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Biomedical subjects

M Fujishima

Publications and source records attributed to M Fujishima.

At least 199 records · Page 11Linked to original sources
PubMed1998

Auditory evoked neuromagnetic response in cerebrovascular diseases: a preliminary study.

OBJECTIVES: Magnetoencephalography (MEG) measures aspects of the function of the auditory cortex of the human brain with high spatial resolution. The objective was to determine whether MEG also accurately identifies the auditory cortex of the brain in patients with ischaemic stroke. METHODS: The auditory evoked magnetic field (AEF) was examined after stimuli of 1 kHz tone bursts in 24 stroke patients without apparent infarcts in the auditory cortex, and compared the topography of sources of 50 ms (P50m) and 100 ms latency deflections (N100m), the most prominent components of middle and long latency AEFs, with that of 12 normal subjects. Cerebral haemodynamics in and around the auditory cortex were evaluated using PET. RESULTS: In nine of 24 stroke patients, the accurate magnetic sources of P50m or N100m were not identified. The distribution of P50m sources varied more widely than N100m. Eight of these nine patients had severe stenotic lesions in the carotid or middle cerebral arterial trunks. Patients with abnormal P50m responses had decreased supratemporal and hemispheric blood flow compared with patients with normal P50m responses. CONCLUSIONS: These findings suggest that large vessel disease with disturbed cerebral haemodynamics in and near the auditory cortex tend to affect AEFs, especially the middle latency components. This is the first combined study of MEG and PET to show a significant correlation between AEF responses in stroke patients and their PET indices.

Adult↗
PubMed1998

Cerebral blood flow and metabolism in patients with silent brain infarction: occult misery perfusion in the cerebral cortex.

OBJECTIVES: Silent brain infarction (SBI) is of growing interest as a possible risk factor for symptomatic stroke. Although morphological characteristics of SBI have been well defined, their characteristic patterns of cerebral blood flow (CBF) and metabolism are in dispute. The purpose of this study was to elucidate CBF and metabolism in patients with SBI in relation to symptomatic stroke. METHODS: The patients underwent PET and were separated into three groups; control group (C group), with no lesions on CT (n=9, mean age 57), SBI group, with no neurological signs or history of stroke, but with ischaemic lesions on CT (n=9, mean age 63), and brain infarction group (BI group), with neurological deficits and compatible CT lesions in the area supplied by perforating arteries (n=19, mean age 56). Regional CBF, oxygen extraction fraction (OEF), cerebral metabolic rate for oxygen (CMRO2), and cerebral blood volume (CBV) were measured by PET. RESULTS: Mean values for CBF to the cerebral cortex and deep grey matter were lower in the SBI group (31.6 (SD 5.8) and 34.3 (SD 6.9) ml/100 g/min, respectively) and in the BI group (30.8 (SD 5.2), 33.9 (SD 5.9), respectively) than in the C group (36.0 (SD 6.6) and 43.5 (SD 9.5), respectively). Although mean CMRO2 of deep grey matter (2.36 (SD 0.52) ml/100 g/min) was significantly decreased in the SBI group compared with the C group (2.76 (SD 0.480), p<0.01), CMRO2 of the cortical area was as well preserved in the SBI patients (2.36 (SD 0.39)) as in the controls (2.48 (SD 0.32)) with a compensatory increase of mean OEF (0.45 (SD 0.06) and 0.41 (SD 0.05), respectively). CONCLUSIONS: Patients with SBI showed decreased CBF and CMRO2 in deep grey matter. On the other hand, decreased CBF with milder increased OEF, resulting in preserved CMRO2 in the cerebral cortex indicates the presence of occult misery perfusion, suggesting that patients with SBI have reduced cerebral perfusional reserves.

Adult↗
PubMed1998

Central nitric oxide attenuates the baroreceptor reflex in conscious rabbits.

We examined the role of central nitric oxide (NO) in the baroreceptor reflex in conscious rabbits. Intracerebroventricular infusion of 20 mumol of N omega-nitro-L-arginine methyl ester (L-NAME) to block central NO resulted in increases in arterial pressure, renal sympathetic nerve activity (RSNA), and plasma catecholamine levels, and the pressor response was suppressed by pretreatment with pentolinium (5 mg/kg i.v.). On the other hand, a subpressor dose of intracerebroventricular L-NAME (10 mumol/h) caused significant increases in baroreflex sensitivities assessed by RSNA and heart rate compared with vehicle infusion [maximum gain: -18.2 +/- 0.9 vs. -9.6 +/- 0.9%/mmHg (P < 0.001) and -14.3 +/- 2.3 vs. -5.7 +/- 0.4 beats.min-1.mmHg-1 (P < 0.05), respectively]. Conversely, an intracerebroventricular infusion of Et2N[N(O)NO]Na, an NO donor (1 mumol/h) significantly attenuated the baroreflex sensitivities. However, intracerebroventricular infusion of N omega-nitro-D-arginine methyl ester (10 mumol/h), an enantiomer of L-NAME, failed to alter the baroreflex sensitivities. These results suggest that 1) the pressor response induced by inhibition of central NO synthesis is mainly mediated by the enhanced sympathetic outflow and 2) central NO attenuates the baroreflex control of RSNA and heart rate in conscious rabbits.

Animals↗
PubMed1998

Crescentic glomerulonephritis due to rifampin treatment in a patient with pulmonary atypical mycobacteriosis.

A 64-year-old male was treated continuously with rifampin, isoniazid and streptomycin for pulmonary atypical mycobacteriosis, Mycobacterium kansasii. Five weeks after beginning the treatment, the patient suddenly developed acute renal failure. A renal biopsy showed crescentic lesions characteristic of rapidly progressive glomerulonephritis with moderate interstitial changes. Serum antirifampin antibody was detected, and the cessation of rifampin treatment was followed by a rapid spontaneous recovery of the patient's renal function. This is, to our knowledge, the first case of rapidly progressive crescentic glomerulonephritis associated with rifampin treatment where circulating antirifampin antibody is demonstrated and the renal function spontaneously improved after discontinuing rifampin treatment.

Antibiotics, Antitubercular↗
PubMed1998

Localization of TGF-beta and its receptors in the kidney.

This paper reviews the expression and localization of proteins of the TGF-beta system in the kidney, i.e. TGF-beta isoforms, latent TGF-beta binding protein, and receptors. There is heterogeneity of TGF-beta isoforms, binding proteins and receptors. TGF-betas are more evenly distributed among different segments of the nephron than TGF-beta receptors, and are expressed by almost all cell types in the kidney. The spatial distribution of TGF-beta and its signaling receptor may help to better understand the biologic function of TGF-beta in the kidney.

Animals↗
PubMed1998

Stretch-activated channels in arterial smooth muscle of genetic hypertensive rats.

Electrical and contractile responses of small arteries to mechanical stress are reportedly enhanced in spontaneously hypertensive rats (SHR), compared with those in Wistar Kyoto rats (WKY). We have previously shown that stretch-activated cation channels exist in arterial smooth muscle membrane, of which opening causes Na+ and Ca2+ influx and membrane depolarization. We thus hypothesize that activation of stretch-activated channels is enhanced in arterial smooth muscle of SHR compared with WKY. To test this hypothesis, stretch-activated currents were recorded in single smooth muscle cells of resistance mesenteric arteries from SHR and WKY (16 to 24 weeks of age). In the whole-cell recording, membrane stretch was applied by inflating the cell with positive pressure to the recording pipette. Cell-inflation evoked Gd3+-sensitive cation currents. This current appeared with less stretch stimulation and its amplitude was larger in SHR cells compared with WKY cells. In the cell-attached recording, suction to the recording pipette evoked single stretch-activated channel currents (conductance of 32 pS with 150 mmol/L Na+), which were blocked by Gd3+. Channels were activated with less negative pressure and their availability was greater in SHR cells than in WKY cells. Results suggest that the activation of stretch-activated channels is enhanced in smooth muscle of resistance arteries from SHR compared with WKY, which may contribute to the enhanced vascular responses to mechanical stress in SHR.

Animals↗
PubMed1998

Antihypertensive treatment and the responsiveness to glutamate in ventrolateral medulla.

We have recently reported that the cardiovascular responses to excitatory amino acids are augmented in the rostral ventrolateral medulla of spontaneously hypertensive rats (SHR). In the present study, we investigated whether the responsiveness to excitatory amino acids would be normalized by antihypertensive treatment. Thus we treated 4-week-old SHR and age-matched Wistar-Kyoto (WKY) rats with either enalapril (25 mg/kg per day in drinking water) or vehicle for 8 weeks. At 12 weeks of age, systolic blood pressure in the untreated SHR (248+/-9 mm Hg) was significantly (P<.01) higher than that in the enalapril-treated SHR (140+/-4 mm Hg), untreated WKY rats (148+/-4 mm Hg), and enalapril-treated WKY rats (117+/-1 mm Hg). The pressor responses to L-glutamate (2 nmol) microinjected into the rostral ventrolateral medulla were similar in enalapril-treated and untreated SHR (40+/-5 and 47+/-3 mm Hg, respectively, NS), and these responses were significantly greater than that seen in the untreated WKY rats (24+/-2 mm Hg, P<.01). On the other hand, the pressor response to either N-methyl-D-aspartate, an ionotropic glutamate receptor agonist, or (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid, a metabotropic glutamate receptor agonist, in the enalapril-treated SHR was slightly but significantly smaller than that in the untreated SHR but was still markedly greater than those in untreated and enalapril-treated WKY rats. These results suggest that the augmented responsiveness to excitatory amino acids in the rostral ventrolateral medulla of SHR may be at least partly genetically determined and cannot be normalized by the treatment with enalapril.

Animals↗
PubMed1998

Role of tyrosine kinase in dilator responses of rat basilar artery in vivo.

We tested the hypothesis that dilator responses of the basilar artery to endothelium-dependent vasodilators are mediated by activation of tyrosine kinase in vivo. Using a cranial window in anesthetized rats, we examined responses of the basilar artery to acetylcholine and bradykinin. Topical application of acetylcholine and bradykinin increased diameter of the basilar artery in a concentration-related manner. Genistein, an inhibitor of tyrosine kinase, did not affect baseline diameter of the basilar artery but inhibited vasodilatation in response to acetylcholine and bradykinin, without affecting vasodilatation produced by sodium nitroprusside. Tyrphostin 47, another inhibitor of tyrosine kinase, attenuated acetylcholine-induced dilatation of the basilar artery without affecting vasodilatation in response to sodium nitroprusside. Tyrphostin 63, an inactive analogue of tyrphostin 47, did not affect acetylcholine-induced vasodilatation. Sodium orthovanadate, an inhibitor of tyrosine phosphatase, enhanced acetylcholine-induced dilatation of the basilar artery. These results suggest that dilator responses of the basilar artery to endothelium-dependent agonists, acetylcholine and bradykinin, are mediated in large part by activation of tyrosine kinase. Because vasodilatation produced by these agonists is mediated primarily by nitric oxide, activation of tyrosine kinase may have an important role in nitric oxide production in the basilar artery in vivo.

Acetylcholine↗
PubMed1998

Enhanced depressor response to nitric oxide in the rostral ventrolateral medulla of spontaneously hypertensive rats.

Possible impairment of the L-arginine-nitric oxide (NO) pathway in the rostral ventrolateral medulla of adult spontaneously hypertensive rats (SHR) was investigated by microinjecting N(G)-nitro-L-arginine methyl ester (L-NAME), NOC 18 (an NO donor), or L-arginine. Unilateral injection of L-NAME (10 nmol/50 nL) into the rostral ventrolateral medulla significantly increased mean arterial pressure (MAP) in both SHR and Wistar-Kyoto rats (WKY). The increases in MAP did not differ significantly between the two strains (15+/-3 versus 10+/-2 mm Hg, respectively; n=8). In contrast, microinjection of L-arginine elicited significant (P<.05) dose-dependent decreases in MAP in both strains, and these depressor responses were significantly greater in SHR than in WKY (in 10 nmol of L-arginine: -29+/-2 versus -15+/-2 mm Hg, respectively; n=8, P<.01). Similarly, microinjection of NOC 18 (10 nmol/50 nL) reduced MAP in both strains, and the depressor response was also significantly greater in SHR than in WKY (-38+/-7 versus -22+/-3 mm Hg, respectively; n=8, P<.05). These results suggest that the L-arginine-NO pathway in the rostral ventrolateral medulla is impaired in SHR and that this impairment may contribute to the increase in arterial pressure in this animal model of genetic hypertension.

Animals↗
PubMed1998

Single L-type calcium channels in smooth muscle cells from resistance arteries of spontaneously hypertensive rats.

The amplitude of the whole-cell L-type Ca2+ channel current recorded from vascular smooth muscle cells is reportedly greater in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto rats (WKY). However, no study has examined properties of single Ca2+ channels in arterial cells from these strains. To further test the hypothesis that activation of L-type Ca2+ channels in arterial smooth muscle cells would be enhanced in SHR, we recorded single Ca2+ channel currents in resistance mesenteric artery cells from SHR and WKY (8 to 9 weeks of age) using a cell-attached patch clamp technique. With 50 mmol/L Ba2+ in the recording pipette, the depolarizing pulse from a holding potential of -40 mV evoked the single L-type Ca2+ channel current. Opening of the single channels was more frequent in cells from SHR than from WKY. Single-channel conductance (20 pS) and open time (1 ms at 0 mV) did not differ in the two strains. The results suggest that an increased amplitude of the whole-cell current can be attributed to the enhanced opening of single Ca2+ channels in the arterial smooth muscle cells from SHR compared with WKY.

Animals↗
PubMed1998

Effects of high atmospheric pressure and oxygen on middle cerebral blood flow velocity in humans measured by transcranial Doppler.

BACKGROUND AND PURPOSE: There are several reports that have studied the effects of hyperbaric oxygen (HBO) on cerebral blood flow (CBF). However, most of the reports have been of animal experiments, and human studies are few so far. The aim of this study is to clarify the relationship between HBO and CBF in humans. METHODS: Middle cerebral arterial blood flow velocity (MCV) was measured using transcranial Doppler (TCD) technique in a multiplace hyperbaric chamber. The Doppler probe was fixed on the temporal region by a head belt, and the transcutaneous gas measurement apparatus (tcPO2 and tcPCO2) was fixed on the chest wall. MCV and transcutaneous gas were measured continuously in eight healthy volunteers under four various conditions: 1 atmosphere absolute (ATA) air, 1 ATA oxygen (O2), 2 ATA air, and 2 ATA O2. On the next step, the effect of environmental pressure was studied in another eight healthy volunteers, in whom the tcPO2 was kept at almost the same level under conditions of both 1 ATA and 4 ATA by inhaling oxygen at 1 ATA. RESULTS: MCV of 1 ATA O2, 2 ATA air, and 2 ATA O2 decreased, and tcPO2 increased significantly in comparison with that of 1 ATA air. A significant difference in MCV was observed between the O2 group and the air group under the same pressure circumstance. On the other hand, there were no differences in MCV or tcPO2 between 4 ATA air and 1 ATA plus O2, and the influence for the MCV of the environmental pressure was not observed. CONCLUSIONS: We conclude that hyperoxemia caused by HBO reduces the CBF, but the high atmospheric pressure per se does not influence the CBF in humans.

Adult↗
PubMed1998

Role of tyrosine kinase in serotonin-induced constriction of the basilar artery in vivo.

BACKGROUND AND PURPOSE: Serotonin is one of the most potent constrictors of cerebral blood vessels and is implicated in several pathological conditions, including migraine and cerebral ischemia. Recent evidence has suggested that tyrosine kinase is involved in vasocontractile responses. The objective of this study was to test the hypothesis that activation of tyrosine kinase contributes to serotonin-induced constriction of the basilar artery in vivo. METHODS: Using a cranial window in anesthetized Sprague-Dawley rats, we examined effects of inhibitors of tyrosine kinase and tyrosine phosphatase on constrictor responses of the basilar artery to serotonin in vivo. RESULTS: Serotonin (10(-8), 10(-7), and 10(-6) mol/L) produced constriction of the basilar artery by 12+/-2%, 27+/-2%, and 37+/-3%, respectively. Genistein (3 x 10(-6) mol/L), an inhibitor of tyrosine kinase, did not affect baseline diameter of the basilar artery but attenuated serotonin-induced vasoconstriction (P<.05 versus control responses). Daidzein, an inactive analogue of genistein, did not affect serotonin-induced constriction of the basilar artery. Tyrphostin 47 (10(-5) mol/L), another inhibitor of tyrosine kinase, also attenuated serotonin-induced vasoconstriction, and tyrphostin 63, an inactive analogue of tyrphostin 47, did not affect the vasoconstriction. Sodium orthovanadate (10(-5) mol/L), an inhibitor of tyrosine phosphatase, enhanced serotonin-induced vasoconstriction. Phorbol 12,13-dibutyrate, a direct activator of protein kinase C, also caused constriction of the basilar artery, which was not affected by genistein or sodium orthovanadate. CONCLUSIONS: These results suggest that serotonin-induced constriction of the basilar artery is mediated, at least in part, by activation of tyrosine kinase in vivo.

Analysis of Variance↗
PubMed1998

Blood pressure control and recurrence of hypertensive brain hemorrhage.

BACKGROUND AND PURPOSE: Recent studies have demonstrated that recurrence of hypertensive brain hemorrhage (HBH) is not uncommon. However, risk factors for the recurrence of HBH have not been evaluated systematically. METHODS: We analyzed 74 patients with HBH who were admitted to our clinic and followed up as outpatients for a mean of 2.8 years. Blood pressure (BP) and other clinical features were compared between the groups of patients with and without rebleeding. We determined the recurrence rate of HBH in relation to BP. RESULTS: Diastolic BP was significantly higher in the recurrence group than in the nonrecurrence group (88+/-8 versus 82+/-7 mm Hg; P=0.04). Systolic BP and other clinical variables were not different between the groups. The recurrence rate was 10.0% per patient-year in patients with diastolic BP >90 mm Hg and <1.5% in those with lower diastolic BP (P<0.001). No patients with diastolic BP <70 mm Hg experienced rebleeding. CONCLUSIONS: Higher diastolic BP was related to an increased rate of rebleeding. Diastolic BP >90 mm Hg may be regarded as a factor predictive of the recurrence of HBH.

Adult↗
PubMed1998

Photothrombotic middle cerebral artery occlusion in spontaneously hypertensive rats: influence of substrain, gender, and distal middle cerebral artery patterns on infarct size.

BACKGROUND AND PURPOSE: To analyze the effects of substrain and gender differences in spontaneously hypertensive rats (SHR) and distal middle cerebral artery (MCA) branching patterns on infarct size, we compared infarct volumes produced by photothrombotic distal MCA occlusion using SHR/Kyushu and SHR/Izumo (Izm). METHODS: Twenty-four male and 8 female SHR/Kyushu, 15 male and 5 female SHR/Izm, and 6 male Wistar-Kyoto rats (WKY)/Izm (5 to 7 months old) were subjected to photothrombotic distal MCA occlusion, and infarct volumes were determined. RESULTS: Although blood pressure levels were essentially the same between the two substrains of hypertensive rats, infarct volumes were significantly larger in the SHR/Kyushu substrain than in SHR/Izm of either sex (P<0.001); infarct volumes in male and female SHR/Kyushu were 83.8+/-11.7 and 58.5+/-9.2 mm3, and those in male and female SHR/Izm were 61.5+/-10.7 and 34.8+/-7.9 mm3, respectively (values are mean+/-SD). Male SHR/Kyushu that had simple Y-shaped MCA showed smaller infarcts (75.8+/-14.6 mm3, n=11) than those with more branching (regular) MCA (93.2+/-19.1, n=13), the difference being significant (P=0.022). Male SHR/Izm with simple distal MCA also produced smaller infarctions than those with regular MCA (51.0+/-3.7 versus 68.9+/-8.7 mm3, P=0.0004). CONCLUSIONS: Photothrombotic occlusion of distal MCA in hypertensive rats provides a simple and reproducible model of focal ischemia. Most importantly, this study emphasizes the substantial variabilities in infarct sizes caused by the differences in substrains of SHR, gender, and distal MCA patterns.

Animals↗
PubMed1998

Circumferential spontaneous coronary artery dissection in an elderly man: a case report.

An 82-year-old man developed acute inferior myocardial infarction. Emergent coronary angiography demonstrated thrombotic occlusion in the right coronary artery. Intracoronary thrombolytic therapy was performed with successful recanalization. However, circumferential dissection with luminal stenosis was revealed at the point of thrombus formation. Repeat angiography 6 months later showed resolution of the dissection. This is the first description of circumferential spontaneous coronary artery dissection. In addition, the present patient is older than any previous patients.

Aged↗
PubMed1998

Asymptomatic moyamoya disease associated with coronary and renal artery stenoses--a case report.

Moyamoya disease is an occlusive intracranial arteriopathy with abnormal cerebral vascular collateral networks. Although this disease is known to be associated with stenosis of extracranial arteries, such as the renal artery, a case associated with stenoses of the coronary and renal arteries has not been reported. We described here a 23-year-old man who had effort angina, renovascular hypertension, and asymptomatic moyamoya disease. Arterioangiography revealed bilateral occlusion of the intracranial carotid arteries and stenoses in the left coronary artery and the left renal artery.

Adult↗
PubMed1998

Obesity induced by neonatal monosodium glutamate treatment in spontaneously hypertensive rats: an animal model of multiple risk factors.

The present study was designed to develop an animal model of multiple risk factors, including obesity, hypertension, non-insulin-dependent diabetes mellitus, and hyperlipidemia. Hypothalamic obesity was induced by neonatal monosodium glutamate (MSG) treatment in spontaneously hypertensive rats (SHR). Female newborn SHR were treated intraperitoneally with 2 or 4 mg/kg body weight of MSG for 5 days. Obesity developed in SHR treated with 4 mg/kg of MSG but not in SHR treated with 2 mg/kg of MSG. Obese SHR had impaired glucose tolerance, hyperinsulinemia, and hypertriglyceridemia. However, the severity of hypertension was attenuated in obese SHR as compared with control SHR. The degree of obesity was closely related to the metabolic abnormalities, but inversely correlated with the blood pressure level. Macrovascular changes were investigated in obese SHR at 14 months of age. Intimal thickening was accelerated in the carotid artery of obese SHR as compared with that of nonobese SHR. Aortic contents of DNA and total cholesterol were significantly increased in obese SHR. SHR associated with MSG-induced obesity showed major manifestations of metabolic syndrome X. This animal model may be useful to study the clustering of risk factors for the development of macrovascular diseases.

Animals↗