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J Misumi

Publications and source records attributed to J Misumi.

At least 37 records · Page 2Linked to original sources
PubMed1989

Angiotensinogen's role in ANG formation, renin release, and renal hemodynamics in isolated perfused kidney.

Isolated perfused rat kidneys were used to investigate the effects of the addition of pure angiotensinogen or renin-free plasma to the perfusate on angiotensin I (ANG I) and angiotensin II (ANG II) generation, renal hemodynamics, and renin release. When no angiotensinogen or plasma is added, a very small amount of angiotensinogen is initially detected in the perfusate. Whereas renin secreted by the kidney accumulates in the perfusate, angiotensinogen disappears during the perfusion and immunoreactive ANG II cannot be detected. The addition of angiotensinogen reactivates the renin-angiotensin system. ANG I, [des-Asp1] ANG I, ANG II, and [des-Asp1] ANG II are progressively generated in the perfusate. At a constant perfusion pressure, as well as at a variable perfusion pressure, a progressive fall in renal perfusate flow is observed that is significantly correlated to the level of immunoreactive ANG II. ANG II significantly blunts the rise in renin, and renin release in the perfusate is negatively correlated to immunoreactive ANG II levels. Comparison of the ANG I and ANG II levels in in vitro incubated perfusates and circulated perfusates shows that in plasma-injected perfusates the level of immunoreactive ANG II is dependent on both the production of ANG I and its conversion to ANG II by renal and perfusate converting-enzyme activity, and on ANG I and ANG II degradation by the kidney and the perfusate.

Angiotensin I↗
PubMed1989

Effects of cefbuperazone on the chemiluminescence of human neutrophils.

To investigate the in vivo effect of antimicrobial agent on neutrophil chemiluminescence and serum opsonic activity, cefbuperazone sodium (CBPZ) was administered to healthy male volunteers via an intravenous drip. A peripheral blood sample (10 ml) was collected 7 times: prior to injection, then 1, 3, 6, 9, 12 and 24 h after injection. Neutrophil chemiluminescence and serum opsonic activity was measured by the simultaneous multiple measurement system based on luminol-dependent chemiluminescence and indicated by peak height and peak time. Neutrophils were activated at hour 1 from the point of view of peak height and statistical significance was observed. The fluctuation of serum opsonic activity was small and statistical significance was not observed. CBPZ has an in vivo effect on neutrophils which was not supposed from in vitro study.

Adult↗
PubMed1986

Metabolism of bradykinin in isolated perfused rat kidney. Measurement of kininase activity in perfusate and urine.

The effect of bradykinin and kininase on renal function and the metabolism of bradykinin in the kidney were examined in isolated perfused rat kidney. In this experimental system, exogenous bradykinin did not affect the water and electrolyte handling by the kidney. Most of bradykinin and kininase in urine were derived from kidney but not from circulating medium. Kininase II may not have a major role in bradykinin destruction by the kidney.

Animals↗
PubMed1985

Effects of vitamin B12 and B6 on 2,5-hexanedione-induced neuropathy.

The therapeutic effect of Vitamin B12 or Vitamin B6 on 2,5-hexanedione induced-neuropathy in animals was examined by using our electrodiagnostic technique in order to investigate the mechanism of the development of the neuropathy. Pyridoxal phosphate and two forms of Vitamin B12 were administered to rats intoxicated by the neurotoxin for a period of 18 weeks, and the sensory and motor fiber conduction velocity and the motor distal latency of the tail nerve were periodically determined. None of the groups treated with the therapeutic drugs exhibited a definite improvement in the nerve fiber conduction velocity and motor distal latency of the rat tail nerve, as compared with those of the 2,5-hexanedione-treated controls.

Animals↗
PubMed1985

Experimental study on the enhancement of the neurotoxicity of methyl n-butyl ketone by non-neurotoxic aliphatic monoketones.

The neurotoxicity of methyl n-butyl ketone is known to be enhanced by combination with methyl ethyl ketone. This study was conducted to clarify the potentiating effect of aliphatic monoketones on the neurotoxicity of methyl n-butyl ketone. Rats were subcutaneously injected in the back with 4 mmol/kg/day of methyl ethyl ketone, methyl n-propyl ketone, methyl n-amyl ketone, or methyl n-hexyl ketone mixed with an equimolar dose of methyl n-butyl ketone five days a week for 20 weeks. The maximum motor fibre conduction velocity and the distal latency were measured every two weeks in the tail nerves of the treated animals and controls. All the monoketones tested enhanced the neurotoxicity of methyl n-butyl ketone. Of the compounds tested, methyl n-hexyl ketone, which had the longest carbon chain, enhanced the neurotoxicity of methyl n-butyl ketone most strongly. These results suggest that the length of the carbon chain of the aliphatic monoketones combined with methyl n-butyl ketone was related to the enhancement of the neurotoxicity of the neurotoxic compound.

Animals↗
PubMed1985

[Kallikrein secretion by the isolated perfused rat kidney. Role of perfusion pressure and the renin-angiotensin system].

The isolated perfused rat kidney (IPRK) releases kallikrein in urine and renin in perfusate. We have previously shown (Kidney Int 24: 58-65, 1983) and confirm here that kallikrein, as well as renin releases are influenced by changes in renal hemodynamics in this model: a rise in perfusion pressure (PP) from 80 to 98 mmHg increases renal perfusate flow (RPF) by 48 +/- 3 p. 100, inhibits renin release and stimulates kallikrein secretion to 234 +/- 84 p. 100 of control values (n = 8). Since the perfusate lacks angiotensinogen, we decided to study the effect on kallikrein of the reconstitution of the renin-angiotensin system in the IPRK by adding angiotensinogen + angiotensin converting enzyme (AG + ACE) to the perfusion medium. After AG + ACE, PP rose to 107 +/- 4 mmHg, RPF decreased by 82 +/- 3 p. 100 as a consequence of the vasoconstrictor effect of angiotensin II, and renin release was suppressed. Again kallikrein secretion was stimulated and increased to 333 +/- 153 p. 100 of control values (n = 4). It is concluded 1) that kallikrein release is influenced by changes in PP but not in RPF on the IPRK. 2) that reconstitution of the renin-angiotensin system by addition of AG + ACE to the perfusate leads to vasoconstriction, suppression of renin release and a marked increase in kallikrein secretion.

Animals↗
PubMed1984

Neurophysiological studies on the relation between the structural properties and neurotoxicity of aliphatic hydrocarbon compounds in rats.

In order to determine the specific structural properties responsible for neurotoxic activity, the comparative neurotoxicity of n-hexane, methyl n-butyl ketone, 2,5-hexanedione, and their relatives was investigated in the peripheral nerves of rats. The maximum conduction velocity of motor and sensory fibres and the motor distal latency of the tail nerves of rats were periodically examined in animals receiving repeated subcutaneous injections of 11 aliphatic monoketone or diketone compounds and their relatives for prolonged periods. A study of the comparative neurotoxicity of n-hexane, methyl n-butyl ketone, and their metabolites showed that 2,5-hexanedione was the most actively neurotoxic. Furthermore, a study of other symmetrical diketones with different carbon numbers showed that 2,4-pentanedione, which is structurally similar to 2,5-hexanedione, possessed a different type of neurotoxic activity than 2,5-hexanedione. Regarding aliphatic monoketone compounds, acetone, 2-pentanone, 2-heptanone, and 2-octanone were confirmed non-neurotoxic for the peripheral nervous system. Evidence from some previous reports, however, suggested that 3-heptanone, 4-octanone, and 5-nonanone might produce neuropathies by being converted to 2,5-diketones under specific conditions.

Animals↗
PubMed1984

Hemoglobin values in adult women of various occupational groups in the community.

In 1966 and 1971, the authors studied hemoglobin values of about 2,000 women of 10 different occupational groups and different social classes in the same district. The mean values of hemoglobin and serum iron were highest in nursing students followed by urban housewives and nutritionists and lowest in 3 groups of farm wives and shoe factory laborers. The difference in the mean values of hemoglobin observed among occupational groups was in principle assumed to be due to the difference of frequency in levels of 11-12 g/dl. Hemoglobin levels between 1966 and 1971 tended to improve as a whole and the differences among occupational groups have been reduced. In this study, some kinds of social conditions as well as some physiological factors related to hemoglobin values were investigated. In the same occupational group, unmarried women had a higher level of hemoglobin than married women. Further, married women with infants showed a relatively lower level than those with no infants. This suggests that hemoglobin values of female workers may be significantly influenced not only by work conditions but also by social conditions including family circumstances.

Adult↗
PubMed1983

Regulation of kallikrein and renin release by the isolated perfused rat kidney.

Rat kidneys perfused in vitro released kallikrein in urine, and renin and kallikrein in the perfusate. The kallikrein was characterized by its kininogenase activity and released bradykinin from bovine and dog substrates. Inactive trypsin activatable kallikrein was present in both perfusate and urine. Kallikrein secretion in urine was influenced by changes in perfusion pressure (PP). Raising the PP strikingly increased urinary kallikrein and lowering PP reduced it. Urinary water and electrolyte output were augmented to the same extent by furosemide and mannitol administration as by raising the PP, but neither drug affected kallikrein. Isoproterenol stimulated the release of renin but not kallikrein. Stopping the oxygen supply to the perfusate suppressed kallikrein secretion in urine and renin release in the perfusate. The kidneys released ten times less kallikrein in the perfusate than in urine, and perfusate kallikrein was not influenced by changes in PP. It is concluded that in this model, changes in PP and/or renal blood flow and/or oxygen supply regulate kallikrein secretion in urine, but that this secretion is unaffected by changes in urinary output. We also conclude that kallikrein release in urine and renin release in perfusate are regulated simultaneously by renal hemodynamic changes but are not affected concomitant by beta-adrenergic stimulation or changes in distal urine composition.

Animals↗
PubMed1983

[An electrophysiological study on peripheral neurotoxicity of 2,3-butanedione, 2,4-pentanedione and 2,5-hexanedione in rats].

A series of studies was made to clarify the relationship of the chemical structures of 2,3-butanedione (2,3-BDione), 2,4-pentanedione (2,4-PDione) and 2,5-hexanedione (2,5-HDione) to neurotoxicity in terms of n-hexane neuropathy and relative neurotoxic potentials, using electrophysiological methods. These compounds are all molecularly symmetrical diketones with 4, 5 and 6 carbons respectively. A 200 mg/kg dose of each compound was administered subcutaneously five days a week to one of three groups of eight rats. This program continued for 40 weeks in the case of 2,3-BDione and 2,4-PDione and for 14 weeks in the case of 2,5-HDione. Electrophysiological studies of the effects of the compounds on the peripheral nerve were performed by measuring maximum motor conduction velocities (MCV) and sensory conduction velocities (SCV) in the tail nerve of the rats. Residual latencies (RL), motor distal latencies (DL), amplitudes of the muscle action potentials (MAP), and amplitudes of the nerve action potentials (NAP) were also estimated. A significant slowing of MCV began to be observed in the 2,5-HDione group at the 6th week and in the 2,4-PDione group at 10th week. At 8th week, a significant decrease in SCV was also observed in these two groups. The degree of reduction in both MCV and SCV was more pronounced in the 2,5-HDione group than in the 2,4-PDione group. In the 2,5-HDione group, the MCV values were more strongly affected than the SCV values. On the other hand, in the 2,4-PDione group the SCV values were slowed more than the MCV values. The amplitudes of MAP and NAP in the 2,5-HDione group decreased significantly at 12th week and at 10th week, respectively. In the 2,4-PDione group, a significant decrease in NAP amplitudes was observed at 16th week and that in MAP amplitudes at 28th week. The 2,3-BDione group showed a decrease in MAP amplitudes at 28th week. The RL and DL were markedly prolonged at an early stage only in the 2,5-HDione group. The gamma-diketone of 6, 7 and 8 normal chains of the aliphatic hydrocarbons has been reported to cause peripheral distal axonopathy with giant axonal degeneration. This disorder is named gamma-diketone neuropathy. In this study, neurotoxic evidence was revealed by 2,4-PDione, which is 5-carbon and symmetrical beta-diketone.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗