Biomedical subjects

Shuji Arakawa

Publications and source records attributed to Shuji Arakawa.

6 recordsLinked to original sources

PubMed2006

Ischemic thresholds for gray and white matter: a diffusion and perfusion magnetic resonance study.

BACKGROUND AND PURPOSE: Although gray matter (GM) and white matter (WM) have differing neurochemical responses to ischemia in animal models, it is unclear whether this translates into differing thresholds for infarction. We studied this issue in ischemic stroke patients using magnetic resonance (MR) techniques. METHODS: MR studies were performed in patients with acute hemispheric ischemic stroke occurring within 24 hours and at 3 months. Cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT), and apparent diffusion coefficient (ADC) were calculated. After segmentation based on a probabilistic map of GM and WM, tissue-specific diffusion and perfusion thresholds for infarction were established. RESULTS: Twenty-one patients were studied. Infarction thresholds for CBF were significantly higher in GM (median 34.6 mL/100 g per minute, interquartile range 26.0 to 38.8) than in WM (20.8 mL/100 g per minute; interquartile range 18.0 to 25.9; P<0.0001). Thresholds were also significantly higher in GM than WM for CBV (GM: 1.67 mL/100 g; interquartile range 1.39 to 2.17; WM: 1.19 mL/100 g; interquartile range 0.94 to 1.53; P<0.0001), ADC (GM: 918x10(-6) mm2/s; 868 to 975x10(-6); WM: 805x10(-6); 747 to 870x10(-6); P<0.001), and there was a trend toward a shorter MTT in GM (GM 4.94 s, 4.44 to 5.38; WM 5.15, 4.11 to 5.68; P=0.11). CONCLUSIONS: GM has a higher infarction threshold for CBF, CBV, and ADC than WM in patients within 24 hours of ischemic stroke onset. Hence, when assessing patients for potential therapies, tissue-specific rather than whole-brain thresholds may be a more precise measure of predicting the likelihood of infarction.

Aged↗

PubMed2006

Inflammation following stroke.

Stroke is one of the leading causes of mortality and morbidity. The stroke process triggers an inflammatory reaction that may last up to several months. Suppression of inflammation using a variety of drugs reduces infarct volume and improves clinical outcomes in animal models of stroke. This benefit occurs even with the initiation of therapy after 3 hours of onset of stroke, beyond the therapeutic window for thrombolysis with tPA. The use of neuroprotectants to suppress inflammation may widen the therapeutic time window for tPA while lessening its side-effects. Suppression of inflammation may also improve outcomes in animal models of haemorrhagic stroke. To date, clinical trials with anti-inflammatory agents in acute ischaemic stroke have failed to improve clinical outcomes. However, because of the potential for broader applicability across all aspects of stroke, a better understanding of anti-inflammatory mechanisms is important.

Animals↗

PubMed2005

Postischemic gene transfer of interleukin-10 protects against both focal and global brain ischemia.

BACKGROUND: Gene therapy may be a promising approach for treatment of brain ischemia, although the efficiency of postischemic gene therapy is not established. Our goal in this study was to examine the effects of gene transfer of interleukin-10 (IL-10), an antiinflammatory cytokine, after induction of brain ischemia. METHODS AND RESULTS: Brain ischemia was produced by either photochemical occlusion of distal middle cerebral artery for focal ischemia or bilateral carotid occlusion for global ischemia in spontaneously hypertensive rats. Adenoviral vectors encoding human IL-10 (AdIL10) or beta-galactosidase (control) were injected into the lateral ventricle 90 or 60 minutes after focal or global ischemia. Five days after ischemia, IL-10, IL-1beta, or tissue necrosis factor-alpha in the cerebrospinal fluid, infarct volume, infiltrations of leukocytes/macrophages in the infarct area, or hippocampal neuronal damages were determined. The transduced IL-10 was released to the cerebrospinal fluid from the ventricular wall and increased to 7623+/-2965 pg/mL 5 days after AdIL10 transfection. Cerebral blood flow during ischemia was not different between treatments in either focal or global ischemia. Brain infarction of the AdIL10 group was significantly smaller and infiltrations of leukocytes and macrophages were fewer in the IL-10 treatment than control. Hippocampal neurons after global ischemia were more preserved, and the terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling-positive cells were diminished by the IL-10 gene transfer with attenuated IL-1beta and augmented tissue necrosis factor-alpha. CONCLUSIONS: Postischemic gene transfer of IL-10 into the lateral ventricle attenuated brain infarction and hippocampal damages, suggesting the promise for treatment of brain ischemia.

Animals↗

PubMed2003

Topographic distribution of misery perfusion in relation to internal and superficial borderzones.

BACKGROUND AND PURPOSE: Whether misery perfusion (MP) commonly accompanies brain borderzones (BZs) in patients with major cerebral artery occlusion remains unclear. We elucidated topographic patterns of chronic hemodynamic failure in such patients. METHODS: Twenty-four patients with unilateral occlusion or severe stenosis (>75% in diameter) of the internal carotid artery (ICA) or middle cerebral arterial (MCA) trunk with minimal or no infarct underwent PET with (15)O-labeled gas inhalation. Mean cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral metabolic rate of oxygen, oxygen extraction fraction (OEF), and CBV/CBF ratio were determined in the superficial BZs, internal BZ, and MCA territory excluding BZs. Values in BZs were standardized and compared with those in controls. Topographic distributions of regions with OEF greater than that in controls were determined. RESULTS: Values in patients and controls were not significantly different. Topographic distributions included matched perfusion in 10 patients, MP in only the ipsilateral internal BZ in four, MP in both ipsilateral internal and superficial BZs in two, MP in the ipsilateral MCA territory including BZs in one, MP in the ipsilateral MCA territory including BZs and contralateral BZs in two, and MP in the ipsilateral MCA territories including BZs in five. CONCLUSION: Only 25% of the patients had MP localized in affected BZs Although localized MP more frequently accompanied the internal BZ than other regions, no patient had elevated OEF in the superficial BZ alone. These results are inconsistent with clinical observations that 80% of BZ infarctions develop superficially. Thus, hemodynamic mechanisms may not cause most superficial BZ infarctions.

Adult↗

PubMed2003

Ultrasonographically predicting the extent of collateral flow through superficial temporal artery-to-middle cerebral artery anastomosis.

BACKGROUND AND PURPOSE: This study was performed to elucidate whether the extent of bypass flow through superficial temporal artery-to-middle cerebral artery (STA-MCA) anastomosis could be indirectly estimated by measuring the blood flow velocity in the superficial temporal artery (STA) by using duplex ultrasonography. METHODS: We analyzed 29 patients (31 sides) who underwent STA-MCA bypass surgery for occlusive cerebrovascular disease (28 sides) or unclippable cerebral aneurysm that required therapeutic occlusion of the internal carotid artery (three sides). The flow velocities of the STA were measured by using ultrasonography. For patients who underwent the surgery unilaterally, the flow velocity ratios of the operated side to the contralateral side for the individual arteries were calculated. The correlation between these flow velocity parameters and the extent of bypass flow, which was graded based on the findings of cerebral angiography, was investigated. RESULTS: Both the affected STA flow velocity and the STA flow velocity ratio, particularly those in the end diastole, increased in patients with more extensive bypass flow. In patients with extensive, moderate, and poor bypass flow, the end diastolic flow velocities of the operated STA were 27.4 +/- 8.8, 23.0 +/- 7.8, and 13.5 +/- 7.5 cm/s, respectively and the end diastolic flow velocity ratios of the STA were 3.4 +/- 0.8, 2.1 +/- 0.5 and 1.3 +/- 0.4, respectively. The pulsatility index and resistance index of the affected STA were significantly lower in the patients with more extensive bypass flow. The optimal threshold value of the end diastolic flow velocity ratio of STA for the group with extensive bypass flow was 2.75, whereas that for the group with poor bypass flow was 1.60. With the obtained values, the sensitivity and specificity were 87.5% and 93.9% for the group with extensive bypass flow and 95.2% and 95.0% for the group with poor bypass flow, respectively. CONCLUSION: The blood flow velocity in the operated STA seems to be a highly sensitive parameter for predicting the extent of bypass flow in patients undergoing STA-MCA anastomosis.

Angiography, Digital Subtraction↗

PubMed2003

[Shrinkage of carotid plaque in a patient with transient ischemic attack].

A 65-year-old man visited to our hospital, because he felt dull pain on the right side of the neck and had transient weakness of the left hand repeatedly. Carotid ultrasonography revealed a large plaque with severe stenosis and ulceration at the bifurcation of right common carotid artery. The plaque was mostly hypoechoic and only the basal part was hyperechoic. Magnetic resonance (MR) study showed multiple high-intensity spots in superficial borderzone area of the right cerebral hemisphere on fluid attenuated inversion recovery images, although diffusion-weighted images revealed no abnormality. Intracranial stenotic lesion was not detected by MR angiography. We diagnosed transient ischemic attacks due to right carotid artery stenosis. Nine days after the symptom onset, he showed no signs of cerebral ischemic attacks and seven days later he began taking aspirin and remained stable. Three months later, carotid ultrasonography showed marked shrinkage of the carotid plaque, of which hypoechoic part virtually disappeared. Release of the atheroma gruel and/or intraplaque hemorrhage due to plaque rupture might lead to dramatic change of the carotid plaque.

Aged↗