Japanese Journal of Stroke
Online ISSN : 1883-1923
Print ISSN : 0912-0726
ISSN-L : 0912-0726
Volume 17, Issue 3
Displaying 1-14 of 14 articles from this issue
  • Haruko Morota, Makoto Kaieda, Atushi Nagazumi, Akiro Terashi
    1995 Volume 17 Issue 3 Pages 209-217
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    To evaluate the influences of incidental cerebral infarction and white matter lesions on cognitive function in patients with diabetes mellitus, we measured the event related potential (P300), number of incidental cerebral infarctions and T2value of the frontal periventricular white matter using magnetic resonance imaging. The subjects comprised three groups : non-insulin dependent diabetes mellitus (NIDDM) cases without dementia or any history of cerebrovascular disease (the DM group : N =50); NIDDM cases with cerebrovascular disease (the DMCVD group : N =18); and normal controls (the NC group : N =23). The DM group was further subgrouped according to the number of incidental cerebral infarctions, as follows : those with no infarction (incidental cerebral infarction, ICI-0 group), a single infarction (ICI-1 group), and multiple infarctions (ICI-2 group). More foci of incidental cerebral infarctions were observed in the DMCVD group than in the DM group. Increases in the T2value of the white matter and the P300 latency were closely correlated with the number of foci. In the DM group, Hasegawa's dementia scale (HDS) and mini-mental state examinations (MMS) were normal. However, an increased P300 latency suggested impaired cognitive function. These results indicate that the impairment of cognitive function in DM patients was caused not only by diabetic encephalopathy but also by incidental cerebral infarction.
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  • Fumihiko Kashiwagi, Yasuo Katayama, Tatsushi Kamiya, Akiro Terashi
    1995 Volume 17 Issue 3 Pages 218-225
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    The effects of three different kinds of protease inhibitors (PI) were studied in cerebral hypoxia or ischemia using spontaneously hypertensive rats. The agents tested were urinastatin (US), gabexate mesilate (GM) and nafamostat mesilate (NM). We investigated the agents under cerebral hypoxia induced by placing rats in a chamber containing 96% nitrogen and 4% oxygen for 30 min. Cerebral ischemia was produced by bilateral common carotid artery occlusion for 2 hr followed by 30 min reperfusion. In the experiment on hypoxia, the brain water content did not change after the hypoxia. The brain ATP levels in the PI-administered groups were higher and the lactate levels in the PI-treated groups were lower than those in the controls. In the experiment on ischemia, the percentage brain water contents was significantly decreased in the PI-administered groups as compared to the control group. The brain ATP levels in the PI-treated groups were higher than those in the control group. The values of the lactate/pyruvate ratio were significantly decreased compared to the control group. These findings suggest that PI agents might be useful in the treatment of cerebral hypoxia or ischemia.
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  • Tsuyoshi Omae, Setsuro Ibayashi, Kenichiro Fujii, Seizo Sadoshima, Mas ...
    1995 Volume 17 Issue 3 Pages 226-231
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    The aim of this survey was to examine the recent trends in the use of antihypertensive drugs for patients with chronic stroke. We studied the age, stroke subtypes, presence of hypertension, type of antihypertensive drugs and blood pressure levels in out-patients with chronic stroke at Kyushu University Hospital and our six satellite hospitals with 17 specialists for stroke. Among 762 patients with chronic stroke, 563 (73.9%) were diagnosed to be hypertensive, and antihypertensive drugs were given in 405 of the hypertensives (71.9%). The average blood pressure was 144 ± 17/82 ± 11 mmHg in the patients receiving antihypertensive drugs (n=405) and 140 ±17/80 ± 10 mmHg in the patients without drug treatment (n=158). The levels of blood pressure observed in the present study suggested that even in patients with drug treatment, hypertension was adequately controlled. Calcium antagonist (Ca antagonist) was most frequently used (58.4%), followed by angiotensin converting enzyme inhibitor (ACEI, 23.9%), β-adrenergic receptor blocker (β-blocker, 16.0%), and diuretics (5.9%). As regards combinations of drugs, 34.8% of the patients were given Ca antagonist alone, followed by the combination of Ca antagonist and ACEI (10.5%), Ca antagonist and fi-blocker (5.9%), ACEI alone (5.7%), β-blocker alone (5.5%), the combination of Ca antagonist, ACEI and fi-blocker (2.3%) and the combination of Ca antagonist, ACEI and diuretics (2.3%). Ca antagonist was more solely and preferably employed in the older patients. Our study revealed that Ca antagonist is the antihypertensive drug most frequently used by stroke specialists. ACEI and β-blocker are next in terms of preferable use.
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  • Toshiya Fukui, Koujiro Sugita, Yukihiro Hasegawa, Hiroo Ichikawa
    1995 Volume 17 Issue 3 Pages 232-240
    Published: June 25, 1995
    Released on J-STAGE: January 25, 2010
    JOURNAL FREE ACCESS
    Silent cerebral infarction (SCI) is often associated with the evolution of symptomatic ischemic vascular accidents and dementia. However, the longitudinal outcome of SCI is unknown. We conducted a preliminary investigation in an attempt to answer this question. Subjects without neurological abnormalities or any history suggesting vascular accident, and in whom cerebral hyperintensity (CH) was detected by magnetic resonance imaging (MRI), were diagnosed as SCI. Forty-three subjects who visited our department in 1991 with non-specific complaints such as headache or dizziness were diagnosed as SCI and enrolled in the present study. We conducted MRI studies and a series of cognitive examinations over an average period of 23 months in order to follow the clinical course, determine the risk factors, and assess the cognitive status of these subjects. The degree of CH was expressed using the rating scale proposed by Scheltens et al., which allocates points according to the size and number of CHs in the periventricular, white matter, basal ganglia and infratentorial regions. Only CHs larger than 3 mm were considered, since they are more likely to represent actual infarctions rather than enlarged perivascular spaces. Over the course of the study, 5 subjects ceased communicating with our department, 3 refused the second evaluation, 2 did not provide complete data, and one developed a fatal subarachnoid hemorrhage. None of the remaining 32 subjects developed symptomatic cerebral infarction and all continued to satisfy the criteria for a diagnosis of SCI at the time of the second evaluation. Fifteen subjects showed an increased CH score (increase group), while 17 subjects displayed no change or a decreased CH score (non-increase group). Increases were most commonly observed in the posterior half of the brain, especially in the periventricular area. Univariate analysis revealed a significantly higher frequency of antiplatelet agent ingestion and a non-significant but higher frequency of diabetes mellitus in the increase group. Multivariate analysis demonstrated that higher CH scores at the first evaluation, longer follow-up intervals, aging, ST-T changes on ECG as well as the ingestion of antiplatelet agents were factors that coincided with a CH increase. Use of antiplatelet agents did not directly cause an increase in CHs, but these agents were more likely to be prescribed to subjects with a large number of risk factors, resulting in higher CH scores. Cognitive functions were not significantly different between the two groups. However, the increase group exhibited longitudinal deterioration on the Raven Colored Progressive Matrices, while the non-increase group showed no deterioration. The results of our study suggest that (1) SCI does not signify an urgent prodrome of symptomatic infarction or dementia; (2) SCI may increase in the presence of prior SCI and ECG changes, and when subjects are aged and under observation for an extended period of time; and (3) appropriate control of associated risks is mandatory for preventing SCI increases.
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  • Makoto Arimitsu, Masahiro Kurisaka, Tatsuo Mima, Koreaki Mori
    1995 Volume 17 Issue 3 Pages 241-246
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    Pyramidal neurons in the hippocampal CAI sector are especially vulnerable to ischemic insult and reveal morphological cell death at several days after transient forebrain ischemia designated as delayed neuronal death (DND). The mechanism of DND remains unknown, although recent studies have indicated that apoptosis is involved in DND demostrations evidence of DNA ladder formation on agarose gel electrophoresis. We examined the time course of DNA fragmentation in the hippocampus after 5 min forebrain ischemia in the gerbil, using immunohistochemical labeling of DNA 3-OH ends generated by DNA fragmentation. In situ end-labeling by the TUNEL method (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling) showed that DNA fragmentation in the hippocampal CAl sector first appeared at 72 hours after transient ischemia and remained up to 7 days in our observations. Our results were similar to those of a previous report describing the time course of DNA fragmentation with agarose gel electrophoresis (Okamoto et al. BBRC, 1993). The present findings indicate that in situ end-labeling by the TUNEL method is appropriate for detecting DNA fragmentation and suggest that apoprosis is at least partially involved in DND.
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  • Hisaji Kobayashi, Tsutomu Kamo, Toyohiro Matsui, Hiroshi Sugihara, Kim ...
    1995 Volume 17 Issue 3 Pages 247-259
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    Diurnal variations of blood pressure and physical activities were analyzed in patients with cerebrovascular disorders (CVDs). Periodic changes were identified and compared between the patients and normal volunteers. The relationship between blood pressure and periodic patterns of physical activities was evaluated. Blood pressure was recorded by ambulatory blood pressure monitoring, and physical activities were estimated by using acceleration sensors. Frequency analysis based on the maximum entropy method (MEM) and curve fitting by the nonlinear least squares method were applied to assess the diurnal changes in 110 patients with CVDs and 50 normal subjects. While the normal subjects showed a periodic pattern with two basic period lengths of 24 ± 3 hours and 12 ± 3 hours, the CVD patients often displayed deviations from this basic pattern. In addition, different types of CVDs were associated with each different periodic pattern. Among the CVD patients, some cases with cerebral thrombosis in the perforating artery revealed disagreement between the physical activities and blood pressure with respect to the period length and/or the acrophase. This finding could indicate that the diurnal periodic pattern of blood pressure is influenced by the individual nature of the CVD as well as by the physical activity.
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  • Nagato Kuriyama, Yasumasa Yamamoto, Kaiyo Oiwa, Hitoshi Satoi, Kenji N ...
    1995 Volume 17 Issue 3 Pages 260-265
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    The diagnosis of transient ischemic attack (TIA) is based on a history of neurological deficit followed by rapid recovery of normal neurological function. TIA has been attributed to microembolic and hemodynamic phenomena associated with atheromatous plaque deposition in large vessels or cardioembolism. However, some cases of TIA have been recognized with no angiographic abnormalities or cardioembolic sources. The present study was therefore conducted to elucidate further the heterogeneous mechanisms of TIA. Forty-five patients with TIA involving the internal carotid artery (age 63.9 ± 9.9 yr, mean ± SD) were initially enrolled in the study. We performed CT/MRI and cerebral angiography (3 or 4 vessels) in all patients. Cases directly attributable to cardioembolism were eliminated from the study. Those with over 25% stenosis of a large extracranial artery were designated as angiographically abnormal (AGA +), and those with less than 25% stenosis, or with normal findings were diagnosed as AGA (-). A total of 26 patients were classified as AGA (+) and 19 patients as AGA (-). These two patient groups were compared on the basis of their CT/MRI findings, frequency and duration of ischemic attacks, and major risk factors. Small infarctions in the basal ganglion and/or subcortical white matter were found in 9 out of the 26 AGA (+) patients (34.6%), as opposed to 16 out of the 19 patients (84.2%) in the AGA (-) group. The incidence of abnormal CT/MRI findings was significantly different between the two groups (p < 0. 001). The symptoms suggestive of TIA were consistent with large vessel abnormalities in 84.6% of the patients. These findings suggested that microembolic mechanisms probably played a major role in the TIA of the AGA (+) group, whereas ischemia at the level of the cerebral perforating arteries was a more important factor in the AGA (-) group. The frequency and duration of ischemic attacks did not differe between the AGA (+) and AGA (-) groups. Similarly, the major risk factors did not differ between the two groups. Seven patients suffered a complete cerebral infarction during the 5-year followup period, but these patients were significantly older (p <0.05) than those who were free of infarction.
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  • Masanori Fujita, Yuji Morimoto, Ryoji Nishioka, Shinji Nakajima, Haruo ...
    1995 Volume 17 Issue 3 Pages 266-270
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    Bilateral medial medullary infarction is relatively rare. Most of the reported cases have demonstrated a poor prognosis because of medullary respiratory failure. We describe the case of a patient who recovered from a bilateral medial medullary infarction limited to the upper portion of the medulla. The patient was a 63-year-old man with mild hypertension who developed temporary respiratory failure, quadriparesis, and disturbance of deep sensation. Magnetic resonance imaging revealed a small infarct bilaterally in the upper third of the medial territory of the medulla oblongata. A magnetic resonance angiogram demonstrated segmental stenosis in the lower basilar artery and atheroscierotic stenosis of the hypoplastic right vertebral artery. Most of his symptoms subsided within 3 months after the onset of the infarction. Our findings suggest that the prognosis of bilateral medial medullary infarct is not necessarily poor.
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  • Satoru Komatsumoto, Masaharu Nara
    1995 Volume 17 Issue 3 Pages 271-277
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    Endothelin-1 (ET-) is a potent and long-lasting vasconstricting peptide that causes vasopasm. However, no systematic evaluation of ET has evere been attempted during the acute stage of cerebrovascular disease (CVD). The present study focuses on the evaluation of changes in ET in the plasma and cerebrospinal fluid (CSF) over 2 weeks following an episode of CVD. Patients with CVD were divided into two groups, 8 with occlusive CVD and 9 with hemorrhagic CVD. The ET levels were assessed from measurements of both the plasma and CSF concentrations of ET. We estimated the immunoreactive ET1 by radioimmunoassay in both the plasma and CSF. In occlusive CVD, the plasma level of Et was 4.75± 1.00 pg/ml on day 1, followed by a gradual decrease to 3.86 ± 1.34 pg/ml on day 3, 3.17± 1.34 pg/ml on day 5 and 3.05 ± 1.05 pg/ml on day 7. The level of ET on day 14 had declined to 2.52 ± 1.5 pg/ml. The levels of ET on both day 1 (p <0.025) and day 3 (p <0.025) were significantly higher, when compared with that on day 14. Hemorrhagic CVD also demonstrated higher levels of ET during the acute stage, with 8.7 ± 7.2 pg/ml on day 1 and 5.84 ± 4.65 pg/ml on day 3, followed by decrease on days 5, 7 and 14 to 4.42 ± 1.94, 2.84 ± 1.11 and 2.50 ± 1.26 pg/ml, respectively. The values from day 1 to day 5 were significantly higher than that on day 14 (p <0.025 on both days 1 and 3; p <0.05 on day 5). In addition, 4 patients who underwent repeated measurements of the ET in their CSF showed a decrease from a value of 28.9 ± 5.2 pg/ml on day 1 to 22.0 ± 6/3 pg/ml after 2 weeks. Elevated concentrations of ET-1 in both the plasma and CSF were thus clarified in the present study. In conclusion, the time course of induction of ET production is consistent with the temporal sequence of derangement of the cerebral hemodynamics following CVD, further supporting the hypothesis that ET may also be closely related to the function of the blood-brain and blood-CSF barrier.
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  • Hiroaki Takahashi, Katsumi Watanabe, Hiroyuki Kuki, Ken-ichi Tamura, H ...
    1995 Volume 17 Issue 3 Pages 278-283
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    We determined the serum concentrations of soluble forms of the adhesion molecules, ICAM-1, VCAM-1, and E-selectin in acute cerebral thrombosis. The subjects comprised 29 post-stroke patients (19 cases of small-vessel disease, SVD; and 10 of large-vessel disease, LVD) and 19 controls. ICAM-1, VCAM-1, and E-selectin were measured by the single step ELISA method (R & D System Europe, UK) in the acute (within 3 days after an initial stroke), subacute (7-10 days), and chronic (28-35 days) phases. We found that the serum ICAM-1 concentration was significantly higher in the chronic phase of LVD (397 ± 123 ng/ml, p < 0.05) than in the controls (277 ± 81 ng/ml) and in the acute phase of LVD (283 ± 71 ng/ml). The serum VCAM-1 concentration was significantly higher in the subacute (SVD, 933 ± 294 ng/ml; LVD, 1223 ± 433 ng/ml) and chronic (SVD, 805 ± 224 ng/ml; LVD, 1030 ± 256 ng/ml) phases of SVD and LVD than in the controls (584 ± 79 ng/ml), the acute phase of SVD (629 ± 157 ng/ml), and LVD (712 ± 203 ng/ml). The serum E-selectin concentration was significantly higher in the acute and chronic phases of SVD and in the chronic phase of LVD than in the controls, but there was no significant differences between the phases. These findings suggest that adhesion molecules may play important roles in the pathophysiology of the acute and chronic phases of cerebral thrombosis.
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  • Yoshio Izumi, Elisabeth Pinard, Simon Roussel, Jacques Seylaz, Yukito ...
    1995 Volume 17 Issue 3 Pages 284-291
    Published: June 25, 1995
    Released on J-STAGE: January 25, 2010
    JOURNAL FREE ACCESS
    The endogenous cation, magnesium, is a natural competitor of calcium and inhibits calcium entry into cells via the voltage-dependent Ca channel and the NMDA receptor-associated channel. We reported previously that systemic administration of MgC12 is neuroprotective, and reduces the ischemic damage in middle cerebral artery (MCA) occluded rats. However, the induced hyperglycemia appeared to affect the infarct undesirably. We therefore investigated the effect of low-dose magnesium in normoglycemia so as to minimize any systemic influence of magnesium. The MCA was occluded under halothane anesthesia employing the method of Tamura et al. Body temperature was regulated during the whole surgical procedure. At 48 hours after the MCA occlusion, TTC was infused via the heart to stain the healthy tissue. Systemic variables and body temperature were measured in an additional group of rats (N = 11). The magnesium-treated group (N = 13) was given MgCl2 (0. 2 mmol/kg) just after the MCA occlusion and again at 1. 5 and 3 hours later. The control group (N = 13) was given saline instead of MgC12. The MgCl2 treatment did not alter any systemic parameter including the blood glucose content, as compared to those of the control group. The total volume of ischemic damage was smaller in the magnesium-treated group (65 ± 9 mm3) than in the control group (111 ± 12 mm3). MgCl2significantly reduced the volume of cortical infarction by 34%, but had no significant effect on the striatum. We conclude that low-dose magnesium can exert a beneficial effect on focal cerebral ischemia without any systemic influence.
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  • Hirokazu Bokura, Shotai Kobayashi, Shuhei Yamaguchi, Kazunori Okada, S ...
    1995 Volume 17 Issue 3 Pages 292-297
    Published: June 25, 1995
    Released on J-STAGE: January 25, 2010
    JOURNAL FREE ACCESS
    We studied the relationship between asymptomatic ischemic lesions on magnetic resonance imaging (MRI) and risk factors for stroke in 460 asymptomatic subjects. Focal lesions were classified into two groups according to their size. Periventricular hyperintensity (PVH) was graded from 0 to 3. We also evaluated equivocal deep white matter hyperintensity as a confluent lesion that was separate from PVH. The incidence of focal lesions below 2 mm in diameter (we regard them as étatcriblé) was 5.7%, and that of lesions over 2 mm was 16.1%. Grade 2 PVH was observed in 12.6% and grade 3 PVH in 2.2%. The prevalence rate of confluent lesions was 8.7%. The age of the group which had white matter lesions was significantly higher than that of the group without lesions. Hypertension was the greatest risk factor for the occurrence of focal lesions, PVH, and confluent lesions. Diabetes mellitus was a significant risk factor only for focal lesions. Other risk factors did not display any relations to white matter abnormalities.
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  • Hideyuki Kita, Katsuji Shima, Iwao Akiyama, Hiroo Chigasaki
    1995 Volume 17 Issue 3 Pages 298-305
    Published: June 25, 1995
    Released on J-STAGE: September 16, 2009
    JOURNAL FREE ACCESS
    It has been reported that abnormalities of systemic coagulation, such as platelet hyperaggregation and hypercoagulation, occur together with vasospasm after aneurysmal subarachnoid hemorrhage (SAH). We evaluated the hemorheological effects of ticlopidine as a means of preventing symptomatic vasospasm. Experimentally, SAH was induced by a single injection of 5 ml of autologous arterial blood into the cisterna magna of hybrid dogs weighing 10-15 kg. The hemorhelogical effects of ticlopidine (100 mg/kg) were determined by examining the platelet aggregation (optical density method), fibrinogen, fibrin/fibrinogen degradation products (FDP), streptokinase-euglobulin lysis time (SK-ELT) and morphological changes in red blood cells and platelets from pre-SAH to the 5th day after SAH. Clinically, we investigated 139 aneurysmal patients admitted within 72 hours after SAH to assess the efficacy of ticlopidine for preventing symptomatic vasospasm. Hemorheological analysis of vasospasm was performed by examining the platelet aggregation using a screen filtration pressure method, platelet counts, fibrinogen, FDP and SK-ELT. In this series, 102 patients (group A) were treated with a regimen that included ticlopidine, and 50 of them were operated on at the early stage; 37 patients (group B) were treated without ticlopidine. Experimental studies demonstrated that ticlopidine reduced platelet hyperaggregation and morphological changes in red blood cells and platelets after SAH. The incidence of symptomatic vasospasm was 33% in group A, 30% in the subgroup of group A that underwent early-stage surgery, and 65% in group B. Fatal vasospasm was significantly less frequent in group A (6%) than in group B (32%). Surviving patients in groups A and B displayed normal or slightly high levels of platelet aggregation and low FDP, but patients who had fatal vasospasm showed low levels of platelet aggregation and high FDP, as observed in the intravascular coagulation syndrome. These results suggest that ciclopidine may be useful for the prevention of symptomatic vasospasm, increasing the proportion of good outcomes. Typical abnormalities of blood coagulation appearing in the acute stage of SAH are closely related to fatal vasospasm and can be employed as an important indicator of prognosis.
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  • Hiroyuki Nozaki, Kortaro Tanaka, Toshitaka Shirai, Eiichiro Nagata, Ya ...
    1995 Volume 17 Issue 3 Pages 306-314
    Published: June 25, 1995
    Released on J-STAGE: January 25, 2010
    JOURNAL FREE ACCESS
    In order to evaluate the influence of cerebral ischemia on the intracellular channels of calcium-induced calcium release (CICR), the alterations of ryanodine receptor binding sites and local cerebral blood flow (LCBF) were examined at 6 hours after occlusion of the right common carotid artery in the gerbil brain. The autoradiographic method developed in our laboratory enabled us to measure both parameters within the same brain. Animals attaining ischemic scores of more than 5, as assessed at 1 hour after the occlusion, were used. LCBF was measured at 6 hours after the occlusion by the [14C] iodoantipyrine method. The ryanodine receptor binding sites were evaluated in vitro using [3H] ryanodine as a specific ligand. LCBF was significantly reduced in most of the cerebral regions on the occluded side. In contrast, a significant reduction in ryanodine binding sites was noted only in the hippocampus CAl on the occluded side. On the other hand, the ryanodine receptor immunoreactivity which was examined with a specific antibody against ryanodine receptor protein, did not reveal any differences between the ischemia and sham groups on both sides, suggesting that the ryanodine receptors may not underego significant morphological degradation. These findings indicate that the suppression of ryanodine binding in the hippocampus CAl may be attributable to a regionally specific perturbation of CICR. Such perturbation may be closely associated with the pathophysiological mechanism of selective ischemic vulnerability of this region.
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