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Biomedical subjects

Y Fukuuchi

Publications and source records attributed to Y Fukuuchi.

At least 145 records · Page 8Linked to original sources
PubMed1994

[Time-course of adenosine deaminase activity in the cerebrospinal fluid in patients with tuberculous meningitis].

The level of adenosine deaminase (ADA) activity in the cerebrospinal fluid is used as a supportive diagnostic measure for tuberculous meningitis. However the time-course of adenosine deaminase activity of the cerebrospinal fluid in patients with tuberculous meningitis remains unknown. The present study describes 4 patients with tuberculous meningitis in whom ADA activity in the cerebrospinal fluid was serially determined in order to clarify the effects of anti-tuberculous chemotherapy on ADA activity in the cerebrospinal fluid. In two of these patients the ADA did not show a high activity in the early stage of the disease. But in all cases the ADA showed a high activity after all, and gradually declined and reached the normal level at approximately 1 month after the initiation of chemotherapy. It seems that the decrease in the ADA activity was seen when T cells in the cerebrospinal fluid returned to a static state upon removal of mycobacterial antigen by the treatment. The level of ADA in the cerebrospinal fluid is considered to be one of the useful measures for diagnosis and follow-up in patients with tuberculous meningitis.

Adenosine Deaminase↗
PubMed1994

[Creutzfeldt-Jakob disease with a point mutation at codon 232 of prion protein--a case report].

We report a 50-year-old female with sporadic Creutzfeldt-Jakob disease who revealed a point mutation at codon 232 of prion protein (Met to Arg). The initial symptom was visual disturbance. The patient then developed progressive dementia, cerebellar ataxia and myoclous. About eight months after the onset, the patient went into the state of akinetic mutism. The electroencephalogram showed periodic synchronous discharges. From the prion protein's DNA sequencing of the patient's family members, the 84-year-old father without any neurological symptoms was also detected to have a point mutation at codon 232. These findings which, have not been reported before, are interesting when considering the relation between the pathogenesis of Creutzfeldt-Jakob disease and mutations of prion protein gene.

Aged↗
PubMed1993

Cerebrovascular NADPH diaphorase-containing nerve fibers in the rat.

Recently, neuronal nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase has been elucidated to be the nitric oxide synthase (NOS) per se. In order to examine the existence and distribution of cerebrovascular nerve fibers containing these substances, NADPH-diaphorase histochemistry was applied to the cerebral blood vessels and the cranial ganglia known to innervate the cerebral vessels in the rat. Numerous nerve fibers with varicosities forming plexuses were observed in the circle of Willis and its branches. In addition, thick nerve bundles were seen to run along the wall of the internal ethmoidal artery. NADPH-diaphorase reaction was prominent in neurons of the sphenopalatine, otic and internal carotid ganglia. This study demonstrated, for the first time, the NADPH-diaphorase-containing nerve fibers in the cerebral vessels and ganglion cells in the parasympathetic and sensory ganglia known to innervate the cerebral vessels.

Animals↗
PubMed1993

Immobilization stress induces alterations of second-messenger systems in the gerbil brain.

The effects of immobilization stress on the cerebral second messenger (adenylate cyclase and phosphoinositide) were investigated autoradiographically in mongolian gerbils. After 10 min (10-min stress group, n = 7), or after 6 h (6-h stress group, n = 7) of fixation on a flat board while supine, in vitro autoradiography was performed using [3H]forskolin (3H-FK) and [3H]phorbol-12,13-dibutyrate (3H-PDBu) as specific ligands to identify the distribution of adenylate cyclase and protein kinase C, respectively. In another group of 7 gerbils (control group), the same autoradiographic procedure was performed immediately after the animals were removed from the cage. In the 10-min stress group, FK binding was significantly decreased in the hypothalamus and amygdala, but significantly increased in the basal ganglia including the caudate-putamen and globus pallidus. FK binding in the 6-h stress group tended to increase throughout the brain, rising significantly in the basal ganglia. PDBu binding in either stress group did not change significantly compared to the control group in any region except the hippocampal CA3 region of the 6-h stress group. Under immobilization stress, the adenylate cyclase system may undergo time-dependent and regionally specific changes, while the phosphoinositide system remains relatively stable.

Adenylyl Cyclases↗
PubMed1993

Transient cerebral vasodilatory effect of neuropeptide Y mediated by nitric oxide.

The effects of intracarotidly injected neuropeptide Y (NPY; 0.1 micrograms/kg) on the local cerebral blood volume (CBV) and blood flow (CBF) in the parieto-temporal cortex were examined by the photoelectric method in 17 anesthetized cats. CBV reflects the cumulative crosssectional area of the cerebral microvascular beds. NPY immediately caused transient but significant increases in CBV and CBF, which lasted for less than 5 min. Thereafter, CBV returned to and remained at the control level, although CBF was decreased by 30-40% for 60 min during the monitoring period. The CBV increases after NPY were prevented by a 15-min preinjection of 0.35 mg/kg/min of NG-monomethyl-L-arginine (L-NMMA), which is a competitive blocker of nitric oxide synthesis. The CBV increases after NPY reappeared following a 15-min administration of 0.25 mg/kg/min of L-arginine, which is a precursor of nitric oxide. We conclude that NPY administered in vivo exerts a previously unreported effect of transient vasodilatation on the cerebral microvessels. This action appears to be mediated by nitric oxide, which is a major candidate as an endothelium-derived relaxing factor (EDRF).

Animals↗
PubMed1993

Reduction in second-messenger ligand binding sites after brain ischemia--autoradiographic Bmax and Kd determinations using digital image analysis.

Changes in forskolin (FK) and phorbol 12,13-dibutyrate (PDBu) binding were evaluated in relation to local cerebral blood flow (CBF) after 6-h unilateral carotid artery occlusion in the gerbil striatum employing a quantitative autoradiographic method, which permitted these three parameters to be measured in the same brain. CBF was measured by the [14C]iodoantipyrine method at the end of the experiment. [3H]FK and [3H]PDBu were utilized as specific ligands to assess the activity of adenylate cyclase (AC) and protein kinase C (PKC), respectively. A saturation study was undertaken to measure the Kd (dissociation constant) and Bmax (maximal binding capacity) of each ligand by digital image processing of sequential autoradiograms employing pixel-by-pixel Scatchard analysis. The Bmax values of FK and PDBu were significantly decreased on the ischemic side, but the reduction in Bmax of FK was greater than that of PDBu. The K4 of each ligand remained unchanged. The FK binding underwent a progressive decline as CBF fell below 30 ml/100 g/min. The PDBu binding showed only a gradual decline in parallel with the CBF reduction. These findings suggest that a reduction in CBF below 30 ml/100 g/min for 6 h may induce a remarkable suppression of the AC system with less significant inhibition of the PKC system in the striatum.

Adenylyl Cyclases↗
PubMed1993

Inhibition of nitric oxide synthesis impairs autoregulation of local cerebral blood flow in the rat.

The effect of intravenous administration of NG-monomethyl-L-arginine (L-NMMA, 30 mg kg-1), a specific inhibitor of nitric oxide (NO) synthesis, on the autoregulation of local cerebral blood flow (LCBF) was examined in the rat using the [14C]iodoantipyrine autoradiographic method. LCBF was significantly lower in various superficial regions such as the cerebral cortices and cerebellar cortex and in several deep brain regions in animals with haemorrhagic hypotension induced after L-NMMA infusion (the L-NMMA + HEM group) compared with animals without haemorrhagic hypotension after L-NMMA infusion (the L-NMMA group). The present findings suggest that NO synthesis may play a crucial role in the autoregulation of LCBF in response to a reduction in blood pressure in the cerebral cortices, cerebellar cortex and several deep brain regions.

Animals↗
PubMed1993

Effects of sumatriptan on the cerebral intraparenchymal microcirculation in the cat.

1. Sumatriptan, a 5-hydroxytryptamine (5-HT)1-like receptor agonist, is effective against the headache of migraine. The effects of sumatriptan injected via the carotid artery on the cerebral microcirculation were studied in 10 anaesthetized cats. 2. The local cerebral blood volume (CBV), mean transit time of blood (MTT) and cerebral blood flow (CBF) in the parieto-temporal cortex were measured by a photoelectric method. CBV represents the cumulative dimensions of the cerebral microvessels. 3. Sumatriptan at 5 and 50 micrograms kg-1 had no significant effects on the CBV, MTT, CBF, and mean arterial blood pressure (MABP); 500 micrograms kg-1 of sumatriptan reduced the CBV, prolonged the MTT, and decreased the CBF (approximately -20%) without affecting the MABP. Sumatriptan, 5 mg kg-1, elicited transient reductions in CBV and CBF, which were attributable to the rapid and marked falls of MABP seen with this dose. 4. Thus, while a high dose of sumatriptan (500 micrograms kg-1) exhibits direct vasoconstrictor actions on the cerebral vessels, low doses of sumatriptan, within the therapeutic range, elicit no vasoconstriction. The data do not support a vasoconstrictor action of sumatriptan playing a primary role in reversing the headache of migraine.

Animals↗
PubMed1993

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

BACKGROUND AND PURPOSE: We examined the effect of ticlopidine hydrochloride on the enhanced erythrocyte aggregability in 14 patients with cerebral infarction during the chronic phase (over 1 month after onset). SUMMARY OF REPORT: Ticlopidine (100 mg BID) was administered for 8 weeks. We measured the rate of erythrocyte aggregation (aggregability), using the whole-blood erythrocyte aggregometer that we developed, before and at 4 and 8 weeks after the initiation of ticlopidine administration. Concomitant measurements were made of such blood factors as the hematocrit, albumin-globulin ratio, and fibrinogen concentration. The erythrocyte aggregation rates before and at 4 and 8 weeks after were 0.147 +/- 0.017/s, 0.138 +/- 0.019/s, and 0.133 +/- 0.017/s, respectively. The erythrocyte aggregation rates at 4 and 8 weeks were significantly lower (P < .05 by Bonferroni's modified t test) than those before ticlopidine administration. At 4 and 8 weeks after the initiation of ticlopidine treatment, the hematocrit value and concentration of fibrinogen were also significantly (P < .05) reduced. CONCLUSIONS: Our results suggest that ticlopidine can improve the enhanced erythrocyte aggregability in patients with cerebral infarction during the chronic phase.

Adult↗
PubMed1993

Changes of pial vessel diameter and CO2 reactivity during insulin-induced hypoglycemia and in the recovery period following glucose administration.

The present study examined the changes of cerebrovascular CO2 reactivity during insulin-induced hypoglycemia and in the recovery period following glucose administration in cats. The diameters of pial vessels were continuously measured using the vidicon camera system. Hypoglycemia was induced by intraperitoneal injection of Actrapid insulin (100 IU/kg). Cerebrovascular CO2 reactivity was estimated by the changes of pial vessel diameters during 3 min inhalation of 5% CO2 in air at each stage of glucose level. CO2 reactivity was impaired in the hypoglycemic stage and this impairment was further enhanced in the early recovery stage. In the late recovery stage, CO2 reactivity was restored particularly in the small arteries which were less innervated by autonomic nerves. These results suggest that the sympathetic activity plays an important role in the impairment of cerebrovascular CO2 reactivity during hypoglycemia.

Animals↗
PubMed1993

Alpha-adrenergic blockade with phenoxybenzamine enhances cerebrovascular CO2 reactivity.

The influence of sympathetic nervous activity on cerebral circulation and cerebrovascular CO2 reactivity was investigated by an alpha-adrenergic blockade with phenoxybenzamine (PBZ). Cerebral oxygen and carbon dioxide tension (BrPo2, BrPco2) and arterial blood pressure were continuously recorded before, during and after intracarotid infusion of 5 mg/kg of PBZ. The effects of 5% CO2 inhalation were measured before and after the infusion of PBZ. Following the intracarotid infusion of PBZ, BrPo2 and BrPco2 did not change significantly. After the alpha-adrenergic blockade the degree of the increase in BrPo2 during 5% CO2 inhalation was significantly enhanced. The increase in the cerebrovascular CO2 reactivity produced by low dose PBZ suggests that the sympathetic nervous system modifies cerebrovascular CO2 reactivity.

Animals↗
PubMed1993

Effect of clonidine on the cerebrovascular system in cats.

The effects of clonidine, a potent alpha 2 adrenergic agonist and an imidazole/imidazoline receptor agonist, were examined in the cat cerebrovascular system, measuring cerebral oxygen and carbon dioxide tension (BrPo2, BrPco2) and arterial blood pressure. Intracarotid injection of clonidine (2 micrograms/kg) produced a gradual decrease in systemic blood pressure without initial hypertension, while BrPo2 decreased slightly but significantly. Before and after intracarotid administration of clonidine, cerebrovascular reactivity to carbon dioxide was estimated by changes in BrPo2 and BrPco2 during and after 3 min inhalation of 5% CO2. Clonidine significantly enhanced cerebrovascular reactivity to carbon dioxide. The data suggest that the alpha 2-adrenoceptor and/or imidazoline receptor play an important role in the regulation of cerebral circulation.

Animals↗
PubMed1993

Effect of sympathetic nervous system stimulation on cerebrovascular CO2 responsiveness.

Cerebrovascular CO2 responsiveness, following noradrenaline (NA) infusion, was studied in the cat by continuous measurement of cerebral tissue oxygen tension (BrPO2), carbon dioxide tension (BrPCO2), pH (BrpH), and blood pressure (BP). Intravenous infusion of NA (1 microgram/kg/min) was done to stimulate the adrenergic nervous system. Inhalation of 5% CO2+air was performed for 3 minutes before, during, and after NA infusion. Cerebrovascular CO2 responsiveness was estimated from changes in BrPO2, BrPCO2, and BrpH. CO2 inhalation increased BrPO2, BrPCO2, and BP, but decreased BrpH, in the respective 3 stages. delta BrPO2 decreased significantly during NA infusion, but recovered after cessation of NA. NA infusion caused a decrease in CO2 responsiveness. This suggests that sympathetic hyperactivity can modify cerebrovascular CO2 responsiveness.

Animals↗
PubMed1993

[Alteration of inositol 1,4,5-trisphosphate receptor binding after 6-hour hemispheric ischemia in the gerbil brain].

Inositol 1,4,5-trisphosphate (IP3) has recently been known to play vital roles as one of the second messengers to control intracellular metabolism of calcium ion. Therefore, alterations of IP3 receptor binding and local cerebral blood flow (1CBF) were evaluated 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 in the same brain. Animals attaining more than 5 in their ischemic scores, which were assessed at 1 hour after the occlusion, were utilized. LCBF was measured by the 14C-iodoantipyrine method at the end of the experiment. After frozen brains were cut into serial slices on a cryostat, the IP3 receptor binding was evaluated in vitro by using 3H-inositol 1,4,5-trisphosphate as the ligand. LCBF fell below 10 ml/100 g/min in most of the cerebral regions on the occluded side. In contrast a significant reduction in IP3 binding was noted only in the hippocampus CA1 on the occluded side. The IP3 binding tended to decrease when the values of 1CBF were reduced below 20 ml/100 g/min in this region. These findings suggest that the selective alteration of IP3 receptor binding in the hippocampus CA1 may be closely associated with the selective vulnerability of this region to ischemia.

Animals↗