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Biomedical subjects

Y Katayama

Publications and source records attributed to Y Katayama.

At least 37 records · Page 2Linked to original sources
PubMed2005

[Extraanatomical bypass grafting for a coarctation of the aorta in the adult: report of a case].

A 49-year-old man with a successful bypass grafting for coarctation of the aorta is presented. He has been suffering from hypertension since his 30s. Angiography and magnetic resonance imaging (MRI) revealed the stenosis of distal aortic arch and developed collateral circulation. After left thoracotomy, bypass grafting using a 16 mm woven Dacron graft was placed between the left subclavian artery and the descending aorta. He had a satisfactory postoperative course with no residual pressure gradient. We recommend this procedure to be a safe and minimally invasive technique that can avoid injury to the collateral.

Aortic Coarctation↗
PubMed2004

A new cytochemical method for ultrastructural localization of Co2+ in rat hippocampal CA1 pyramidal neurons in vitro.

This paper describes new cytochemical method for the ultrastructural localization of Co(2+) following blockade of synaptic transmission. In the CA1 region of rat hippocampal slices, electrical stimulation of the Schaffer collaterals elicited field excitatory postsynaptic potentials (fEPSPs). The fEPSPs were completely blocked within 2 min after the addition of Co(2+) (2 mM). The slice was then fixed and precipitated Co(2+) was examined by means of a solution containing 2.5% glutaraldehyde and 10 mM K(3)[Fe(3+)(CN)(6)] in 90 mM NaCl. Electron spectroscopic imaging confirmed Co in the precipitate. The precipitates were found as clusters on the membranes of the fine apical dendrites and their spine heads of CA1 pyramidal neurons. No clustered precipitate was found when slices were treated: (1) without Co(2+); (2) after recovery from the Co(2+)-induced blockade of fEPSPs; (3) without electrical stimulation of the Schaffer collaterals; and (4) with dl-2-amino-5-phosphonopentanoate and 6-cyano-7-nitroquinoxaline-2,3-dione. After administrating glutamate (5 mM) in the presence of tetrodotoxin (1 microM) and Co(2+), precipitates were found on dendritic membranes and spine heads. These results indicate that the Schaffer collaterals stimulation induces the binding of Co(2+) on CA1 pyramidal neuron membrane.

2-Amino-5-phosphonovalerate↗
PubMed2004

Response durations encode nociceptive stimulus intensity in the rat medial prefrontal cortex.

We examined whether the medial prefrontal cortex (mPFC) encodes nociceptive stimulus intensity by applying mechanical pressure stimulation, for 2 s at 50, 100, or 300 g constant force (gf) to the tails of urethane-anesthetized rats. In a total of 1208 neurons sampled, 242 (20.0%) were responsive to mechanical stimuli. One hundred thirteen of the 242 (46.7%) were mechanical high threshold neurons (nociceptive specific neurons, NS; threshold >or=100 gf), and 35 (14.5%) exhibited a graded increase in excitator responses to a stepwise increase in stimulus intensity (wide dynamic range-like neurons, WDR-L). These 148 response discharges persisted during stimulation followed by post-stimulus discharges. The nociceptive response duration of NS neurons, but not discharge frequency, was reduced dose-dependently by intraventricular injection of morphine (0.3, and 30 microg/3 microl). Different doses of morphine may set the stimulus intensity at relatively different brain activity levels. Thus, the NS neurons used the response duration as a sensory transduction code. In WDR-L neurons, the response duration, but not always the firing frequency, was linearly related to stimulus intensity. The WDR-L neurons in the mPFC encoded stimulus intensity with response duration, although the coding method is not likely to be the same as that of sensory discriminating WDR cells in the primary somatosensory cortex. Both types of mPFC neurons encode nociceptive (absolute or relative) stimulus intensity and transform the information into the temporal duration of the next stage of pain-related modulation in animal behavior.

Action Potentials↗
PubMed2004

Midbrain hypometabolism as early diagnostic sign for progressive supranuclear palsy.

OBJECTIVE: Progressive supranuclear palsy (PSP) is often misdiagnosed in early phase. The purpose of this study is to investigate the feature of [(18)F]fluoro-2-deoxy-d-glucose (FDG) positron emission tomography images for the early diagnosis of PSP. METHODS: We studied 15 patients with PSP and 16 normal subjects. Using SPM99 and analysis of covariance to eliminate the effect of aging, the differences between PSP and normals were displayed as a statistical map. In the PSP, we also investigated the correlation with duration and with the subscores of Unified Parkinson's Disease Rating Scale. RESULTS: The glucose metabolism of midbrain was significantly lower in PSP than in normals. However, correlation was not found between the metabolism of midbrain and clinical deterioration. CONCLUSIONS: The statistical map clearly demonstrated the hypometabolism of midbrain in PSP, which is independent of the clinical deterioration. The hypometabolism of midbrain is one of the most promising sign for early diagnosis of PSP.

Adult↗
PubMed2004

Sympathetic skin response in patients with spinal cord injury.

PURPOSE: To assess the effectiveness of sympathetic skin response in evaluating peripheral sympathetic nerve activity of patients with spinal cord injury, and to report on the basic properties of sympathetic skin response. METHODS: Sympathetic skin response evoked by electrical stimulation was recorded from the palms and soles of healthy volunteers and patients with spinal cord injury. RESULTS: Sympathetic skin response was recorded in 17 healthy volunteers and 14 patients with spinal cord injury. Of the 4 waveforms, the shortest latency was obtained from the palm; the sympathetic skin response was 1.2 to 1.4 ms at all stimulated sites, 1.9 to 2.0 ms at the sole, with a difference of about 0.6 ms between the palm and the sole. None of the patients with spinal cord injury responded at either the upper or lower limbs. In patients with a thoracic cord injury, some responded at the upper limbs but none at the lower limbs; some responded at neither upper nor the lower limbs; and some responded at both upper and lower limbs. The conducting pathway of sympathetic skin response in the spinal cord for the upper limbs descends to the upper thoracic cord (T4-6), and the conducting pathway for the lower limbs departs from the spinal cord at the lower thoracic cord (T9-10). CONCLUSION: It appears that sympathetic skin response should be used for the evaluation and morbid investigation of the functional abnormalities of the sympathetic nervous system in patients with spinal cord lesions such as spinal cord injuries, cervical spondylosis, and spinal canal stenosis.

Adolescent↗
PubMed2004

[Intraaortic balloon pumping in patients undergoing coronary artery bypass grafting].

UNLABELLED: Beneficial effect of preoperative intraaortic balloon pumping (IABP) treatment in high-risk patients who had open heart surgery have been demonstrated. The purpose of this study is to determine the impact of preoperative IABP use on survival in high-risk patients undergoing coronary artery bypass grafting (CABG). METHODS: Two hundred seventy-seven consecutive patients having CABG at our institution were reviewed. Patients having an IABP were identified retrospectively and grouped into one of 3 groups as follows. Group A (n = 14): preoperative IABP for high-risk urgent or elective cases. Group B (n = 26): preoperative IABP for emergency cases. Group C (n = 6): unplanned intraoperative or postoperative IABP. RESULTS: Forty-six patients had an IABP (16.6% of total). Parsonnet score in group B was significantly higher (p < 0.05). Length of operation for group C was significantly longer (p < 0.05). Overall hospital mortality in the total group of 277 cases was 4.2%. Hospital mortality was 7.1% in group A, 7.7% in group B, and 50% in group C. Hospital mortality in group C was significantly higher (p < 0.01). CONCLUSIONS: The beneficial effect of preoperative treatment with IABP in high-risk patients undergoing CABG was confirmed. This approach resulted in a significantly lower hospital mortality.

Aged↗
PubMed2004

[Re-coronary artery bypass grafting necessitated by flow insufficiency of right internal thoracic artery; report of a case].

A 75-year-old woman required re-coronary artery bypass grafting due to flow insufficiency of the right internal thoracic artery (RITA). After the first operation, coronary angiography revealed a narrowed RITA. Myocardial ischemia occurred when the native coronary artery was occluded by the catheter. A stringlike internal thoracic artery is probably unable to increase blood supply immediately in response to the demand created by acute obstruction of the recipient native coronary artery.

Aged↗
PubMed2004

[Surgical treatment for the valvular disease through partial sternotomy].

213 patients who underwent surgical treatment for the valvular disease through partial sternotomy were studied. We started the minimally invasive valvular surgery in July 1997. All the valvular diseases were indicated for the minimally invasive surgery except for the annulo-aortic ectasia and the concomitant disease with coronary artery bypass surgery. Ascending aorta was selected as an arterial cannulation place if we could choice it through intraoperative echocardiography. Venous cannulae 22-24 Fr were inserted into the venae cavae directly or through right atrium. Negative pressure venous drainage (maximally 90 mmHg) was performed if necessarily. We did single approach as possible. Mortality rate was 3.8%. We could complete 96.2% of our series as a minimally invasive surgery. Post operative intensive care unit (ICU) stay and hospital stay through partial sternotomy were significantly shorter than those through full sternotomy.

Aged↗
PubMed2003

Metabolic derangements in interstitial brain edema with preserved blood flow: selective vulnerability of the hippocampal CA3 region in rat hydrocephalus.

Hydrocephalus induces interstitial brain edema, which causes neurological deficits, even if the intracranial pressure is maintained within the normal range, and the cerebral blood flow (CBF) does not decline to an ischemic level. The precise mechanisms underlying such edema-induced neuronal dysfunction remain unclear. In the present study, in an attempt to elucidate the metabolic derangements in brain tissue with interstitial edema, we evaluated the changes in CBF and oxidative/glucose metabolism using a rat model of kaolin-induced hydrocephalus. Hydrocephalus was produced in male Wistar rats by intrathecal injection of 0.1 ml aluminum silicate suspension (200 mg/ml) via the cisterna magna. CBF was determined by 14[C]-iodoantipyrine autoradiography. Oxidative metabolism was evaluated by cytochrome oxidase (CYO) histochemistry, and glucose metabolism by hexokinase (HK) histochemistry. CBF declined with the development of hydrocephalus, but did not reach an ischemic level. The CYO activity was diffusely depressed in both the cortex and hippocampus. The HK activity was preserved at the early stage of hydrocephalus. At the advanced stage, the HK activity was reduced in the hippocampal CA3 region first, and diffusely thereafter. In conclusion, interstitial brain edema impairs oxidative metabolism even at the early stage of hydrocephalus, and shifts the metabolism to anaerobic glycolysis despite a preserved CBF. Impairment of glucose metabolism was first observed in the CA3 region, suggesting that the CA3 is metabolically vulnerable, and CA3 dysfunction may contribute to the memory deficits seen in hydrocephalus.

Animals↗
PubMed2003

FK506 attenuates the post-ischemic perturbation of protein kinases and tyrosine phosphorylation in the gerbil hippocampal CA1 sectors.

To explore effects of Immunosuppressant FK506 on signal transduction pathway. we studied changes in subcellular distribution of protein kinase Cgamma (PKCgamma), CaM kinase II (CaMKII), as well as changes of tyrosine phosphorylation levels after ischemia. Male Mongolian gerbils were divided into 3 groups; FK506 (1 mg/kg, 3 mg/kg) and vehicle. FK506 was administered intravenously after 5 min ischemia. At the designated time points (0 time, 5 min ischemia, 1 hour, or 24 hour recovery), heads were frozen and samples were taken from CAI subfield of hippocampus. Western blot analysis was carried out with specific antibodies for PKCgamma, CaMKII, and phosphotyrosine. FK506 administration significantly decreased translocation of PKCgamma and CaMKII at 24 h of recovery (p < 0.05, ANOVA followed by Student-Newman Keuls' test) in P2 fraction. The levels of tyrosine phosphorylated p160, p140, p100, p90, and p80 in P2 fraction were also significantly decreased with FK506 treatment at 24 h of recovery. The persistently elevated PKCgamma and CaMKII level in P2 fraction which may be related to cell death, are attenuated with FK506 treatment. FK506 may contribute to recover calcium homeostasis in the post ischemic phase and promote cell survival.

Animals↗
PubMed2003

Infiltration of tissue plasminogen activator through cerebral vessels: evaluation using a rat thromboembolic stroke model.

In recent years, evidence has been accumulating that tissue plasminogen activator (tPA) possesses neurotoxic effects. However, such deleterious effects have been attributed to endogenously generated tPA. In the present study, focusing on exogenously administered tPA for the purpose of fibrinolysis, we evaluated the extent and the degree of extravasated tPA in a rat model of thromboembolic stroke. Even after early recanalization of occluded cerebral vessels, significant infiltration of tPA occurred through the cerebral vessels. It is assumed that exogenous tPA also exerts neurotoxic effects in the ischemic brain tissue.

Animals↗
PubMed2003

Mild hypothermia enhances the neuroprotective effects of a selective thrombin inhibitor following transient focal ischemia in rats.

The aim of this study is to determine whether a selective thrombin inhibitor, Argatroban, would prevent neuronal cell death and whether extra-mild hypothermia (35 degrees C) would enhance the neuroprotective effect of a selective thrombin inhibitor following transient focal ischemia in rats. Sprague-Dawley rats were subjected to MCAo using an intraluminal suture technique for 2 hrs. The rats were reperfused for 24 h and decapitated for infarct and edema analysis. Argatroban-treated animals received a continuous injection of argatroban (3.0 mg/kg) for 24 hrs after onset of ischemia, while vehicle-treated groups received same dose of vehicle. During ischemia, temporal muscle and rectal temperatures were monitored and maintained at 37 degrees C in the normothermic animals and at 35 degrees C in the hypothermic animals. Argatroban ameliorated the cortical ischemic damage significantly (p < 0.05). Moreover, argatroban with mild hypothermia decreased the cortical infarct or edema volume significantly compared with those of groups I and III (p < 0.05). Argatroban improved neurological symptoms significantly and also improved survival rate. These results demonstrate that extra-mild hypothermia (35 degrees C) enhances neuroprotective effects of a selective thrombin inhibitor, argatroban, suggesting that this combined therapy may be a new therapeutic strategy for the treatment of acute stroke.

Animals↗
PubMed2003

The neuroprotective effect of a free radical scavenger and mild hypothermia following transient focal ischemia in rats.

Edaravone, a novel free radical scavenger, has been reported to reduce ischemic damage in rats subjected to transient focal ischemia. The aim of this study is, therefore, to investigate the effect of a combined therapy with edaravone and mild hypothermia of 35 degrees C. Sprague-Dawley rats were subjected to MCA occluding an intraluminal suture technique for 2 hrs. The rats were reperfused for 24 h and decapitated for infarct and edema analysis. Animals were randomly devided into four groups: (I) vehicle + normothermia (control) (II) vehicle + mild hypothermia (III) Edaravone + normothermia (IV) Edaravone + mild hypothermia. Mild hypothermia alone had no reduction of the brain damage. The edaravone alone significantly reduced edema volume. The combined treatment with edaravone and mild hypothermia reduced both infarct and edema volume. In addition, this treatment provided for the best functional outcome. These results demonstrate that free radical scavenger, edaravone attenuates brain edema and that the combined therapy with edaravone and mild hypothermia significantly reduces not only edema but also infarct on transient focal cerebral ischemia in rats. The neuroprotective effects seen in this study may be due to the combined interaction of antiedema activity between edaravone and mild hypothermia, suppressing free radical production.

Animals↗
PubMed2003

Cerebral blood flow index image as a simple indicator for the fate of acute ischemic lesion.

BACKGROUND AND PURPOSE: To evaluate the feasibility of utilizing cerebral blood flow (CBF) index images, we attempted to investigate 1) whether CBF index images can reveal the resulting infracted area, 2) whether the CBF index can correlate other modality (SPECT). METHODS: DWI and DPI were obtained in 17 patients within 12 hours of stroke onset and follow up MRI. On three DPI delivered images, namely relative regional cerebral blood volume (rrCBV), uncorrected mean transit time (MTTu) and CBF index images, correlations between initial lesion volume of and follow up infarction volume of three images and rCBF images delivered with singular value decomposition (SVD) methods were assessed. Then 99mTc-ECD SPECT was taken immediately after MRI to correlate to MRI data. RESULTS: Among the three images, lesion volume of CBF index images against follow up infarct volume had the highest correlation (r = 0.995) to a linear fit and the slope was closest to 1.0 (0.91) and had identical accuracy to the regression coefficient of rCBF images. CBF index well correlated to SPECT delivered CBF. CONCLUSION: CBF index images can accurately predict final infarct volume. Evaluating CBF index images together with DWI can guide the initial assessment in the acute stage of cerebral ischemia.

Acute Disease↗
PubMed2003

Edema fluid accumulation within necrotic brain tissue as a cause of the mass effect of cerebral contusion in head trauma patients.

The early massive edema caused by severe cerebral contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 hours post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In order to elucidate the mechanisms underlying the early massive edema, we have carried out a series of detailed clinical studies. Diffusion magnetic resonance (MR) imaging and apparent diffusion co-efficient (ADC) mapping suggest that cells in the central area of contusion undergo shrinkage, disintegration and homogenization, whereas cellular swelling is predominant in the peripheral area during the period of 24-72 hours post-trauma. The ADC values in the central and peripheral areas are maximally dissociated during this period. A large amount of edema fluid accumulates within the necrotic brain tissue of the central area beginning at approximately 24 hours post-trauma. We have found that fluid-blood interface formation within the central area does not represent an uncommon finding in various neuroimaging examinations of cerebral contusions, indicating layering of red blood cells within the necrotic brain tissue accumulating voluminous edema fluid. Intravenous slow infusion of gadolinium-DTPA and delayed MR imaging revealed that the central area of contusion can be enhanced at 24-48 hours post-trauma. implying that water supply from the blood vessels is not completely interrupted. Necrotic brain tissue sampled from the central area of contusion during surgery demonstrates a very high osmolality. It appears that the capacitance for edema fluid accumulation increases in the central area, whereas cellular swelling in the peripheral area elevates the resistance for edema fluid propagation. Combination of these circumstances may facilitate edema fluid accumulation in the central area. We also suggest that the dissociation of ADC values and high osmolality within the necrotic brain tissue may generate an osmotic potential across the central and peripheral areas and contribute to the early massive edema caused by cerebral contusion.

Body Fluids↗
PubMed2003

Ultra-early study of edema formation in cerebral contusion using diffusion MRI and ADC mapping.

OBJECTIVE: Our previous studies have reported that heterogeneous mechanisms exist in early edema formation in cerebral contusion, and cytotoxic edema plays an important role within 48 hours post-trauma. It is remains unclear, when edema begins to develop following injury. In order to determine the time course of edema development, diffusion imaging and ADC (apparent diffusion co-efficient) mapping was performed in 10 patients within 24 hours post-trauma with cerebral contusion. METHODS: Diffusion imaging and ADC mapping were performed employing 1.0 T echo planar MRI. ADC values were indicated as a ration relative to the values of intact brain areas. RESULTS: Within 3 hours post-trauma, diffusion MRI showed no remarkable changes, and the ADC values were within normal limit (ADC ratio (=contused/normal brain) = 1.00 +/- 0.21, (mean +/- SD)). At 6 hours post-trauma, diffusion images demonstrated a low intensity core in the contusion proper and a high intensity rim in the peripheral area of contusion. The ADC value increased in the contusion proper (ADC ratio = 1.26 +/- 0.13) and decreased in the peripheral area (ADC ratio = 0.58 +/- 0.19). CONCLUSIONS: These findings indicated that early cellular swelling in the peripheral area of contusion begins within 6 hours following injury. This delayed occurrence of contusion-induced cellular swelling suggests that the CBF does not decrease to ischemic level immediately following injury.

Brain Edema↗
PubMed2003

BOLD functional MRI may overlook activation areas in the damaged brain.

Clinical applications of blood-oxygenation-level-dependent contrast functional MRI (BOLD-fMRI) have been rapidly moving toward routine non-invasive cortical mapping in the patients with brain disorders. However, it is not yet clear whether the damaged brain shows same cerebral blood oxygenation (CBO) changes during neuronal activation as those in the normal adult. We compared the activation mapping obtained by BOLD-fMRI and the evoked-CBO changes measured by near infrared spectroscopy (NIRS) in normal adults (6 cases) and patients with damaged brain (6 cases of cerebral ischemia and 10 cases of brain tumors in or adjacent to the motor cortex). BOLD-fMRI demonstrated robust activation areas in the primary sensorimotor cortex (PSMC) during contralateral hand grasping tasks in all of the normal adults; however, in the cerebral ischemia (6 cases) and the brain tumors (2 cases), BOLD-fMRI demonstrated only limited activation areas in the PSMC on the lesion side during the task. NIRS demonstrated an increase of focal concentration of oxyhemoglobin and total hemoglobin at the PSMC during the task in all of the normal adults and the patients, indicating the presence of rCBF increase in response to neuronal activation. A focal concentration of deoxyhemoglobin decreased during the task in the normal adults, however, in the patients that showed limited activation areas by BOLD-fMRI, deoxyhemoglobin concentrations increased during the entire course of the task. In summary, the evoked-CBO changes occurring in the damaged brain differed from those in the normal brain. This indicates that BOLD-fMRI may overlook activation areas in the damaged brain.

Brain Ischemia↗