Japanese Journal of Stroke
Online ISSN : 1883-1923
Print ISSN : 0912-0726
ISSN-L : 0912-0726
Volume 2, Issue 3
Displaying 1-16 of 16 articles from this issue
  • Kenichi Tanaka, Tadaatsu Nukada, Shotaro Yoneda, Masahito Kusunoki, Yo ...
    1980 Volume 2 Issue 3 Pages 179-185
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Ultrasonic Doppler sonography has been applied to evaluate the patency of superficial temporal artery (STA) to middle cerebral artery (MCA) anastomosis. This study included 13 patients with internal carotid artery occlusion or stenosis who had undergone STA-MCA anastomosis. The blood flow patterns of the STA, ophthalmic and major aortocranial arteries in all patients were analysed by Doppler sonography. Futhermore, long-term follow-up studies were also performed in ten cases.
    In patients with good patency demonstrated by postoperative angiograms, the flow pattern of STA showed increase in systolic and diastolic velocities and changed to an internal carotid type from an external carotid type. The findings of Doppler sonograms of STA were well consistent with the postoperative angiograms and precisely represented the bypass patency. In long-term follow-up cases, the alterations of STA flow on the sonograms were concurrent with those of the blood flow distribution via anastomosis on the second postoperative angiograms. In ten cases with reverse flow direction in ophthalmic arteries before the operation, the reverse flow decreased in eight cases postoperatively. But no significant changes of the reversed ophthalmic flows were detected in the remaining two cases. The flow direction of ophthalmic artery was vulnerable to the pressure change, especially, in the case with internal carotid occlusion and easily affected by infusion pressure of the contrast material. Therefore, Doppler flowmetry is suitable for detecting the change of the ophthalmic flow in the physiological condition. The blood flow velocity patterns of major aortocranial arteries showed no change postoperatively.
    In conclusion, it was proved that the detection of the STA and the other collateral flow using the ultrasonic Doppler sonography was an excellent and reliable means for assessment and monitoring of bypass patency.
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  • Takefumi Kageyama
    1980 Volume 2 Issue 3 Pages 186-196
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    There have been many experimental reports concernig early ultrastructural changes of ischemic brain tissue. Common morphological changes of the early stage of the ischemic brain tissue are said to be mitochondrial swelling in the neuron and edematous enlargement of perivascular spaces. In this paper, it was reported that the actions of various agents such as Dexamethasone, Mannitol, Ergot-Alkaloids, Pentobarbital to these ischemic conditions experimentally. The ischemic conditions were obtained by ligation of both internal and right external carotid arteries of Wistar rats. The regional cerebral blood flow (rCBF) were measured in the area of the cortex and the basal ganglia of the right hemisphere.
    In 73 cases of 258 experimental rats, the rCBF decreased up to 50-60% to the preoperative flow rate in 30 minutes after ligation and gradually reduced subsequently. Therefore, these animals were used for experiments.
    Morphological changes of these ischemic brains were observed by electron microscope chronologically. The ischemic conditions produced mitochondrial changes in the neurons which were disintegrated with vacuolation and separation of cristae. These irreversible morphological changes of mitochondrias were increased when their ischemia were prolonged, and 3 hours after ligation, the proportion of the irreversible mitochondrias in cortical neurons attained to 54%.
    Pentobarbital and Ergot-Alkaloids had significant inhibitory effect for these ischemic mitochondrial changes.
    Dexamethasone and Mannitol showed no apparent protective effect for them. However, the latter two drugs reduced perivascular edema remarkably. Especially, Mannitol showed an effect to increase circulatory blood volume after recanalization by removal of the clip. Namely, the brain tissue of the group, which was administrated Mannitol during the ischemic condition, showed minimal histological changes after the blood circulation was regained, and active vesicular transports were not seen.
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  • Yoshio Miyasaka, Nobuyuki Kawano, Masako Murakami
    1980 Volume 2 Issue 3 Pages 197-206
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    The no-reflow phenomenon (NRP) after cerebral ischemia has been proposed as a factor limiting brain recovery. However, there have been other reports which denied the occurrence of the NRP. The purpose of this study is to reinvestigate the presence or absence of the NRP after circulatory arrest by using strict quantitative analysis.
    Nineteen adult mongrel dogs were used. Circulatory arrest was accomplished by occluding the ascending aorta for 15 minutes. The patency of cerebral microvasculature was assessed by carbon black perfusion study. The perfusion was performed without circulatory arrest (control; 6 dogs) and either immediately after releasing the circulatory arrest (group A; 7 dogs) or after reestablishment of normal blood pressure for 15 minutes (group B; 6 dogs).
    In order to judge the presence or absence of the NRP quantitatively, a modification of Mitchell's point counting method was used. All the vessels under 10 μ in diameter were traced with × 125 magnification. Then, points counting screen tone, which had 500 points in 25 cm2 of areas, was overlied on the traced vessels. The number of points lying on vessels were counted. The ratio of the number to 500 was calculated and expressed as a percentage which was termed “The Density of Minute Blood Vessels (DMBV)” (Fig. 2). Samples for the calculation were taken from 15 regions as shown in Fig. 3. The calculation was made five times in each region. The results were compared in 3 groups.
    In the control, it was shown quantitatively that the DMBV varied from one region to another over a wide range. The maximum DMBV was observed in the inferior colliculus. The minimum DMBV was recognized in the anterior hypothalamus. However, the standard deviation of the mean in the each region in the control was very small. Its value was 1.3 to 4.8% (average; 3.1%) (Fig. 5). The DMBV of the group A was significantly smaller than that of the control (p<0.01-0.05) (Fig. 6), but there was no difference of the DMBV between the control and the group B (Fig. 7). The MABP (mean arterial blood pressure) at the carbon black perfusion was 84 (±S.D. 24) mmHg in the control, 25 (±20) mmHg in the group A and 103 (±26) mmHg in the group B (Fig. 8).
    On the basis of the above data, in order to discuss the presence or absence of the NRP using carbon black perfusion study, it is absolutely necessary to use quantitative method. And also the comparison must be made in the same region. By using this method, it was clarified that the NRP is present right after the circulatory arrest, but it is reversible if the sufficient recirculation is established within short period of time.
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  • 1, biochemical study of tissue lipids
    Tadashi Nagayama, Toshihiko Atobe, Shigeo Ichimori, Kazuaki Tsuchiya, ...
    1980 Volume 2 Issue 3 Pages 207-214
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    In order to study the role of tissue lipids in cellular reaction to injury in cerebral tissue, we produced cerebral infarct in rats by way of embolization of homologous blood, and we chemically, chronologically measured tissue lipids in the infarcts. The corresponding tissue changes were histologically studied as well.
    Tissue phospholipids, essential components of membranes of cells and organellae, rapidly decreased to 79.8% of the controls in a day or two after injury. Histological changes at this time corresponded to tissue edema. On 3rd to 5th day when tissue damage was most advanced with many foamy macrophages in the center of infarcts, phospholipids still remained significantly low associated with a slight increase of triglycerides in the infarcted areas. The foamy macrophages were full of sudanophilic and osmiophilic granules. Later on, along with healing process, phospholipids gradually recovered to the same level as the controls by the 14th day. The infarcted areas at this point showed prominent proliferation of astroglia with still remaining foamy macrophages.
    We presume that catabolized tissue phospholipids by released enzymes in the infarcted areas will return into blood circulation, and that uncatabolized phospholipids as well as certain other lipids will be phagocytized by macrophages. It is suggested that sudanophilic and osmiophilic granules in the foamy macrophages must be made up of not only triglycerides but also free fatty acids and cholesterol ester.
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  • Kenichi Nakazawa, Jonosuke Atarashi, Akiro Terashi, Kosuke Iyoda
    1980 Volume 2 Issue 3 Pages 215-220
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    There still remain many unexplained points concerning the incidence mechanism of the disturbance of glucose metabolism recognized in cerebrovascular diseases.
    The authors have already reported that hyperglycemia in cerebrovascular diseases is related to the level of cortisol and epinephrine in the blood. This time, using the rabbits with experimental cerebral hemorrhage, our studies are concerned with the relationship between the blood glucose and α- and β-effects of epinephrine, the relationship between the blood glucose and glycogen levels, periodic change of glycogen in hepatic cells, and the influence of dexamethasone on these rabbits.
    Consequently, the blood glucose that gradually rises following the experimental cerebral hemorrhage has been controlled by β-adrenergic blockade (propranolol). The glycogen level was in parallel with blood glucose level. In order to find out the origin of blood glucose, we carefully observed the liver sections in formaline and found out that the glycogen in the liver cells was gradually decreased.
    Therefore, the blood glucose level is closely related to cortisol, β-effect of epinephrine, and glycogen. Hepatic glycogen is responsible for the blood glucose increase.
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  • Kazuo Suzuki, Kenji Nakajima
    1980 Volume 2 Issue 3 Pages 221-225
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    A 55-year-old man showed ocular bobbing during the course of hypertensive pontine hemorrhage.
    Ocular bobbing appeared intermittently and synchronized with electroencephalographic changes.
    When electroencephalogram showed α patterns, ocular bobbing was observed, and when electroencephalogram changed to spindle patterns, ocular bobbing disappeared and skew deviation was observed.
    Caloric test revealed no response bilaterally. Light reflex of the pupils persisted during the course of this illness, therefore the function of the midbrain was considered to be intact.
    He died 49 hours after the onset. Necropsy was done. The hematoma was situated mainly in the ventral pons and extended from the rostral end of the medulla to the caudal end of the midbrain.
    Small amount of blood was observed in the fourth ventricule.
    We concluded that the ocular bobbing was caused by the lesion of the pons and the lower midbrain, and speculated the mechanism as follows.
    1) The horizontal eye movement was disturbed by the hematoma in the pontine lateral gaze center.
    2) Irregular neural discharges from the midbrain made the eye balls to move downward, and the eye balls remained in this position for a few seconds.
    3) When neural discharges disappeared eye balls returned to the middle position.
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  • Hisao Tachibana
    1980 Volume 2 Issue 3 Pages 226-234
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    The purpose of the present study was to investigate the possibility to estimate CBF autoregulation by the retinal vascular responsiveness to changes in perfusion pressure.
    The retinal arterial diameter and its response to changes in blood pressure were measured by means of a fundus camera in 46 control subjects and in 26 patients with cerebrovascular disease (CVD), 7 with Parkinson's disease and 1 with Shy-Drager syndrome.
    Reduction of effective mean arterial blood pressure was induced by the postural change from a supine to an erect position.
    Changes in diameter of the retinal vessel were quantitatively analysed by the use of Retinal Vasomotor Index (RVI) [-a change in diameter (%) /a change in effective mean arterial blood pressure (mmHg)].
    The results obtained are summarized as follows :
    1) RVI in control subjects showed no significant differences between male and female or between right and left eye. The reduction of RVI correlated with advancing age (r=-0.299, P<0.01).
    2) RVI in patients with Parkinson's disease was significantly lower when compared with that in control subjects (p<0.005). In a patient with Shy-Drager syndrome, there was no significant response of the vessels to the fall in perfusion pressure.
    3) RVI in cases with supratentorial infarction, infratentorial infarction, intracerebral hemorrhage and vertebrobasilar insufficiency was all significantly lower than that in control subjects (p<0.001, p<0.02, p<0.05, and p<0.01, respectively). In cases with unilateral supratentorial infarction, there was no significant difference in RVI between affected and non-affected side of the lesion. RVI in each side was lower than that in control subjects (p<0.001 and p<0.001, respectively).
    4) RVI in cases without orthostatic hypotension was significantly higher than that in cases with orthostatic hypotension (p<0.01).
    Present data indicate that autonomic nervous system play a role in the mechanism of autoregulation of retinal blood flow and are compatible with previous data of CBF autoregulation. It is concluded that the observation of the retnial blood flow autoregulation is a useful and non-invasive method to estimate the CBF autoregulation.
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  • Significance of a risk factor
    Hideaki Kotoh
    1980 Volume 2 Issue 3 Pages 235-239
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Total cholesterol, triglyceride, HDL-cholesterol (by heparin-Mn2+ precipitation method) and lipoprotein fractionation (by cellulose acetate electrophoresis) were measured in 113 patients (83 men, 30 women) with TIA and cerebral infarction.
    The diagnosis was determined by clinical course, clinical signs and neurological specific examinations of cerebrospinal fluid, computerized tomography and angiography.
    The data of patients were compared with age-adjusted data in control groups of 110 men and 134 women.
    Male patients with TIA and patients with cerebral infarction showed significantly lower HDL-cholesterol levels and all showed significantly lower a-lipoprotein (%) levels and significantly higher triglyceride, pre β- lipoprotein (%) and atherogenic index (TC-HDL.C/HDL.C) levels than those of the controls.
    On the contrary, no differences were observed in total cholesterol and β-lipoprotein (%) levels of the patients with TIA and cerebral infarction.
    HDL-cholesterol level was measured monthly after the attack for nine months in 16 cases with TIA and cerebral infarction. However, no significant changes in HDL-cholesterol levels were observed.
    Thus, it might be considered that lower HDL-cholesterol and α-lipoprotein (%) levels are a negative risk factor of cerebral infarction.
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  • Tsutomu Sato
    1980 Volume 2 Issue 3 Pages 240-245
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    The efficiency in autoregulation of regional cerebral blood flow (CBF) was compared in the carotid and vertebral arterial systems. A newly developed photoelectric method was used with 6 rhesus monkeys to measure the mean transit time of blood (t), together with the cerebral blood volume (CBV) in the tissue of the parietotemporal area supplied by the carotid artery and of the cerebellar tonsil supplied by the vertebral artery. From values of t and CBV, the CBF was calculated using the Stewart-Hamilton equation. During continuous recording of CBV and frequent determination of t in both territories simultaneously, various levels of hypotension were induced by stepwise exsanguination through a femoral vein. As had been expected, CBF tended to decrease when blood pressure fell below a certain threshold. However, the author found that the mode of the decreases in CBF in the two arterial systems was quite different. The CBF in the carotid arterial system tended to be preserved even when the blood pressure fell below 60 mmHg while that in the vertebral arterial system started to decrease from as high as 70 mmHg of blood pressure. In addition, the decrease in the vertebral arterial system became more marked in accordance with the progress of hypotension. The difference in the CBF decreases in the two arterial systems at blood pressure less than 60 mmHg was statistically significant (p<0.05).
    From these data, the author concluded that the efficiency in autoregulation of regional blood flow in the vertebral arterial system was inferior to that in the carotid arterial system.
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  • With particular reference to the correlation between the midbrain lesion and cause of death
    Yasuaki Hosaka, Mitsuo Kaneko, Noboru Goto
    1980 Volume 2 Issue 3 Pages 246-254
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Since we proposed the extremely early operation or the operation within 7 hours after the apoplectic attack for the lateral type of hypertensive intracerebral hemorrhage in 1973, the excellent surgical results could have been obtained for them. But there are still fulminant cases in approximately 10% of the lateral type, in which even if they are admitted in a short period of time after the attack, they progress too rapidly and develop into the irreversible state due to damage of the brainstem. In these fulminant cases cerebral herniation is not caused by the secondary edema of the brain but by the direct compression of huge hematoma possibly caused by the rupture of the large caliber of the artery.
    This is the first report, at least in our investigation, as the clinicopathological study on these fulminant hemorrhage in the basal ganglia.
    We reviewed 13 autopsy cases of the fulminant type clinically and pathologically, particularly regarding to the midbrain lesion.
    During the past 6 years, a total of 650 cases of cerebrovascular accident have been admitted in our hospital. Of these cases the hypertensive intracerebral hematoma was located laterally in 145 cases, medially (thalamic hemorrhage) in 48 cases and 18 cases of them took the fulminant course in the former (10 autopsy cases) and 11 cases in the latter (autopsy cases). The clinical findings in 13 autopsy cases were presented in Table 1. 11 cases admitted within 3 hours were not indicated for operation at that time, because they already showed the damage of the brainstem. Some types of respiratory disturbance were always observed from the onset of the attack until the death in every case.
    In the neuroradiological examination, carotid angiography was performed in 5 cases which revealed findings of huge hematoma and CT was performed in other 5 cases, which showed huge high density area with marked midline shift and ventricular perforation of hematoma. The sign of downward transtentorial herniation was observed in every case. In the rest of 3 cases, no neuroradiological examination could be done because of the too rapid progression.
    In autopsy findings, all brains were extremely edematous. Schemata of the extension of hemorrhage is presented in Fig. 1. The ventricular perforation of hematoma were observed in all cases of the lateral type, either into the anterior horn, the trigone or the body of the lateral ventricle. In the thalamic hemorrhage, the hematoma extended downward and destructed the hypothalamus and the midbrain directly. (Secondary lesion of the brainstem was presented in Table 1.) In the lateral type, there were 7 cases of secondary midbrain hemorrhage, 4 cases of upper pontine hemorrhage. But we could not find out any damage to the medulla macroscopically. Other lesions of the midbrain which was proposed by Blackwood et al. (Fig. 5) were checked in our cases as Table 1.
    As a conclusion, 1) In this type of the fulminant lateral hemorrhage, cerebral herniation and secondary midbrain lesion were caused by the hematoma itself in a short period of time. 2) In the fulminant thalamic hemorrhage the midbrain were damaged directly by the extension of hemorrhage. 3) In these fulminant types of basal ganglionic hemorrhage, there were secondary hemorrhage, squeezing or destruction of the midbrain in all cases, but could not find any lesion in the medulla. 4) Therefore, we were strongly impressed that the cause of death in these fulminant basal ganglionic hemorrhage could be destruction of the midbrain.
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  • Masahiko Shizuka, Ken Nagata, Kazuta Yunoki, Goro Araki, Masahiro Mizu ...
    1980 Volume 2 Issue 3 Pages 255-261
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Seventy-one cases of hypertensive thalamic hemorrhage were studied with special reference to neurological symptoms and extention of the hematoma on CT.
    The patients were classified into three groups according to CT findings; thirty cases had hematomas localized in the thalamus, twenty had small intraventricular hematomas and twenty-one had large intraventricular hematomas.
    All the patients with intraventricular hematoma showed the neuro-ophthalmological manifestations which were described by Fisher; Mitotic pupils, anisocoria, absence of light reflex and downward ocular deviation. Among them. anisocoria that the pupil on the side of hemorrhage was larger was considered to be a poor prognostic sign.
    Twenty-two patients were able to move their fingers although they were not able to move their shoulder or elbow joint in the early stage, and/or their hemipareses were improved from the distal portion of the extremities in advance of the proximal portion in the stage of recovery. This type of hemiparesis was previously unrecognized in the patients with thalamic hemorrhage and we would propose to call it “thalamic hemiparesis”.
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  • Yasutaka Shimizu, Shotai Kobayashi, Norihisa Furuhashi, Tadashi Kanda, ...
    1980 Volume 2 Issue 3 Pages 262-268
    Published: September 25, 1980
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Although pseudoxanthcma elasticum (PXE) is known to involve multiple systems including the skin, the eye and other several organs, a few cases with the manifestation of central nervous system have been reported. In this report, a case of PXE associated with two episodes of brainstem infarction is described. A 38 year old man suffered from the second attack of brainstem infarction one year after the first attack, which was followed by complete recovery. The patient had loosening of the skin in the neck and the trunk and angioid streaks of the optic fundi. Based on neurologic examination, he was diagnosed as Wallenberg's syndrome. Vertebral angiography revealed occlusion of the right posterior inferior cerebellar artery. The ischemic attacks were presumed to be due to cerebrovascular involvement of PXE which was confirmed by skin biopsy.
    Only 23 cases of PXE with the involvement of central nervous system have been found in Japanese literature, since Kawamura reported the first case in 1957. Following results were obtained by reviewing the 23 cases :
    1. The mean age of the onset of neurological symptoms was 37.9 years (range 14 to 67).
    2. Mortality was low, but functional recovery of the nervous system was poor.
    3. The involvement of central nervous system was for the most part due to ischemic cerebrovascular disease.
    4. In the majority of cases, cerebral angiography revealed the lesion in the internal carotid artery.
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  • 1. Acute experiment
    Kortaro Tanaka
    1980 Volume 2 Issue 3 Pages 269-279
    Published: September 25, 1980
    Released on J-STAGE: January 22, 2010
    JOURNAL FREE ACCESS
    The pathophysiology of cerebral arterial spasms after subarachnoid hemorrhage (SAH) are not well known yet. This study was designed to clarify the role of noradrenergic system in the spasm.
    Effects of fusaric acid (F.A.), a potent inhibitor of dopamine-β-hydroxylase, on pial arterial diameter and regional cerebral blood flow (r-CBF) were investigated in 16 cats with pial arterial spasm after experimental SAH. Cats were anesthetized with α-chloralose (50 mg/kg) and urethane (500 mg/kg). After the administration of alcuronium chloride, respiration was maintained constant throughout the experiment. Parietal craniectomy was performed for the microphotographic observation of pial vessels. r-CBF were measured by the hydrogen clearance method in four regions of the brain. Vasospasms were induced by the cisternal injection of the fresh autogenous blood (group 1 (8 cats)) or the mixture of autogenous blood and CSF incubated for 4 days (group 2 (8 cats)). F.A. (50 mg/kg) was administered intravenously 45 to 50 minutes after the cisternal injection.
    The following results were obtained.
    1) In both groups, the diameters of pial arteries began to decrease significantly (p<0.001-0.005) immediately after the cisternal injection. These arterial spasms continued up to the time of administration of F.A. r-CBF showed. a reduction almost in parallel with the decrease of pial arterial diameters in all regions. The degree of vasospasm and r-CBF reduction in group 2 were more marked than those in group 1.
    2) Intravenous injection of F.A. resulted in a complete disappearance of the spasm (p<0.001) and the r-CBF rapidly restored and even exceeded the control level in spite of a moderate fall of blood pressure. In either group maximum effects of the drug were observed 40 minutes after the administration of the agent.
    The above data suggest the participation of the activity of noradrenergic nerve endings in the pathogenesis of cerebral arterial spasm after SAH.
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  • 2. Chronic experiment
    K. Tanaka, F. Gotoh, Y. Fukuuchi, T. Amano, H. Okayasu
    1980 Volume 2 Issue 3 Pages 280-290
    Published: September 25, 1980
    Released on J-STAGE: January 22, 2010
    JOURNAL FREE ACCESS
    In the earlier communication of the experimental subarachnoid hemorrhage (SAH), one of the authors (Tanaka) reported that the administration of fusaric acid, a potent inhibitor of dopamine-β-hydroxylase, completely relieved the vasospasm in the acute phase of the disease, and that the noradrenergic system seemed to participate in the pathogenesis of the vasospasm. The present study was designed to know whether the same mechanism is operating on the vasospasm in the chronic phase of SAH.
    Twenty cats of either sex, weighing 1.8 to 3.5 Kg, were used, and the experimental SAH was produced by the cisternal injection of fresh autogenous blood. The effect of intravenous injection of fusaric acid (50 mg/kg) on the diameter of pial arteries was evaluated either 3 days (Experiment 1) or 7 days (Experiment 2) after SAH by means of the microphotographic technique through a cranial window. The cerebral blood flow was also measured by the hydrogen clearance method.
    The results of the experiments were as follows;
    Experiment 1 : The pial arteries were dilated significantly (p<0.005-0.01) after the administration of fusaric acid. The degree of the dilatatory response was greater than that in the control group.
    Experiment 2 : The vasospasm, which appeared immediately after SAH, showed a spontaneous gradual relief on the first day, but it recurred 4 days later and continued to show an aggravation until the 7th day when fusaric acid was administered. Immediately after the injection of the agent the vasospasm started to ameliolate and disappeared completely 90 minutes later. Fusaric acid also remarkably improved the cerebral blood flow in spite of the reduction of arterial blood pressure.
    The above data suggest that the noradrenergic system participates in the vasospasm of the chronic phase of SAH.
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  • Hidenori Ohta, Shiro Tominaga, Akifumi Suzuki, Zentaro Ito, Matsutaro ...
    1980 Volume 2 Issue 3 Pages 291-298
    Published: September 25, 1980
    Released on J-STAGE: January 22, 2010
    JOURNAL FREE ACCESS
    There are a few reports which indicate a close relationship between cerebral vasospasm in subarachnoid hemorrhage (SAH) and metabolic impairment of cyclic adenosine 3', 5'-monophosphate (cyclic AMP) in the vascular smooth muscle.
    Ten patients with SAH due to ruptured intracranial aneurysm admitted to our hospital within 5 days after the onset were analyzed concerning the correlations between the concentrations of cyclic AMP in body fluids, and clinical grading of SAH (Hunt & Hess's) and degree of vasospasm on angiograms, respectively.
    Body fluids were collected into syringes moistened with 0.5 M. disodium ethylene-diaminetetraacetate and centrifuged, and supernatants were analized for the concentrations of cyclic AMP applying a competitive protein binding method (Radiochemical Co.). The body fluids consisted of plasmas obtained from the antecubital vein (AVP), the internal jugular bulb (IJP) and the femoral artery, and cerebrospinal fluids. Cerebrospinal fluids were obtained by lumbar puncture or from the tube of continuous ventricular drainage.
    In the early stage of SAH, cyclic AMP concentration in AVP showed an increase over the normal range (8-18 picomolese/ml) in 7 cases. This elevation of cyclic AMP concentration returned to the normal range within 10 days after the onset. In cases without vasospasm, the level of cyclic AMP concentration in AVP had a tendency to take higher level than in cases with vasospasm within 4 days after the onset of SAH.
    The cyclic AMP concentration in CSF showed scattering values in each case, but showed a gradual increase during 2 weeks after the onset in majority of cases.
    IJP had a tendency to take the highest concentration of cyclic AMP among plasmas obtained simultaneously in each patients. This phenomenon might suggest the release or leakage of cyclic AMP from the brain. But, whether the origin of cyclic AMP is the brain tissue or the vascular smooth muscle, has not yet been clarified.
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  • Tadashi Kanda, Hidehito Hayashi, Shotai Kobayashi, Norihisa Furuhashi, ...
    1980 Volume 2 Issue 3 Pages 299-306
    Published: September 25, 1980
    Released on J-STAGE: January 22, 2010
    JOURNAL FREE ACCESS
    Plasma catecholamines were measured in 19 control subjects and 64 patients with acute stroke, admitted within 48 hours of onset. Plasma norepinephrine (pNE) and epinephrine (pE) were determined by the application of high speed liquid chromatograph combined with trihydroxy indole method. Markedly elevated levels of pNE and pE were observed in patients with massive cerebral hemorrhage and cerebral embolism with large hemispheric infarcts. The levels of pNE gradually decreased over the next few days. The mean pNE values for cerebral hemorrhage, cerebral infarction and subarachnoid hemorrhage within 48 hours of onset were 753±116 pg/ml (SEM), 397±65 pg/ml and 630±291 pg/ml, respectively. The mean value for cerebral hemorrhage was significantly higher than that of 292±29 pg/ml for control subjects (p<0.005) and that for cerebral infarction (p<0.01). The mean value of pE for cerebral hemorrhage was also significantly higher than those for cerebral infarction and control subjects.
    The mean pNE levels of 1199±162 pg/ml in 13 died patients (11 cerebral hemorrhage, 2 cerebral infarction) were significantly higher than that of 362±39 pg/ml in 43 survived patients (p<0.001), suggesting that the plasma levels of NE within 48 hours of onset well reflect the prognosis.
    These results indicate that excessive sympathetic nerve discharge occurred concomitantly with adrenomedullary hyperfunction following the onset of stroke.
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