Search PubMed⌕ Search

Biomedical subjects

Y Fukuuchi

Publications and source records attributed to Y Fukuuchi.

At least 109 records · Page 6Linked to original sources
PubMed1996

Flow threshold for reduction of cyclic AMP binding in the hippocampus CA1 and other brain regions during stroke development in gerbils.

The flow threshold for alterations of the in vitro [3H]cyclic AMP (cAMP) binding, an indicator of the total amount of particulate cAMP-dependent protein kinase, was evaluated in the gerbil brain after 30 min, 2 h, and 6 h of unilateral common carotid artery occlusion, respectively. The autoradiographic method developed in our laboratory enabled us to measure the [3H]cAMP binding and local CBF in each region of the same brain. The ischemic flow thresholds for reduction of the cAMP binding in the hippocampus CA1 were 18, 34, and 49 ml 100 g-1 min-1 after 30-min, 2-h, and 6-h ischemia, respectively. These values were higher than those in other regions such as the hippocampus CA, and temporal cerebral cortex in each duration of ischemia. These findings indicate that (a) the ischemic flow threshold for perturbation of the cAMP system may be higher in the hippocampus CA1 than in other brain regions, suggesting that the hippocampus CA1 could be especially vulnerable to acute ischemic stress; and (b) the level of the aforementioned threshold may increase progressively during the time course of ischemia in particular regions such as the hippocampus CA1 and CA3, suggesting that the duration of ischemia exerts a definite influence on the viability of the ischemic neuronal cells in these regions.

Animals↗
PubMed1996

Swift transformation and locomotion of polymorphonuclear leukocytes and microglia as observed by VEC-DIC microscopy (video microscopy).

The detailed assembly used by us for video-enhanced contrast-differential interference contrast (VEC-DIC) microscopy (video microscopy is first described. Employing such video microscopy, we then examined the morphological changes occurring during locomotion and activation processes of polymorphonuclear leukocytes (PMNL) and microglia at an almost electron microscopic magnification. Upon contacting the substratum, PMNL transformed into a polarized ameboid shape and crawled extending pseudopodia, as has been well documented previously. The PMNL sometimes displayed a peculiar locomotion as if they were stepping on "tiny legs", or sliding on a treadmill of cell membrane. Cultured microglia were observed to exist in 4 forms; ramified, reactive, villous, and ameboid. Microglia in the reactive form pivoted, circled and crawled on the astroglial cell layer using their transparent lamellipodia with no morphological changes in their cell body. Unlike PMNL, reactive microglia exhibited no agitated movements of their intracellular organelles, including granules and cytosol, during locomotion. Lamellipodia on the undersurface of the cell body touching the cell layer adhesively, appeared to serve as the locomotive apparatus. When activated, both floating PMNL and microglia of villous form assumed an ameboid shape within a few seconds. Microglia occasionally swam in the medium waving their lamellipodia towards a target object (e.g. zymosan A particles), remodelling to an amorphous ameboid form and covering up the target. We attempt to discuss such swift morphological changes from the standpoint of thermodynamic potential of Gibbs free energy which is stored within the cells.

Cell Movement↗
PubMed1996

[A case of posttraumatic spinal pseudomeningocele which caused spinal cord compression 20 years after injury].

We reported an extremely rare case of posttraumatic spinal pseudomeningocele which caused spinal cord compression 20 years after getting injury, and demonstrated that sequelae of an injury may occur many years after the original wound. A 39-year-old man, who got left cervical root avulsion due to a traffic accident when he was 17 years old, began to complain of progressive muscle atrophy and weakness of left lower extremity 1 year ago. Myelography demonstrated pseudomeningocele at left C6-C8 level, and MRI and CT myelography revealed that the pseudomeningocele extends through the intervertebral foramen and compresses the spinal cord to the right side in the spinal canal. Bilateral functional compression of spinal cord dorsal and lateral column was also verified with SEP and MEP electrophysiologically.

Accidents, Traffic↗
PubMed1996

Aspirin improves the enhanced erythrocyte aggregability in patients with cerebral infarction.

We examined the effect of aspirin on the enhanced erythrocyte aggregability in 19 patients with cerebral infarction during the chronic phase. Aspirin (81 mg/day) was administered for 8 weeks. The rate of erythrocyte aggregation (aggregability) was measured using the whole-blood erythrocyte aggregometer developed by us (Am. J. Physiol. 251, H1205-H1210, 1986) before, and at 4 and 8 weeks after initiation of the aspirin administration. Concomitant measurements were made of certain blood factors such as the hematocrit, albumin-globulin (A/G) ratio and fibrinogen concentration. The erythrocyte aggregation rates before, and at 4 and 8 weeks were 0.154 +/- 0.019/s, 0.144 +/- 0.020/s, and 0.143 +/- 0.020/s, respectively. The erythrocyte aggregation rates at 4 and 8 weeks were significantly (P < 0.05, Bonferroni's modified t-test) lower than that before aspirin administration. Although the hematocrit value and A/G ratio were not changed at 4 and 8 weeks after the initiation of aspirin, the concentration of fibrinogen were significantly (P < 0.05) reduced at 4 weeks. The above results suggest that aspirin can improve the enhanced erythrocyte aggregability in patients with cerebral infarction during the chronic phase.

Adult↗
PubMed1996

-Clinical features of 10 cases of tuberculous meningitis--with special reference to patient's delay and doctor's delay.

We retrospectively evaluated the clinical findings of 10 cases of tuberculous meningitis who had been admitted to our department from 1987 to 1994. Four patients were male and six were female. All of them were Japanese, and their age ranged from 17 to 74 years old. Regarding the patient's delay, nine patients visited a doctor in 1 to 20 days after the onset of headache, and one patient visited a doctor in 14 days after the onset of general malaise. It is suggested that the patient's delay could not be longer than 3 weeks because of progressively worsening symptoms of tuberculous meningitis such as severe headache and fever. The time interval between the first contact of the patient to a doctor and the commencement of antituberculous therapy (doctor's delay), ranged from 14 to 66 days. When the diagnosis of meningitis was obtained based on the findings of the cerebrospinal fluid (CSF), focal neurological signs including psychological symptoms, cranial nerve palsies and seizure were noted besides meningeal signs or the disturbance of consciousness in 4 patients. The CSF revealed an increase in cell counts with mononuclear cell dominance in 9 patients, but the findings typical for tuberculous meningitis such as increase in total protein content and a decrease in glucose concentration were obtained in only 5 patients. Mycobacterium tuberculosis had not been detected in all cases when the antituberculous chemotherapy was started. Later, it was found to be positive in the CSF sample from only three patients by culture or polymerase chain reaction (PCR) method. When the antituberculous therapy was completed, meningitis was cured without remaining any symptom or sign in all patients. All patients had no active pulmonary tuberculosis when the meningitis was diagnosed, and only one of them had sequels of lung tuberculosis. Four patients had the past history of tuberculosis, and 1 had the familial history of pulmonary tuberculosis. At the first contact to a doctor, seven patients were diagnosed as having common cold or headache related with fever because of the lack of typical signs of meningitis. Similarly three other patients were initially diagnosed as having meningitis due to viral infection or unknown etiology. In summary, it was difficult to obtain the solid diagnosis of tuberculous meningitis at the initial stage of this disease, since the symptoms and signs at its onset often similar to those of common cold or non-specific headache. Therefore, when we see the patients with subacute onset of headache and fever followed by the meningeal signs, tuberculous meningitis should always be included in the list of diseases requiring differential diagnosis. In addition, when tuberculous meningitis is suspected, the antituberculous therapy should be started without any delay.

Adolescent↗
PubMed1995

Calcitonin gene-related peptide (CGRP) and the regulation of cerebral parenchymal vessels.

The role of calcitonin gene-related peptide (CGRP) in the cerebral microcirculation was examined in fourteen anesthetized cats. The local cerebral blood volume (CBV) and blood flow (CBF) in the temporoparietal cortex were measured by our photoelectric method. CBV represents the cumulative dimensions of the parenchymal vascular network. Intracarotid injection of 0.1, 1, and 10 micrograms/kg CGRP8-37, a CGRP antagonist, had no significant effects on CBV and mean arterial blood pressure (MABP). Intracarotid injection of 0.1 and 1 microgram/kg CGRP, but not 0.01 microgram/kg CGRP, increased CBV in a dose-dependent manner (P < 0.05). CBV was initially reduced following 1 microgram/kg CGRP injection, possibly reflecting the marked fall in MABP (P < 0.01) with this dose. Following injection of 0.1 and 1 microgram/kg CGRP, CBF was also increased by +7.3 +/- 7.7 (+10.7%) and +13.1 +/- 4.8 ml/100 g brain/min (+20.4%, P < 0.05) at 15 min. The CBV increase elicited by 1 micrograms/kg CGRP was inhibited (P < 0.05) by preinjection of 10 micrograms/kg CGRP8-37. It is concluded that CGRP has no significant role in the maintenance of resting tone of intracerebral microvessels. However, circulating CGRP dilates the small parenchymal vessels through a specific CGRP receptor, and thereby is involved in the evolution of pathologic conditions.

Animals↗
PubMed1995

Non-amoeboid locomotion of cultured microglia obtained from newborn rat brain.

The movements of cultured microglia obtained from newborn rat brain were examined by video enhanced-differential interference contrast (VEC-DIC) microscopy. Active microglia measured 9.03 +/- 1.06 microns in diameter (mean +/- SD, n = 33; range, 7.03-10.36 microns). The microglia appeared to become smaller with spread of lamellipodia. The short axis of actively moving microglia measured 7.03 +/- 0.49 microns (n = 7). The lamellipodia were thin, transparent and developed rapidly around the cell body (maximal speed of extension, 4 or 5 microns/s). When shear stress from the medium was applied to the surface of cultured cells, the microglia swam with flat lamellipodia serving as sails in the stream. Spontaneous non-amoeboid movements of microglia were observed: they pivoted, circled and marched in various directions using their lamellipodia. The angular speed of rotation was maximally 3 degrees/s. In 5 marching cells, the average speed (distance/s) was calculated at 1.01 +/- 0.54 microns/s (ca. 60 microns/min or 3.6 microns/h).

Animals↗
PubMed1995

Chronic transection of post-ganglionic parasympathetic and nasociliary nerves does not affect local cerebral blood flow in the rat.

The role of post-ganglionic parasympathetic nerve fibers from the sphenopalatine ganglion and nasociliary nerve fibers from the trigeminal ganglion in the regulation of basal cerebral blood flow (CBF) was examined using rats, which had been divided into three groups; a sham group, a denervation group and a denervation+NG-monomethyl-L-arginine (L-NMMA) group. In the denervation and denervation+L-NMMA groups, unilateral chronic transection of the above nerve fibers had been performed at the ethmoidal foramen (EF) for 2 weeks. In the sham group, the above nerve fibers were only exposed at EF and not severed 2 weeks before the CBF measurement. Local CBF was measured by the [14C]iodoantipyrine autoradiographic method after intravenous administration of saline in the sham and denervation groups or L-NMMA (30 mg/kg) in the denervation+L-NMMA group. No significant difference in CBF was noted on each side in any of the regions between the sham and denervation groups. L-NMMA induced a significant reduction in local CBF on either side in each brain region. Neither the animals which were administered saline nor those with L-NMMA showed any side-to-side differences in local CBF in any of the brain regions examined. These findings suggest that the perivascular nerve fibers running through the EF, which are known to contain substantial nitric oxide synthase (NOS), may not play a pivotal role in the regulation of basal CBF. The reduction in CBF induced by the acute administration of L-NMMA was not affected by the chronic denervation of the above NOS-containing perivascular nerves.

Animals↗
PubMed1995

Flow threshold for enhanced phorbol ester binding in the ischemic gerbil brain.

The correlation between regional phorbol ester binding and cerebral blood flow (CBF) was evaluated in the gerbil brain after 2-hour unilateral common carotid artery occlusion. [3H]phorbol 12,13-dibutyrate (PDBu) was used as a specific ligand for estimating the translocation of protein kinase C (PKC), and CBF was determined by the [14C]iodoantipyrine method. A quantitative autoradiographic method permitted concurrent measurement of these two parameters in the same brain. In the ischemia group of the animals, statistically significant, inverse correlations were noted between the CBF and PDBu binding in the hippocampus (CA1 and CA3 regions and dentate gyrus), the caudate-putamen and lateral nuclei of the thalamus. In these regions, the PDBu binding increased progressively as CBF fell below 35-40 ml/100 g/min. On the other hand, the PDBu binding in the cerebral cortices did not show any significant changes even when CBF was decreased to below 35 ml/100 g/min. The above data suggest that (1) the translocation of PKC to the cell membrane may be regionally specific in response to ischemia, and may remain in the regions particularly vulnerable to ischemia such as the hippocampus, caudate-putamen and lateral nuclei of the thalamus in the early ischemic phase; (2) the threshold of CBF below which PKC begins to translocate to the cell membrane in the above regions, may be 35-40 ml/100 g/min in 2-hour ischemia.

Animals↗
PubMed1995

Levodopa-induced local cerebral blood flow changes in Parkinson's disease and related disorders.

Local cerebral blood flow (CBF) in the steady state and after intravenous administration of levodopa (1 mg/kg) was measured by xenon-enhanced computed tomography in patients with Parkinson's disease (PD, n = 16), progressive supranuclear palsy (PSP, n = 6), olivopontocerebellar atrophy (OPCA, n = 5), and arteriosclerotic parkinsonism (AP, n = 7). Three patterns of local CBF changes following levodopa were observed: (1) diffuse CBF increases, especially in striatum and thalamus, as found in patients with PD; (2) no significant changes in CBF, as in patients with OPCA and AP; and (3) CBF reductions in basal ganglia and thalamus, as seen in patients with PSP. The CBF increases after levodopa in PD may be secondary to metabolic activation of the nigrostriatal dopaminergic system. The poor CBF responses in patients with OPCA, AP, and PSP appeared to reflect degeneration of the dopaminergic neurons and dopamine receptors to various degrees. The CBF increases, especially in striatum and thalamus, tended to be greater (not significant) among responders to oral levodopa therapy. Levodopa-induced CBF measurements may be useful for the differential diagnosis of parkinsonian syndromes of various etiologies, but are not necessarily sufficient for predicting outcomes of long-term levodopa therapy.

Adult↗
PubMed1995

Pentoxifylline ameliorates postischemic delayed hypoperfusion of the cerebral cortex following cardiac arrest in cats.

Two major events occurring in the cerebral hemodynamics after successful resuscitation from cardiac arrest are reactive hyperemia and postischemic hypoperfusion. We examined the effect of pentoxifylline on the feline cerebral hemodynamics following cardiac arrest. Fifteen cats were anesthetized and artificially ventilated. Using our photoelectric method, the local cerebral blood volume (CBV), mean transit time of blood (MTT), and cerebral blood flow (CBF) in the parietotemporal region were measured. Thoracotomy was performed, and cardiac arrest (ventricular fibrillation) was induced by direct application of a 2-V DC countershock. The heart was resuscitated with a DC countershock at 30 sec after cardiac arrest. In 9 cats, pentoxifylline (25 mg/kg) was infused into the femoral vein at 5 min before cardiac arrest (PTX group). The other 6 cats served as controls (control group). In both groups, the CBV, CBF and mean arterial blood pressure (MABP) overshot the control levels just after resuscitation, whereas the MTT was decreased. In the control group, postischemic hypoperfusion was detected at 30-180 min after resuscitation from cardiac arrest (CBF (ml/100 g/min): 51 +/- 4 (control), 38 +/- 4 (30 min, p < 0.05), and 23 +/- 3 (180 min, p < 0.05)). However, the postischemic hypoperfusion was not observed in the PTX group. Pentoxifylline ameliorated postischemic delayed hypoperfusion in the cerebral cortex after a short period of cardiac arrest. Pentoxifylline may be useful in the emergency situations following cardiac arrest.

Animals↗
PubMed1995

Effects of ventricular arrhythmia on the cerebral microcirculation in cats.

To test the widely believed but poorly proved hypothesis that the cerebral symptoms observed during ventricular arrhythmia are caused by a reduced cerebral blood supply, we examined the effects of single and multiple ectopic ventricular beats (or ventricular tachycardia of short duration) on the cerebral microcirculation. Six anesthetized cats were used. Ectopic ventricular systoles of various sequences were produced by electrically stimulating the ventricle through a bipolar needle-type electrode for 1 to 50 times at a rate of 300/min. The local cerebral blood volume (CBV) and blood flow (CBFLD) in the cortex were measured continuously employing the photoelectric and laser Doppler methods. CBV reflects the cumulative dimensions of the cerebrocortical microvessels. Ectopic ventricular contractions, as confirmed by electrocardiograms, always reduced the CBV and arterial blood pressure in a total of 104 attempts. The CBV reductions ranged from 0.20 +/- 0.03 vol% for a single ectopic beat to approximately 0.6-0.8 vol% for runs of 8 or more beats. The CBFLD reductions measured with the laser Doppler flowmeter were 10-35%. The reductions in CBV and CBFLD during the ventricular arrhythmia could be attributed to the abrupt and marked reductions in arterial blood pressure. Runs of ectopic ventricular beats have significant effects on the cerebral microcirculation, whether clinically apparent or not.

Animals↗
PubMed1995

Activated leukocytes, endothelial cells, and effects of pentoxifylline: observations by VEC-DIC microscopy.

Using video-enhanced contrast (VEC)-differential interference contrast (DIC) microscopy, ultrastructural observations were made of the activation of polymorphonuclear leukocytes (PMNLs), the interaction between activated PMNLs and endothelial cells (ECs), and the effects of pentoxifylline (PTX). The ECs were obtained from a commercial source as human umbilical cord vein endothelial cells (HUVECs) or were obtained from pig or rat brains. They were cultured on a coverglass with DMEM for about 1 week. The human PMNLs were obtained from the authors' venous blood. The control appearance of the PMNLs resembled an elastic ball covered with fine villi. The PMNL was activated spontaneously and became flattened on the glass surface within 10 min in the observation chamber. The activation of the PMNLs was estimated arbitrarily from the polymorphous changes in cell shape, agitation of the intracellular granules, and apparent increase in adhesiveness. Preadministered PTX prevented such PMNL activation, and the PMNLs remained round for more than 15 min. PMNL activation was accelerated by chemoattractants (PAF, fMLP, and PMA). In one case, a PMNL that had been activated by PMA tended to recover its round shape with PTX, but finally ended by swelling and bursting. When PMNLs were introduced into the EC-containing chamber, they became entrapped by the ECs and activated, with degranulation followed by release of a smoke-like material. After about 3 h, the EC with an attached PMNL shrank and fell into a state of coagulation necrosis. When PTX was introduced at the time of adhesion of the flattened PMNL, the PMNL appeared to be deactivated, becoming smaller and assuming its previous round shape, and detached from the EC. PTX prevented the spontaneous activation of PMNLs, and of deactivated PMNLs even after their adherence to the endothelium.

Animals↗
PubMed1995

[A case of spontaneous arteriovenous fistula presenting as the partial oculomotor nerve palsy].

We report a case of partial oculomotor nerve palsy due to spontaneous arteriovenous fistula. A 62-year-old man noticed double vision on downward gaze and periorbital pain. Clinical examination revealed inability to move the left eye downwards and to the right, and also anisocoria. No conjunctival injection or proptosis was noted. Findings of computed tomographic scan, magnetic resonance imaging and magnetic resonance angiography of the orbits, cavernous sinus region and brainstem were all normal. Carotid angiography demonstrated arteriovenous fistula via the left ophthalmic artery, the dural branch of the left external carotid artery, and the dural branch of the right internal carotid artery. Partial oculomotor palsy in this case indicated that the left inferior branch of the oculomotor nerve was affected. Inferior branch palsy of the oculomotor nerve in spontaneous arteriovenous fistula has not been described in the literature, while it is reported in cases of trauma, tumor, or aneurysm of the cavernous sinus.

Arteriovenous Fistula↗
PubMed1995

Effect of thyrotropin-releasing hormone (TRH) on cerebral blood flow in spinocerebellar degeneration and cerebrovascular disease.

The effect of TRH on cerebral blood flow in patients with spinocerebellar degeneration and cerebrovascular disease was investigated. Cerebral blood flow was measured by the 133Xenon arterial injection method before, and 30 min after, the intravenous administration of 1000 micrograms of TRH. TRH had no effect on mean arterial blood pressure in either group. In the spinocerebellar degeneration group, cerebral blood flow increased slightly after the injection of TRH, from 52.7 +/- 10.5 to 56.7 +/- 16.0 ml/100 g brain/min. In two patients with spinocerebellar degeneration, whose autonomic function was normal and whose brainstem structure appeared normal in the CT scan, cerebral blood flow increased from 54.8 to 66.4 ml (21.2%), and from 68.6 to 79.9 ml (16.5%), respectively. In the patients with cerebrovascular disease, cerebral blood flow did not change (49.7 +/- 10.8 ml before and 49.4 +/- 12.6 ml after TRH). Cerebral blood flow reportedly increases following an intravenous injection of TRH in animals, supposedly due to the activation of intrinsic cerebral vasodilative fibers situated in the submesencephalic brainstem region. Our results are consistent with this hypothesis and with the clinical finding that TRH especially improves ataxia in spinocerebellar degeneration where there is no pyramidal involvement or disorder of deep sensation.

Autonomic Nervous System↗
PubMed1994

Role of nitric oxide in regulation of cerebral microvascular tone and autoregulation of cerebral blood flow in cats.

The role of nitric oxide in the regulation of cerebrocortical microvascular tone and autoregulation of cerebral blood flow (CBF) was examined in 24 anesthetized cats. The local cerebral blood volume (CBV), mean transit time of blood (MTT), and CBF in the cortex were measured by our photoelectric method. CBV represents the cumulative dimensions of the cerebral microvessels. Intravenous injection of 0.35-0.7 mg/kg/min NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide synthesis, significantly increased mean arterial blood pressure (MABP; 8.4-14.1%, P < 0.01), decreased CBV (15.2-28.7%, P < 0.01), and decreased CBF (20.0-29.8%, P < 0.01) in a dose-related manner. The changes in MABP, CBV, and CBF elicited by L-NMMA were inhibited (P < 0.05) by simultaneous infusion of 35 mg/kg/min L-arginine. Autoregulation of CBF was examined during controlled hypotension of -30 to -40 mmHg (artificial bleeding) and recovery of blood pressure (reinfusion of blood). Although CBF remained constant with blood pressure changes in the control state (delta CBF/delta MABP of 0.037 +/- 0.155 with hypotension), CBF became dependent on blood pressure changes (delta CBF/delta MABP of 0.478 +/- 0.135, P < 0.05) during infusion of 0.35 mg/kg/min L-NMMA. It is concluded that nitric oxide participates in both the regulation of basal tone of cerebral microvessels and the autoregulation of CBF.

Animals↗