The Authors evaluated the effects of high-dose administration of 25% albumin solution on the vasospastic basilar artery and rCBF in adult mongrel cats. A comparative analysis was made based upon the experiments done in the following 3 groups; Group I : Vasospasm was induced by infusion of hemolysate solution, and simultaneously, physiological saline (12 ml/kg) was administered intravenously in 2 hours. Group II : Vasospasm was induced by the same method as Group I, and simultaneously, 3 g/kg (12 ml/kg) of 25% human albumin solution was administered intravenously in 2 hours. Group III : Without inducing vasospasm, 25% human albumin solution was administered exactly the same way as in group II. General hemodynamic state, caliber of the basilar artery and rCBF in the thalamus were measured.
In Group I, the basilar artery constricted throught its length following the infusion of hemolysate solution (Fig. 1) resulting in a decrease in rCBF in the thalamus (Fig. 2). During this period, no significant change was observed in general hemodynamic state (Fig. 3-6). In Group II, the basilar artery constricted to the same extent as that in Group I. However, despite the decrease in the caliber of the artery, rCBF in the thalamus significantly increased (Fig. 2). During this period, marked increase in cardiac output, increase in the central venous pressure, marked decrease in Hct and moderate increase in the mean systemic blood pressure were observed (Fig. 3-6). Group III showed mild vasodilation and significantly higher degree of increase in rCBF than the increase in Group II. (Fig. 2) Hemodynamic state was similar to that of Group II. (Fig. 3-6)
The result indicates that : 1) High-dose albumin administration had no vasodilating effects on the spastic basilar artery; 2) Despite the decrease in the caliber of the cerebral blood vessel caused by vasospasm, high-dose albumin administration increased rCBF; 3) High-dose albumin administration produced a marked hyperhemodynamic state.
As the cause of increase in rCBF following administration of human albumin under the condition of the vasospasm, following three mechanisms are being assumed since albumin was proved to have no influence on the caliber of the large artery which is in the state of vasospasm : 1) increase in flow through collateral vessels 2) increased blood flow through the spastic vessel caused by decreased viscosity of the blood. 3) mild increase in blood pressure.

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Effect of lowering of blood pressure on acutely-induced cerebral ischemia was studied using spontaneously hypertensive rats (SHR). Cerebral ischemia was produced by bilateral common carotid artery ligation (BLCL). Reserpine was administered intraperitoneally for antihypertensive treatment after producing cerebral ischemia. Blood pressure was moniterd and regional blood flow (r-CBF) in the occipital deep brain was measured periodically. Cerebral metabolites (ATP, lactate, c-AMP) and brain water content were also measured 3 hr after the BLCL. They were determined in the frontal and the occipital brain of each hemisphere, because the experimental cerebral ischemia induced by BLCL was severe in the frontal region and was mild in the occipital.
There was a tendency of a decrease in r-CBF by the lowering of blood pressure. Also it was shown that r-CBF had positive correlation to the blood pressure at 3 hr after BLCL. Brain ATP was remarkably decreased in the frontal and the occipital region and brain lactate was markedly accumulated in both regions. c-AMP was not changed remarkably. The ATP levels in the occipital region were reduced in the antihypertensive treated group compared to those in the untreated group. The lactate levels in the occipital region were increased in the treated group compared to those in the untreated group. There was no differences in the c-AMP levels between the treated and the untreated group in the frontal and the occipital regions. The ATP levels in the occipital had positive correlation to the blood pressure at 3 hr after BLCL. The lactate levels in the occipital had negative correlation to the blood pressure, while the c-AMP levels had no correlation to the blood pressure. Brain water content in the frontal and the occipital regions in the treated group was higher than that in the untreated. The brain water content had negative correlation to the blood pressure at 3 hr after BLCL in the frontal and the occipital areas.
It is shown that lowering of blood pressure in cerebral ischemia in the acute stage results in reduction of r-CBF and aggravates cerebral metabolism and brain edema. Also the effect of lowering of blood pressure is more prominent in the occipital region. Therefore hypertension in the acute stage of ischemia should be carefully managed.

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The pathogenesis of the dural arteriovenous malformation in the posterior fossa has not yet come to an agreement, whether it is congenital or acquired. The authors experienced a case of such dural malformation accompanied by multiple cerebral aneurysms. The case was a 76-year-old woman who suffered from sudden severe headache and vomiting, and was diagnosed as subarachnoid hemorrhage with intraventricle rupture by CT scan. Cerebral angiography revealed an anterior communicating aneurysm and a left middle cerebral aneurysm as well as a dural arteriovenous malformation in the posterior fossa. This malformation had the meningeal branches of the left occipital artery as feeding arteries and the left transverse sinus and the sigmoid sinus as draining veins. The malformation of the present case was suggested to be congenital because of its coexistence with multiple cerebral aneurysms on one hand, but to be acquired because of its occasional appearance on an aneurysmal rupture at such advanced age as 76 years, and of the irregularity and stenosis on the sinus wall due to thrombosis, on the other. On the basis of the present case, the authors offer a hypothesis of the pathogenesis of such malformation with additional considerations in literature.

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Of the 298 cases of ruptured intracranial aneurysm experienced at the Shimane Prefectural Central Hospital, there were 18 cases (6.0%) of aneurysms of the distal anterior cerebral artery (DACA). DACA were classified into 3 groups according to the location of the aneurysm, that is, Group A in which the aneurysm is located between the anterior communicating artery and genu of corpus callosum, Group B in which the aneurysm is located in genu of corpus callosum, and Group C in which the aneurysm is located in trunk of corpus callosum, and a comparative review was made of the cases by incidence, clinical features, neuroradiological findings and prognosis.
1) As for the location of DACA, 72% of cases belonged to group B.
2) Clinical grade IV-V at time of admission was 0% for Group A, 31% for Group B, and 100% for Group C.
3) Disturbance of consciousness was 0% for Group A, 62% for Group B, and 100% for group C, while motor disturbance was 0% for Group A, 46% for Group B, and 67% for Group C.
4) The level of subarachnoid hemorrhage evaluated by computerized tomography showed no difference among the three groups, but in the cases complicated with intracerebral hematoma, the level was 0% for Group A, 46% for Group B and 100% for group C.
5) The prognosis showed no difference among the three groups for the non-operated group, being poor in all groups. For the operated group, the prognosis of group C could not be said to be favorable when compared to Group A and B.
In DACA, the more distal the location of the aneurysm, the higher was the complication rate of intracerebral hematoma and the greater was the tendency for the clinical features and prognosis to become poorer.

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The effects of hematocrit (Ht) on the size of infarction and functional outcome of thrombotic internal carotid artery (ICA) occlusion with antegrade or retrograde collateral circuration were studied. According to the angiographic findings of the collaterals, the subjects were devided into the two groups, one the antegrade group (Group A : N=31), in whom the collateral blood flow was circulating in an antegrade manner through the circle of Willis, and the other the retrograde group (group R : N=36), in whom the collateral blood flow was circulating in a retrograde manner through the branches of external carotid artery and/or leptomeningeal anastomosis. The size of infarction was determined from CT on the chronic phase of infarction and calculated from following formula : Area of maximum low density/Area of maximum hemisphere on CT. Functional outcome was graded upon the ability of walking.
In Group A, there was no significant correlation between Ht and size of infarction (r=0.19) and no significant correlation between Ht at functional outcome. On the otherhand in Group R, a significant correlation existed between Ht and size of infarction (r=0.41), p<0.05), and functional outcome of high Ht (Ht≥45%) group was poorer than low Ht (Ht<45%) group.
The results of the present study suggest that Ht may give more important effects on the prognosis of ICA occlusion with retrograde collaterals than that with antegrade collaterals. In the retrograde collaterals, the blood flow has to go through the resistance vessels twice, while once in the antergrade collaterals. Moreover, the retrograde collaterals are generally longer in distance compared to the antegrade collaterals. Therefore, the flow velocity in the retrograde collaterals is likely to be slower than in the antegrade collaterals. The difference in flow velocity (shear rate) may contribute to the effects of Ht on the prognosis of ICA occlusion with retrograde collaterals.

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A clinical analysis was made on seven patients of cerebral infarction localized in the territory of anterior cerebral artery (ACA). The incidence was 0.55% of whole 1283 cases of cerebral infarction. The pathogenesis of cerebral infarction of ACA territory was thought to be mainly due to the intracranial arteriosclerotic changes rather than the embolic mechanisms. The characteristics of clinical symptoms were hemiparesis with crural predominance, psychiatric symptoms and muteness at onset. Neurological recoveries were good in these patients. Two cases revealed disconnexion syndrome.
In two cases local cerebral blood flow measurements were done by use of stable Xenon and CT scanner, and local oligemia was noted not only in the ACA territory but also in the territory of the ipsilateral middle cerebral artery. From this evidence it was suggested that appeared symptoms in the acute stage were thought to be modified by such mechanism as intracranial redistribution of local cerebral blood flow.

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A model of brain stem ischemia has been developed in the dog by occluding the perforators of the posterior cerebral arteries bilaterally as far as the junctions with the posterior communicating arteries. The animals survived for 7 days with severe consciousness disturbance, tetraparesis, and oculomotor palsy. In acute models, which were sacrificed immediately after occlusion, carbon defects in the brain slices or avascular areas on microangiogram were mainly located in the midbrain, but also extended to the posterior portion of the thalamus rostrally and to the upper pons caudally. A wedge-shaped filling defect was seen on the coronal sections, its base being ventral and its apex pointing to the fourth ventricle. The anemic or partly hemorrhagic infarction was constantly found in chronic models which were kept alive for 7 days and was confirmed to correspond to the avascular areas mentioned above. Using this model, regional cerebral blood flow (rCBF), brain stem auditory evoked potential (BAEP), and electroencephalography (EEG) were measured until 6 hours after vascular occlusion.
Responses of rCBF to perforator occlusion was remarkable. rCBF in the ischemic region decreased from 52.5 ± 13.3 to 8.4 ± 2.5 m1/100 g/min 6 hours after occlusion. rCBF in the surrounding area of the ischemia was about 20 m1/100 g/min, compared with about 58 m1/100 g/min as control value. These results appeared to define the critical flow for infarction in the brain stem. When r-CBF fell below about 13 m1/100 g/min, local infarction resulted.
There was no changes in BAEPs in 8 out of 11 animals. The lesion in the midbrain of this model is not detected by BAEP and the accompanying events with the ischemia such as edema have little effects on the BAEP within 6 hours after occlusion.
In EEG, low voltage fast activity appeared in 7 out of 9 animals which were semicomatose state. This finding is also reported in clinical cases of brain stem strokes and is known as so-called β-coma. The ischemic lesion in the restricted midbrain tegmentum containing reticular formation is correlated with the appearance of desynchronization.

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Ring form contrast enhancement of CT scans are frequently observed in the cases of hypertensive cerebral hemorrhage in subacute stage.
A mechanism of the appearance of ring enhancement was investigated by multiparameter analysis of local cerebral circulation in ten patients, including one case with thalamic hemorrhage and nine with putaminal hemorrhage. Mean age of the cases was 57 years old. The size of hematoma observed in CT scans was moderate in all cases. hemodynamic indices were measured 2-96 days after the onset. The instrument used was GE CT/T 8800 scanner.
The local cerebral blood flow (L-CBF) was estimated by the inhalation of high concentration (65%) of nonradioactive Xenon. And local mean transit time was measured by dynamic CT scans after intravenous bolus injection of Iodine. The width value calculated from the time concentration curve was used as an index of mean transit time. The map of local cerebral blood volume (L-CBV) index was prepared by multiplying L-CBF map by width map in each pixels.
The degrees of brain edema, contrast effects, and local vascular bed volume in each maps were estimated as minor; 1, moderate; 2 and severe; 3 grades. The maps were evaluated by those multiple parameters, and following results were obtained. : 1) Brain edema tended to increased until around 20 days after the onset and gradually decreased thereafter. 2) Contrast ring enhancement showed two peaks around 20 and 40 days after the onset. 3) The local vascular bed volume of perihematoma was increased around 40 days after the onset.
1) Ring form contrast effect in subacute stage of hypertensive cerebral hemorrhage was biphasic, showing early and late enhancement. 2) The early contrast enhancement was related to extravasation of contrast medium, which coincided with deterioration of brain edema. And 3) the late contrast enhancement was closely related to an increase of local vascular bed volume.
Assessment by simultaneous use of CT, nonradioactive Xenon, and Iodine enables more detailed in vivo evaluation of the pathophysiology of hypertensive cerebral hemorrhage.

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The underlying mechanisms that lead to brain edema following ischemic insult have been subject to much debate.
In the first study, experimental cerebral infarction was produced in 25 dogs by injecting 1 or 2 silicon rubber cylinders through the cervical internal carotid artery. The animals were sacrificed 24 hours after embolization. Freezefracture studies were conducted on the plasma membrane of the capillary endothelium from 15 control and 25 ischemic dogs. No definite findings of tight junction opening were made in the ischemic preparations. Pinocytotic vesicles were seen as concave area on the protoplasmic face (PF) of the plasma membrane and as protrusions on the exoplasmic face (EF). The average pinocytotic vesicle count per square micron was increased in ischemic animals. On the luminal side, it reached 22.0 ± 1.2 sq μ in the 50 PF samples and 29.5 ± 1.31 sq p in the 50 EF samples in the experimental preparations, as compared to 7.2± 0.5 sq μ in the 50 PF samples and 9.0 ± 0.6 sq μ in the 50 EF samples in normal cortex. The average area of the vesicles was also enlarged in experimental animals : 4, 990 ± 798 sq nm in the 50 PF samples and 4, 762± 878 sq nm in the 50 EF samples, as compared to 3, 765 ± 570 sq nm in the 50 PF samples and 3, 404 ± 573 sq nm in the 50 EF samples in normal cortex (p>0.01). These results indicate that transcellular transportation by pinocytotic vesicles plays an important role in the increase of capillary permeability observed in an ischemic model.
In the second study, ischemic cerebral edema was produced in 10 rats by means of transcarotid embolization which have been previously immunized by horseradish perioxidase (HRP). The animals were sacrificed 24 hours after embolization. Immnuohistochemical technique was used to observe the location of anti HRP antibodies. Leakage of anti-HRP antibodies from venules and capillaries in the ischemic lesion was clearly observed. Uptakes of anti-HRP antibodies in the neurons and glial cells were also observed. Anti-HRP anti-boddies migrated along the nerve fibers in the white matter and reached the subependymal layer of the lateral ventricle. The drainage sites of anti-HRP antibodies in the brain were the site being devoid of the blood-brain barrier, that is, the subfornical organ at the root of the choroid plexus of lateral ventricle, the pineal body at the root of the choroid plexus of third ventricle, also the hypophysis and its vicinity, and the choroid plexus itself.

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A case of cerebral embolism, showing marked capillary blush on the right perforating arteries of the middle cerebral artery (MCA) is reported.
A hypertensive 57-year-old man experienced weakness in his left upper and lower extremities with headache in the early morning. He was admitted to the hospital. Physical examination revealed atrial fibrillation, slight dysarthria and left hemiparesis with accelerated deep tendon reflexes and positive pathological reflexes. Brain CT revealed a low density area on the right basal ganglia and internal capsule. Cerebral embolism of cardiac origin was diagnosed clinically. Angiography, taken 12 hours after onset, revealed marked capillary blush on the perforating arteries of the MCA. Early venous filling of the thalamostriate vein and the Rosenthal vein in the arterial phase was noted as well as occlusion of the right MCA branches with retrograde filling through the leptomeningeal anastomosis from the anterior and posterior cerebral arteries. These neurological deficits improved gradually 8 days later and angiogram, studied 33 days after onset, was almost normal.
In general, capillary blush and early venous filling are frequently seen after reopening of ischemic regions caused by cerebral embolism. Capillary blush was considered as hyperemia, while early venous filling as hyperperfusion. The former was especially noted over the cortical region, but rare in the deep areas where brain edema was induced by infarction. In this case, however, ischemia was mild. Therefore, it appeared that dilatation of the capillary lumen resulted in hyperemia after reperfusion in addition to hyperperfusion due to vasoparalysis of arterioles.

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For the purpose to elucidate the relationship between cerebrovascular disease (CVD) and disorders of lipid metabolism, we analysed serum lipids, lipoproteins and apoproteins in CVD with a particular emphasis on the chemical composition and the size of LDL. CVD were classified according to the findings on the lesions by brain computed tomography as cerebral bleeding, perforating artery infarction and cortical artery infarction, the results being compared between CVD and the control, and among the CVD subgroups.
The subjects employed in this study were 63, only male patients with CVD, and 38 normal healthy control. The patients were all on rehabilitation program for 2 to 12 months after stroke episode, among whom 27 had cerebral infarction within cortical artery region, 21 infarction within perforating artery region, and 15 cerebral hemorrhage.
They were examined on fasting blood plasma for total cholesterol (TC), triglycerides (TG) by enzymatic methods, lipoproteins of VLDL, LDL and HDL by ultracentrifugation with a use of Lp-42 Ti rotor, and apoproteins of A-I, A-II, B, C-II, C-III and E by single radial immunodiffusion. LDL isolated were stained negatively and viewed under transmission electron microscopy, and their diameters measured on enlarged photographs. When we compared the total CVD with the control, TG and VLDL-c were significantly higher in the CVD than in the control, while HDL-c, apo-A-I and A-II were significantly lower in the CVD than in the control. Apo C-II and E tended to be higher in the CVD but not significant, apo C-III had no difference.
Cholesterol ratio (TC-HDL-c/HDL-c) and LDL-c/HDL-c ratio were significantly higher in CVD, while the ratios of A-I/B and A-II/B were significantly lower in CVD when compared with those of the control.
When we looked into the CVD subgroups, TC, LDL-c, apoB and LDL-apo B were higher in the infarction of cortical artery region than in the control, while they were lower in the cerebral bleeding than in the control, among which statistically significant were the elevation of LDL-c, apoB in cortical infarction group, and the low levels of TC and LDL-apoB in cerebral bleeding group.
Since LDL differed significantly in cholesterol and apoB contents among CVD subgroups, we examined the size of LDL in each group, and found that LDL was significantly larger in the descending order of cortical artery infarction, perforating artery infarction, control, and cerebral bleeding.
We computed by multivarite analysis the contributing factors (s) to determine LDL-size, setting LDL-c as criteion variable and lipoprotein and apoprotein parameters as explenary variables. We gained a multiple regression equation, whose partial regression coefficients were greater in the order of VLDL-c, HDL-c and apo E, indicating that these three factors were the major determinants of LDL-size.
This is in good concrdance with hypertriglyceridemias observed in common with CVD subgroups, and with the fact that serum triglyceride level or triglyceride content in VLDL affects via VLDL-HDL cycle the size of LDL and the level of HDL-c, Yet, the relation between LDL-size and exact mechanism for pathogenesis of arterisclerosis in cerebral arteries remains to be studied.

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Among consecutive 126 cases of ruptured intracranial aneurysms admitted to our clinic, fifteen cases had rebleeding during admission. Three cases died within a week after the second ictus. Twelve cases were operated on. Seven cases were operated on within 24 hours and five cases more than 24 hours after the second bleeding. It seemed that operations as early as possible after the rebleeding would have better clinical results. Thus five out of seven cases operated on earlier had good recoveries, while only one recovered well in later operated five cases.

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