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Biomedical subjects

S Kikuchi

Publications and source records attributed to S Kikuchi.

At least 433 records · Page 24Linked to original sources
PubMed1986

Isolation and partial characterization of a very long-chain fatty acid desaturation system from the cytosol of Mycobacterium smegmatis.

The supernatant fraction after 105,000 X g centrifugation of an extract of sonically disrupted cells of Mycobacterium smegmatis catalyzed the desaturation of lignoceroyl-CoA to a delta15-monounsaturated derivative in the presence of molecular oxygen and NADPH. This desaturation system was separated by ammonium sulfate fractionation, gel filtration, DEAE-cellulose column chromatographies, and affinity column chromatography on immobilized dye, into three components; a NADPH-oxidase, a ferredoxin-containing fraction and a desaturase, all of which were required for the reconstituted desaturation system for lignoceroyl-CoA. This system was inhibited by FMN and ferrous ions but not by KCN. All of these features clearly distinguish this system from the previously known fatty acid desaturation systems of various origins.

Acyl Coenzyme A↗
PubMed1986

Anatomic features of the furcal nerve and its clinical significance.

Attention must be paid to the furcal nerve when analyzing lumbosacral radicular symptoms, especially when neurologic findings are atypical and the responsible level cannot be assessed. An anatomic and clinical study of the furcal nerve showed the following: the furcal nerve was found in all dissections, and it arises at the L4-root level in most dissections (93%); the furcal nerve has its own anterior and posterior root fibers and its own dorsal nerve root ganglion. This proves that the furcal nerve is an independent nerve root. Neurologic symptoms, suggestive of two roots being involved, are frequently due to furcal nerve compression.

Adult↗
PubMed1986

Antihypertensive action of a non-sulfhydryl angiotensin converting enzyme inhibitor (CV-3317) in various hypertensive models.

The antihypertensive action of N-[N-[(S)-1-ethoxycarbonyl-3-phenyl-propyl]-L-alanyl]-N-(indan-2-yl) glycine hydrochloride (CV-3317), a nonsulfhydryl compound characterized as an angiotensin converting enzyme inhibitor in our previous work, was examined in hypertensive animal models. In 2-kidney, 1 clip hypertensive rats and dogs, CV-3317 (3 and/or 10 mg/kg, p.o.) produced a sustained antihypertensive action of about 15 to 25 mmHg. Daily oral administrations of CV-3317 (1 to 10 mg/kg/day) to spontaneously hypertensive rats (SHR) for 5 weeks produced a sustained antihypertensive action of 20 to 40 mmHg. When CV-3317 (3 mg/kg) was combined with hydrochlorothiazide (10 mg/kg), its antihypertensive action was intensified in potency and duration. CV-3317 (30 mg/kg) induced a slight hypotension (5 to 10 mmHg) in normotensive rats, but had no effect on the blood pressure of 1-kidney, 1 clip hypertensive rats and on that of a low renin type of DOCA/salt hypertensive rat. The antihypertensive activity of CV-3317 was more potent than that of captopril. In pithed SHR, the pressor response induced by an electrical stimulation of the preganglionic sympathetic nerve, but not the pressor response to norepinephrine, was attenuated by both agents (0.3 mg/kg, i.v.). Both agents may exert their antihypertensive action not only primarily by inhibiting the renin-angiotensin system, but also by inhibiting norepinephrine release from the sympathetic nerve terminals indirectly by reducing the formation of vascular angiotensin II.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

Inhibition of angiotensin converting enzyme by CV-3317, a non-sulfhydryl compound.

N-[N-[(S)-1-Ethoxycarbonyl-3-phenylpropyl]-L-alanyl]-N-(indan-2- yl)glycine hydrochloride (CV-3317) and its de-esterified products, CV-3317-COOH and CV-3317-(5-OH)-COOH, inhibited rabbit lung angiotensin converting enzyme (ACE) with the IC50s of 1.2 X 10(-7), 4.0 X 10(-8) and 4.9 X 10(-8) M, respectively, angiotensin I (A-I)-induced vasoconstriction of the rat aorta (IC50: 2.6 X 10(-7), 2.6 X 10(-8) and 5.4 X 10(-8) M, respectively), and A-I-induced pressor response of the rat kidney (IC50: 3.9 X 10(-7), 3.5 X 10(-8) and 2.8 X 10(-8) M, respectively). In these 3 experiments, both de-esterified products were 4 to 14 times more potent than captopril. In rats, CV-3317 (0.0138 to 138 mumol/kg, p.o.) inhibited plasma and lung ACEs, and the effects at a dose of 0.46 mumol/kg lasted more than 8 hr. CV-3317 inhibited the A-I-induced pressor action in rats (0.138 to 13.8 mumol/kg, p.o. or 0.046 to 0.138 mumol/kg i.v.) and dogs (0.46 to 4.6 mumol/kg, p.o.) in a dose-related manner. CV-3317 was more potent and longer acting than captopril in these in vivo ACE inhibitions. CV-3317 augmented bradykinin-induced hypotension (dogs) and contraction of the ileum (guinea pigs) less potently than captopril. In spontaneously hypertensive rats (SHR), CV-3317 (3 mg/kg, p.o.) markedly inhibited plasma and tissue (aorta, kidney, lung and brain) ACEs; and when administered daily for 2 weeks, it inhibited the plasma, aorta, kidney and lung ACEs; in particular, it markedly inhibited the aortic ACE. Captopril (30 mg/kg, p.o.) markedly inhibited tissue ACEs and slightly plasma ACE, but its inhibitory effects on tissue ACEs, except for the aorta, were unclear by repeated dosings and its effect on plasma ACE was rather enhanced. Thus, the inhibition of vascular ACE may be particularly important for the antihypertensive effect of the ACE inhibitors, including CV-3317, in SHR.

Angiotensin I↗
PubMed1986

[Glucose metabolism in the rat cerebral cortex in chronic hepatic failure with reference to glucose-derived amino acids].

In order to investigate metabolic derangements in hepatic failure brains, glucose utilization was studied in regard to glucose-derived amino acids. For this purpose, chronic hepatic failure models were produced in adult male Wistar rats by successive carbontetrachloride injection (0.20 ml/100 g, B. W., twice/week) for 13 weeks. They were confirmed to develop chemical changes compatible with hepatic failure, showing markedly elevated serum levels of NH3, GOT and ALP. Animals were killed by decapitation during fasting and the brains were removed immediately. After the parietal cortical slices were incubated with D-(U-14C) glucose for 15 min, they were homogenized in 75% ethanol and deproteinized with water saturated chloroform. And the radioactivities of liberated CO2 and glucose-derived amino acids (glutamate, glutamine, aspartate, alanine and GABA) obtained from the supernatants were measured. In chronic hepatic failure brains as compared to normal controls, the amount of radioactivity of the two major metabolites, namely glutamate and CO2, decreased (p less than 0.01), but that of aspartate and alanine changed insignificantly, while GABA formation increased (p less than 0.05) and glutamine synthesis tended to increase. The above results indicate not only that the overall glucose oxidation in chronic hepatic failure brains declines reflecting low production of glutamate and CO2, but also that glucose-derived glutamate is actively metabolized through GABA shunt and energy-consuming ammonia fixation.

Amino Acids↗
PubMed1986

[Glutamate metabolism in cerebral cortex obtained from chronic hepatic failure rats].

The present investigation was carried out in order to elucidate the amino acid metabolism in hepatic failure with particular emphasis placed on glutamate. For this purpose, chronic hepatic failure models were produced in adult male Wistar rats by successive carbontetrachloride injection (0.20 ml/100 g. B. W., twice/week) for 13 weeks. They were confirmed to develop chemical changes compartible with hepatic failure, showing markedly elevated serum levels of NH3, GOT and ALP. Animals were killed by decapitation during fasting and the brains were removed immediately. After the parietal cortical slices were incubated for 45 min at 37 degrees C together with L-(U-14C) glutamate in O2-saturated Gey's balanced salt solution, they were homogenized in 75% ethanol and deproteinized with water saturated chloroform. The radioactivities of liberated CO2, glutamate and its metabolites (glutamine, aspartate and GABA) obtained from the slices were measured. The amount of radioactivity recovered from CO2, glutamine and aspartate revealed a significant increase (p less than 0.001), while that of glutamate and GABA remained unchanged. The main source of the CO2 is believed to originate from TCA cycle rather than the decarboxylation of glutamate to form GABA, and glutamate forms glutamine when it fixes ammonia. Furthermore, glutamate is converted into aspartate via TCA cycle when the carbon was labeled. Therefore, the results indicate that in chronic hepatic failure brains glutamate metabolism is enhanced through TCA cycle as well as ammonia fixation mechanism.

Animals↗
PubMed1986

[A comparative study of free amino acid levels in the serum and cerebral cortex in hepatic failure rats].

In order to elucidate the role of amino acid changes in hepatic encephalopathy, free amino acids in serum and cerebral cortex were measured in the experimental hepatic failure models. The acute and chronic models were produced in adult male Wistar rats by carbontetrachloride (CCl4) administration. Acute model was produced by a single intraperitoneal injection of CCl4 (0.35 ml/100 g, B.W.) after the daily pretreatment of phenobarbital (6 mg/100 g, B.W.) for 4 days, while chronic model was established by successive injections CCl4 (0.20 ml/100 g, B.W., twice/week) for 13 weeks. They were confirmed to develop chemical changes compatible with hepatic failure, showing markedly elevated serum levels of NH3, GOT and ALP. Animals were killed by decapitation during fasting and the brains were removed immediately. The parietal cortexes were homogenized in 75% ethanol and deproteinized with water saturated chloroform. The supernatants were subjected to amino acid analyzer. In serum, almost all amino acid concentrations were elevated in acute hepatic failure, reflecting massive release of amino acids from severely damaged liver cells. Chronic hepatic failure rats, however, showed moderately elevated levels of valine and leucine and markedly high levels of phenylalanine and tyrosine, which eventually led to a reduction of the ratio of branched chain amino acids to aromatic amino acids. Regarding urea cycle related amino acids, there were decreases of aspartate and arginine and an increase of ornithine, while citrulline was not affected. In cerebral cortex, no different pattern was observed in acute heptic failure with the exception of increases in threonine, glycine and leucine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗