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Biomedical subjects

S Fujiwara

Publications and source records attributed to S Fujiwara.

At least 541 records · Page 30Linked to original sources
PubMed1983

[Echocardiographic findings in 3 cases of mucopolysaccharidosis].

Mucopolysaccharidosis (MPS) has been shown to cause cardiac involvements. However, echocardiographic features of MPS were not well understood. We examined echocardiographic findings in three adult patients with MPS. The diagnosis was confirmed by measuring urinary acid mucopolysaccharide and alpha-L-iduronidase activity in the white blood cell and skin fibroblast. The age ranged from 29 to 54 years. Two patients were Scheie syndrome (MPS I-S) and one was suspected to be Maroteaux-Lamy syndrome (MPS VI). All patients had a systolic heart murmur suggestive of aortic stenosis, and one had an additional apical systolic murmur consistent with mitral regurgitation. The echocardiogram revealed the following findings; 1) an abnormal thickening of all aortic leaflets with reduced valve opening in all cases, 2) diffuse and marked thickening of the mitral leaflets, chordae and papillary muscles, no upward motion of the posterior mitral leaflet in spite of reduced E-F slope (13, 23 and 17 mm/sec, respectively), and slight narrowing of the mitral orifice, and 3) a slightly thickened and dilated left ventricle (IVS: 11, PW: 12, EDd: 58, and ESd 44 mm) in the case with Maroteaux-Lamy syndrome. The last finding was probably due to deposition of mucopolysaccharide in the myocardium, because the coronary arteriogram in this case did not demonstrate any significant lesions. The echocardiographic characteristics in our adult MPS cases were similar to those reported in infant or juvenile cases with Hurler syndrome (MPS 1-H) or Hunter syndrome (MPS II). However, our Maroteaux-Lamy patient may be the first case, in which myocardial involvement by mucopolysaccharide was suggested echocardiographically.

Adult↗
PubMed1982

Development of glutamate:glyoxylate aminotransferase in the cotyledons of cucumber (Cucumis sativus) seedlings.

Glutamate:glyoxylate aminotransferase had been reported to be present exclusively in the peroxisomes of plant leaves and to participate in the glycollate pathway in leaf photorespiration (Tolbert (1971) Annu. Rev. Plant Physiol. 22, 45-74]. Glutamate:glyoxylate aminotransferase activity was already present in the etiolated cotyledons of cucumber (Cucumis sativus) seedlings, and increased during greening. The enzyme was present only in the cytosol of the etiolated cotyledons and appeared in the peroxisomes during greening. The enzyme was purified to homogeneity from the cytosol of the etiolated cotyledons and from the peroxisomes of the green cotyledons of cucumber seedlings. The two enzyme preparations had nearly identical enzymic and physical properties. On the basis of these findings, roles of glutamate:glyoxylate aminotransferase in the glycollate pathway in photorespiration, and the mechanism of its appearance in the peroxisomes during greening, are discussed.

Glutamates↗
PubMed1982

Coronary circulatory failure and thromboxane A2 release during coronary occlusion and reperfusion in anaesthetised dogs.

Attempts were made to demonstrate release of vasoactive substances from the heart during coronary occlusion (for 60 min) and reperfusion (for 60 min), and to clarify the pathophysiological significance of them. Vasoactive substances were detected by superfusion of rabbit aortic and dog coronary arterial strips with great coronary venous blood. Plasma thromboxane (TX) B2 was radioimmunologically assayed. Gradually developing, sustained contraction of both vascular strips was noted during coronary occlusion and reperfusion, while a transient contraction in rabbit aortic and relaxation in dog coronary arterial strips were seen immediately after reperfusion. The TXB2 released into the great coronary venous blood significantly increased during occlusion and reperfusion. Indomethacin treatment of the dog abolished the sustained contraction of both vascular strips and TXB2 release. The transient contraction of rabbit aorta after reperfusion was inhibited by phenoxybenzamine. Reactive hyperaemia following a 60 min occlusion was significantly depressed, as compared with that following 30 s to 30 min occlusion, and the depression was alleviated by indomethacin and imidazole. These results suggest that catecholamine(s) and TXA2 are released during coronary occlusion and reperfusion, and that the latter might be responsible for the coronary circulatory failure during reperfusion of irreversibly damaged myocardium.

Animals↗
PubMed1982

Proton magnetic resonance spectroscopy of an essential histidyl residue in a milk-clotting acid protease, Mucor rennin.

The location and state of an essential histidyl residue in a milk-clotting acid proteases, Mucor rennin, were investigated by NMR spectroscopy. Assignment of the C2H resonance peak of the essential histidyl residue was possible by comparison of the NMR spectrum of the native enzyme with that of the photo-oxidized enzyme. The pH titration curve for the chemical shift of the C2H proton showed two inflections, a major one with pKa = 7.4 and a minor one with pKa = 3.5 at 30 degrees C. The major inflection, corresponding to an intrinsic protonation of the imidazole ring, shifted toward the alkaline side upon addition of acetyl pepstatin, an inhibitor specific for the acid protease. Modification of an essential carboxyl group in the enzyme with diazoacetyl-DL-norleucine caused disappearance of the minor inflection as well as an acidic shift of the major pKa value. Perturbation effects on the C2H resonance of the lanthanide metals, Pr3+, Eu3+, and Gd3+, suggested their selective binding to a carboxyl group and location of the bound metal atom close to the essential histidyl residue. All data suggested that the essential histidyl residue of Mucor rennin is located close to one of the two essential carboxyl groups in the catalytic site of the enzyme.

Animals↗
PubMed1982

Metabolism of urea and glyoxylate, degradative products of purines in marine animals.

In marine fish and crustacean liver, degradative enzymes able to convert purines to urate have been shown to be located only in the cytosol, and degradative enzymes able to convert urate to urea and glyoxylate, only in the peroxisomes (Noguchi, T., Takada, Y., & Fujiwara, S. (1979) J. Biol. Chem. 254, 5272-5275). The subcellular distribution of these two enzymes involved in further metabolism of urea and glyoxylate in marine animal species was examined by centrifugation in a sucrose density gradient. Urease was located only in the cytosol of crustacean and mollusc liver; no activity was detected with fish liver. In fish, crustacean and mollusc liver, the conversion of glyoxylate to glycine may be mainly catalyzed by alanine : glyoxylate aminotransferase. Hepatic alanine: glyoxylate aminotransferase was located both in the mitochondrial matrix and in the cytosol in each species studied. These findings suggest that peroxisomal urea is transported to the cytosol then degraded to NH3 for the excretion of purine nitrogens, while peroxisomal glyoxylate is transported to the cytosol or mitochondria then converted to glycine for the reutilization of purine carbons.

Animals↗
PubMed1982

Diltiazem-induced vasodilatation of smooth muscle cells of the canine basilar artery.

1 The effects of diltiazem on smooth muscle cells of the canine basilar artery were investigated by means of microelectrode, double sucrose gap and isometric tension recording methods. 2 The mean membrane potential of the smooth muscle cells was -49.8 mV and they were electrically quiescent. Diltiazem (over 10(-5) M) depolarized the membrane. After pretreatment with 5 and 10 mM tetraethylammonium (TEA), an outward current pulse (1 and 2 s in duration) produced a spike and this spike was abolished by application of 10(-5) M diltiazem. 3 The spike could also be generated by the excitatory junction potential (e.j.p.) evoked by perivascular nerve stimulation (0.05 ms in pulse duration) in the presence of 5 mM TEA. Diltiazem (greater than 10(-6) M) suppressed both the spike and the e.j.ps, the suppression being more apparent for spike generation. The amplitude of the e.j.ps was reduced by diltiazem in concentrations greater than 10(-6) M. The effects were dose-dependent: when the amplitude of e.j.ps was reduced by application of diltiazem, the resulting mechanical response was also proportionally smaller. 4 The contractions evoked by 128 mM [K]o, 10(-3) M adenosine 5'-triphosphate (ATP) or, NaCl-free solution were abolished in Ca-free solutions containing 2 mM EGTA, but the amplitude of caffeine-induced contraction (10 mM) was only slightly reduced. Diltiazem, in concentrations above 3 X 10(-7) M suppressed the contraction evoked by excess [K]o, ATP or caffeine, but the inhibitory action of diltiazem on the K-induced contraction was greatest. 5 Following pretreatment with 2.5 mM [Ca]o, a contraction was evoked by caffeine in Ca-free solution. The amplitude of the caffeine-induced contraction was increased by simultaneous application of 2.5 mM [Ca]o with 128 mM [K]o and to a lesser extent by simultaneous application of 2.5 mM [Ca]o with 5.9 mM [K]o. The amplitude of the caffeine-induced contraction generated in the presence of 5.9 mM or 128 mM [K]o was suppressed to the same extent by application of diltiazem [10(-5) M) during preincubation in [Ca]o. This result suggests that the Ca stored in cell is replenished by Ca-influx from [Ca]o during the resting and active states of the membrane, and that diltiazem has no effect on the mobilization of Ca stored in the cell. 6 Thus, diltiazem acts on the canine basilar artery suppressing the Ca-influx during the active condition as a Ca-spike suppressor and the voltage-dependent Ca-influx induced by excess [K]o or by chemical depolarization. Diltiazem has no effect on the Ca mobilization from the store site. This agent also suppresses the amplitude of e.j.ps due to inhibition of the release of chemical transmitter from nerve terminals following the suppression of the Ca-influx. Diltiazem appears to act as a vasodilator on the canine basilar artery.

Adenosine Triphosphate↗
PubMed1982

Membrane properties and excitatory neuromuscular transmission in the smooth muscle of dog cerebral arteries.

1 Drug actions on electrical and mechanical properties of smooth muscle cells and neuromuscular transmission in the canine cerebral arteries were investigated by use of microelectrode and isometric tension recording methods. 2 In the basilar and middle cerebral arteries, the resting membrane potentials were--49.4 mV and -51.7 mV, respectively, the length constants 0.57 mm and 0.45 mm, respectively and the time constants 142 ms and 118 ms, respectively. 3 Outward current pulses did not evoke the spike in either artery but did evoke the spike under conditions of pretreatment with 10 mM tetraethylammonium (TEA). 4 The maximum slope of depolarization produced by a ten fold increase in [K]o plotted on a log scale was 40.1 mV in the basilar artery and 42.2 mV in the middle cerebral artery. 2-Nicotinamidoethyl nitrate, the K-permeability accelerator, had no effect on the membrane potential. 5 K-free or ouabain [10(-5)M] treatment slightly depolarized the membrane. Re-addition of K [5.9 mM] hyperpolarized the membrane by several mV. Thus, the contribution of an active Na-K pump in the membrane potential seems to be small. 6 In both arteries, acetylcholine, adenosine, noradrenaline and isoprenaline in concentrations up to 10(-5)M did not modify the membrane potential and resistance, while 5-hydroxytryptamine (over 10(-8)M) and ATP (over 10(-5)M) depolarized the membrane, decreased the membrane resistance and produced a dose-dependent contraction. Adenosine suppressed the contraction evoked by excess [K]o (39.8 mM). 7 Perivascular nerve stimulation produced excitatory junction potentials (e.j.ps). Often e.j.ps were followed by a hyperpolarization. Repetitive stimulation produced facilitation after several stimuli and depression followed. In some cells, this depression appeared without facilitation. 8 The e.j.ps ceased with pretreatment with guanethidine (10(-6)M) or tetrodotoxin (3 X 10(-7)M), while phentolamine (10(-7)M) and yohimbine (10(-7)M) enhanced the amplitude of e.j.ps. ATP (10(-5)M) and noradrenaline (10(-6)M) suppressed and prazosin had little effect on the e.j.ps. Atropine (10(-6)M) also had no effect on the e.j.ps. 9 Specific features of the cerebral artery and systemic vascular beds were compared, and the features of adrenoceptors on the smooth muscle membrane were compared with findings in other vascular beds.

Animals↗
PubMed1982

Impaired lactate production by skeletal muscle with anaerobic exercise in patients with chronic renal failure. A possible consequence of defective glycolysis in skeletal muscle.

The lactate concentration in antecubital venous blood was determined in 33 patients before and after ischemic forearm exercise. Before exercise, there wa no significant difference in serum lactate level between uremic patients and controls. However, after ischemic exercise the means serum lactate level in uremic patients was significantly lower than that of controls. The results may lead to the conclusion that uremic patients have a markedly reduced ability to form lactate with anaerobic exercise probably due to inhibition of glycolytic enzymes of skeletal muscle.

Adult↗
PubMed1982

Neurogenic electrical responses of single smooth muscle cells of the dog middle cerebral artery.

Electrical responses induced by perivasascular nerve stimulation were recorded intracellularly from the smooth muscle of dog middle cerebral artery. With nerve stimulation, the muscle membrane produced excitatory junction potential and then a slow hyperpolarization. The excitatory junction potential showed facilitation and the slow hyperpolarization showed depression phenomena, when the nerves were stimulated with twin pulses. Generation of the slow hyperpolarization was associated with an increase in the potassium conductance of the membrane and was suppressed by tetraethylammonium, which depolarized the membrane, reduced the membrane conductance, and increased the amplitude of the excitatory junction potential. Treatment with 6-hydroxydopamine abolished the excitatory junction potential, but not the slow hyperpolarization; the latter was suppressed by tetrodotoxin. The amplitude of slow hyperpolarization was decreased by application of tetraethylammonium or ATP, but was not affected by application of atropine, neostigmine, theophylline, apamin, ouabain, norepinephrine, propranolol, or guanethidine. ATP produced transient depolarization of the membrane with associated decrease in the membrane resistance. The excitatory junction potential was attributed to activation of the noradrenergic nerves, whereas the slow hyperpolarization was not generated by activation of adrenergic, cholinergic, or purinergic receptors. Inasmuch as the electrogenic Na-K pump, cAMP, and ATP were not involved in the generation of slow hyperpolarization, the possibility of an unidentified chemical transmitter should be given attention.

Animals↗