneurysms occluded by thrombi to all the arterial lesions responsible for small infarction in the basal ganglia had increased in recent years.
The reasons of the decreased incidence of cerebral hemorrhage in Japan of late years were considered to be the increased thrombotic occlusion of the arterionecrosis or microaneurysms, which was caused by increased thrombosis due to high lipid diets, which were brought about by the modernization of dietary life of the Japanese, in addition to the prevention of the medial muscle cell necrosis by the high lipid diets.

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The neurological examination is fundamental for the diagnosis; further observations were undertaken to confirm the diagnosis. Recently, computerized tomography (CT) has been employed making it possible to differentiate cerebral hemorrhage and cerebral infarction by non-invasive techniques. However, diagnosis of hemorrhage due to ruptured aneurysm and localization of the occluded point of the artery in cerebral infarction still must depend on cerebral angiography. As the utilization of CT is limited, the neurological examination must be considered the fundamental procedure for the diagnosis.
We have observed nearly 1250 cases of cerebrovascular disease in Mihara Memorial Hospital during last 5 years. Cerebral infarction accounted for approximately 50% of the cases, followed in frequency by cerebral hemorrhage (30%) and subarachnoid hemorrhage (10%).
In our study of 300 cases of cerebral hemorrhage, putaminal hemorrhage accounted for 60% of the cases, thalamic bleeding for 26% and other site for 14% respectively. Among the other sites, pontine hemorrhage and cerebellar hemorrhage were found in a almost the same number and subcortical hemorrhage was less frequent than the above mentioned two. I would like to make special comment about the clinical diagnosis of putaminal and thalamic hemorrhage. We made up our criteria for these diagnosis according to the disturbance of consciousness and grade of paralysis. When the disturbance of consciousness is absent or in slight degree, the diagnosis is made on the basis of the presence at the thalamic syndrome which is confirmed in cases of incomplete paralysis. However, thalamic bleeding is diagnosed when Parinaud's sign is present, and putaminal bleeding is suspected when the thalamic syndrome is absent and aphasia is observed due to lesion in the dominant hemisphere. When there is moderate or severe disturbance of consciousness, putaminal bleeding is indicated by the presence of contralateral deviation of the eyes. Signs such as biocular deviation of the eyes inward and downward, loss of light reflex, or deviation to the “wrong side” in severe cases were considered to indicate thalamic bleeding.
In a randomized study by cerebral angiography in 300 cases of cerebral infarction, the number of cases with occlusion, with stenosis, and without occlusion or stenosis each accounted for approximately one third of the total. Among the cases with occlusion, occlusion of the middle cerebral artery was most frequently observed followed by occlusion of the internal carotid artery.
Treatment : Surgical procedures include evacuation of hematoma, in cases of putaminal hemorrhage, cerebellar hemorrhage and subcortical hemorrhage. Thalamic hemorrhage is not the object of evacuation. In cases of cerebral thrombosis, superficial temporal artery-middle cerebral artery anastomosis is considered to be effective in some instances, although final evaluation is still not completed and will require more clinical experience. Endoarterectomy of the internal carotid artery is performed in some cases of transient ischemic attacks. A comparative study of medical (79 cases) and surgical (175 cases) treatment of putaminal hemorrhage was evaluated. In cases of moderate to large hematoma showing ventricular hemorrhage and with a disturbance of consciousness between stupor and semicoma, surgical treatment was significantly better than conservative treatment in improving both activities of daily living and mortality rate.

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During the past 14 years from 1965 to 1978, the total incidence of post-transfusion hepatitis (PTH) in our patients undergoing thoracic surgery was 20.4%. In the first phase of this study from 1965 to 1967, almost bloods were supplied from commercial blood bank.The post-transfusion hepatitis markedly developed in 45.4% of 33 patients. The hepatitis risk of PTH was very high in this period. So based on these fact, every possible means were tried to exclude bloods from hepatitis carriers. And we converted donor blood from paid to volunteer origin from 1968. But no significant reduction in PTH could be shown and incidence was still 20.3%. Fortunately, we were able to screen all donors blood for HBs Ag prior to transfusion and the incidence of PTH fell to 12.5% as would be expected.
In 94 transfused recipients, 8 cases (8.5%) had HBs Ag and 22 cases (23.4%) had HBs Ab. There have been 12 cases of PTH, 8 cases (8.5%) of type B hepatitis and 4 cases (4.3%) of non-B hepatitis. In 137 non transfused cases, 6 cases (4.4%) with HBs Ag positive and 9 cases (6.6%) with HBs Ab positive were observed and unexpectedly, 14 cases (10.2%) suffered from hepatitis were revealed.
Conclusively, the exclusion of commercial and HBs Ag positive donor blood has markedly reduced the incidence of type B post-transfusion hepatitis. But it was very interested that 14 cases suffered from hepatitis without transfusion. So the development of new serologic detection methods for non-B hepatitis virus is necessary to prevent post-operative hepatitis.

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In eighteen patients with subacute thyroiditis, serum triiodothyronine (T₃), thyroxine (T₄), thyrotropin (TSH) and 4-hour ¹³¹I-uptake were measured during the course of the illness. In the acute stage, serum T₃ and T₄were markedly elevated, (T₃ : 343±36 ng/dl, T₄ : 11.0±0.9 ug/dl) and ¹³¹I-uptake was low. (2.9 ±0.6%) Serum TSH was undetectable in 14 patients out of 18.
In five cases, TRH test was performed.There was no significant response in serum TSH in the acute stage.
This indicates that in the acute stage of subacute thyroiditis, the thyroid hormone level is increased sufficiently to inhibit TSH release. The mean value of an increment in serum TSH was only 1.8μU/ml during the recovery phase when ¹³¹I-uptake was normal or hypernormal. In addition, an elevated ¹³¹I-uptake was not necessarily associated with an immediate increase in serum T₃ and T₄.
These observation suggests that the resumption of the iodide pump is more important than an increment in serum TSH in producing normal or hypernormal ¹³¹I-uptake during the recovery phase.
There appears to be dissociation between the reestablishment of ¹³¹I-uptake and the resumption of hormone synthesis and secretion in the thyroid.

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The relationship between pacemaker potential and C-fibre's potential evoked by stimuli of the vagus nerve was studied intracellularly in the frog's sinus venosus. In all experiments the heart of Rana catesbeiana was excised together with the vagosympathetic nerve trunk. The ventricle and a large part of the auricles were cut away and the sinus venosus was pinned on wax in a bath with dorsal wall underneath. Vagal cardiac branches entering along the venae cavae superiores were dissected 5 mm to the point at which the division of pulmonary and cardiac branch could be seen (50μ or less in diameter). The extracellular recording electrodes were applied there. On the other hand the pacemaker potential was recorded intracellularly from the sinus venosus through a glass microelectrode.
The following results were obtained.
1) There were three major groups of nerve fibres as judged by conduction velocity in the cardiac nerve branch.
2) The fast groups vary in conduction rate from 20 m per sec. to approximately 8 m per sec., may be regarded as B fibre. 3) The slow groups vary in conduction rate from 2 m per sec. to approximately 0.3 m per sec., regarded as C-fibre.
4) The other groups had an intermediate velocity between. them, regarded as B₂ fibre.
5) The fast groups had a lower threshold and the slow and intermediate groups had a higher threshold.
6) The post tetanic hyperpolarization (PTH) in the C-fibre showed the maximum value in stimulus duration between 30 and 75msec. It agreed very closely with that of hyperpolarization of pacemaker.
7) Both hyperpolarization of C fibre and pacemaker cell were inhibited by K and ouabain.From these results it could be presumed that spontaneous activity in pacemaker cell was similar to activation of electrogenic sodium pump of C fibre in the PTH.

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Left inferior vena cava was incidentally demonstrated in a 54-year-old male during a right heart catheterization performed under a clinical diagnosis of cardiomyopathy. No other congenital intracardiac anomalies were associated in this case.

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Many investigators suggested the role of lysosomal hydrolases released into systemic circulation as a causative factor of cardiovascular depression during shock. The present study was undertaken to clarify the nature of circulatory derangement induced by intravenous administration of lysosomal extracts. The liver of mongrel dogs was excised for the separation of contents of lysosomal pellets with homogenization and centrifugation.
Cardiovascular function including myocardial contractility and peripheral vascular performance was assessed during and some time after the infusion of lysosomal extracts. Profound hypotension and decrease in cardiac output were observed. However, myocardial contractility was not impaired on the measures such as dp/dt/p and Vmax obtained by left ventricular catheterization. Peripheral vascular resistance was observed to be significantly lowered in the constantly perfused hind limb circuits of dogs.
These results indicate that lysosomal hydrolases released into systemic circulation may cause vasodilation and pooling of blood in peripheral vascular bed and may not deteriorate myocardial contractility.

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