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Biomedical subjects

K Shimoji

Publications and source records attributed to K Shimoji.

At least 91 records · Page 5Linked to original sources
PubMed1995

[Possible involvement of smoking in the development of asthma-like conditions in patients with chronic obstructive pulmonary disease].

Indicies of asthma were measured in smokers with chronic bronchitis (CB) + pulmonary emphysema (PE), smokers with CB only, and non-smokers with CB, to examine whether smoking is involved in the development of asthma-like condition in patients with chronic obstructive pulmonary disease (COPD). Airway hypersensitivity was measured with an Astrograph method, and the reversibility of airway obstruction was measured as improvement in FEV1.0 and as percent change in FEV1.0 after inhalation of a beta-agonist. Both hypersensitivity and reversibility were significantly higher in smokers with CB+PE and in smokers with CB only than in non-smokers with CB. The number of eosinophils in sputum, but not in peripheral blood, was slightly higher in the smokers than in the non-smokers. The serum levels of IgE were significantly higher in the smokers than in the non-smokers. No significant difference in the rate of positive skin tests for common allergens was observed among the three groups, but the rate of positive tests for Broncasma Berna was very high in the smokers, and all such tests were negative in the non-smokers. These results indicate that among patients with COPD an asthmatic component is more frequently found in smokers than in non-smokers, and suggest that smoking plays some part in the development of asthma-like condition in these diseases.

Aged↗
PubMed1995

[The effects of prostaglandin E1 and epidural anesthesia on peripheral blood flow].

We compared the effects of prostaglandin E1 (PGE1) and epidural anesthesia on peripheral blood flow by laser Doppler tissue flowmetry during lower abdominal surgery. Epidural anesthesia increased the blood flow of the toe, where the sympathetic nerve supply is of the same spinal cord segments as that of pelvic organs. On the other hand, PGE1 could not prevent the decrease of the blood flow of the toe, but increased that of the index finger, which did not receive the nociceptive stimuli from operative site. Thus, the use of epidural anesthesia together with PGE1 is considered to be effective to increase peripheral blood flow.

Abdomen↗
PubMed1995

[Problems of commercially available heparinized syringes in measurements of blood gases and electrolytes].

We compared the measured values of blood gases and electrolytes by commercially available heparinized syringes (PZ-II, Quick-lite and QS90) with normal and decreased calcium concentrations. With normal calcium concentration, the measured value of [Ca2+] in PZ-II was significantly less than that in Quick-lite and QS90, seemingly due to contained heparin. With hypocalcemia, the measured values of [Ca2+] in Quick-lite and QS90 were significantly greater than those in non-heparinized syringe. The pH and PO2 decreased, and PCO2 increased as time passed. The [Ca2+] was suggested to be more influenced by heparin than by acid-base balance.

Blood Gas Analysis↗
PubMed1994

Prior mechanical injury inhibits rise in intracellular Ca2+ concentration by oxygen-glucose deprivation in mouse hippocampal slices.

Prior mechanical brain microinjury has been found to have a preventive effect on brain ischemia. To investigate the mechanism responsible for this, the effect of mechanical brain injury on changes in intracellular free Ca2+ concentration ([Ca2+]i) in response to ischemic insult was studied in mouse hippocampal slices. The mechanical injury was made by inserting a 25G hypodermic needle into the CA1 region of the hippocampus in mice anesthetized with pentobarbital. Sagittal slices of the hippocampus were prepared two hours, and 1, 3, 7, and 14 days after the brain injury. Changes in [Ca2+]i in the slices by oxygen-glucose deprivation were analyzed from fluorescence images, using fura-2. Increases in [Ca2+]i induced by oxygen-glucose deprivation were inhibited in the vicinity of the injury 1 and 3 days after injury. [Ca2+]i levels were lower in the posterior side from the injury than in the anterior side 1 and 3 days after injury. No significant regional differences in [Ca2+]i responses were found 2 h or 7 and 14 days after the injury. Membrane potential and membrane resistance of CA1 neurons in the vicinity of the injury measured 1 day after the injury were not significantly altered in comparison with non-injured slices. These results indicate that mechanical brain injury inhibits ischemic [Ca2+]i increase. This inhibition may be induced not only by damage of the presynaptic fibers projecting to the CA1 neurons but also by the other certain factor(s) that prevent [Ca2+]i increase, and it appears to be related to the protective effect of prior mechanical injury against ischemic neuronal damage.

Animals↗
PubMed1994

Synaptic responses of substantia gelatinosa neurones to dorsal column stimulation in rat spinal cord in vitro.

1. To study the mechanism of dorsal column stimulation-induced depression of nociceptive transmission in the spinal cord, synaptic responses evoked in dorsal horn neurones by dorsal column and dorsal root stimulations were examined in a horizontal spinal cord slice of the adult rat. Intracellular recordings were made from substantia gelatinosa (SG) neurones. 2. All SG neurones examined received monosynaptic inputs and/or polysynpatic inputs from both dorsal column and dorsal root. A delta fibres were probably responsible for the synaptic responses. The responses evoked by dorsal column stimulation were similar to those evoked by primary afferent A delta fibre stimulation. 3. Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by dorsal column A delta fibres were depressed by 6-cyano-7-nitroquinoxaline-2,3-dione, suggesting that these fibres released L-glutamate or a related amino acid as a transmitter. 4. In 38 of 101 SG neurones, dorsal column stimulation evoked an initial EPSP followed by fast and/or slow inhibitory postsynaptic potentials (IPSPs). These IPSPs reversed polarity at a membrane potential of -73 +/- 2 mV. The fast IPSPs observed in 16 of the SG neurones (42%) that received inhibitory inputs were depressed by strychnine, while the slow IPSPs observed in 22 SG neurones were depressed by bicuculline. In a few cells, a long-lasting slow IPSP with a much slower time course was detected; this IPSP was insensitive to strychnine and bicuculline, and reversed polarity at a membrane potential near -90 mV. 5. Repetitive stimulation of the dorsal column depressed the amplitude of monosynaptic EPSPs evoked by dorsal root stimulation. 6. The responses of SG neurones to dorsal column stimulation had configurations and durations similar to responses to dorsal root stimulation, and may be mediated largely by the same A delta fibres. However, a C fibre-mediated response could not be detected in SG neurones from dorsal column stimulation, although dorsal root stimulation could evoke C fibre-mediated monosynaptic EPSPs in 18 of 88 SG neurones (20%). 7. These observations suggest that SG neurones receive abundant A delta but not C fibre inputs from the dorsal column and that dorsal column stimulation inhibits primary afferent transmission in the spinal cord both by reducing transmitter release from primary A delta fibres and by hyperpolarizing SG neurones.

2-Amino-5-phosphonovalerate↗
PubMed1994

Endogenous 12(S)-HETE production by tumor cells and its role in metastasis.

12(S)-Hydroxyeicosatetraenoic acid [12(S)-HETE] is the 12-lipoxygenase metabolite of arachidonic acid. Previously, we have demonstrated that exogenous 12(S)-HETE can activate protein kinase C, increase cell surface expression of integrins, enhance adhesion, induce endothelial cell retraction, and increase experimental metastasis of tumor cells. Because of these prominent effects of exogenous 12(S)-HETE on tumor cell metastatic potential, it is important to determine whether there is endogenous 12(S)-HETE production by tumor cells. In the present study, mRNAs from human, rat, and mouse platelets as well as human colon carcinoma (Clone A), rat Walker carcinoma (W256), and mouse melanoma (B16a) and lung carcinoma (3LL) were reverse transcribed and amplified by polymerase chain reaction with platelet 12-lipoxygenase specific primers. Identity of the polymerase chain reaction fragments was confirmed by sequencing. 12-Lipoxygenase protein was detected by Western blotting. Tumor cell-derived 12-HETE was determined by reverse phase-high performance liquid chromatography analysis. In addition, the effect of endogenous 12(S)-HETE on tumor cells was studied by using a platelet-type 12-lipoxygenase selective inhibitor (N-benzyl-N-hydroxy-5-phenylpentanamide). Our results suggest that some tumor cells express platelet-type 12-lipoxygenase mRNA, protein and metabolize arachidonic acid to 12(S)-HETE and that endogenous 12(S)-HETE, like the exogenous 12(S)-HETE, may play an important role in tumor cell adhesion to matrix in vitro and lung colonization in vivo.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1994

Mild acidosis inhibits the rise in intracellular Ca2+ concentration in response to oxygen-glucose deprivation in rat hippocampal slices.

Changes in the intracellular Ca2+ concentration ([Ca2+]i) induced by ischemia in vitro (oxygen-glucose deprivation) were continuously recorded using fura-2-loaded hippocampal slices under normal (pH 7.4), acidotic (pH 6.8) and alkalotic (pH 7.8) conditions. Oxygen-glucose deprivation induced an initial slow and a subsequent characteristic rapid increase in [Ca2+]i in most of the normal and alkalotic preparations regardless of whether or not Ca2+ was present in the bathing solutions. This characteristic rapid increase in [Ca2+]i was observed in a minority of the acidotic preparations and its latency was significantly longer in acidotic preparations than in normal and alkalotic preparations. The rise in [Ca2+]i at 10 min of oxygen-glucose deprivation was significantly smaller in the acidotic preparations than in the normal and alkalotic preparations, regardless of whether or not Ca2+ was present. At 15 min, the differences in the increase in [Ca2+]i between normal and acidotic preparations in Ca(2+)-containing solutions (2.5 mM) were insignificant. However, significant differences were still observed between the acidotic preparations and either the normal or alkalotic preparations under Ca(2+)-free conditions. These results suggest that acidosis inhibits the ischemia-induced rise in [Ca2+]i by attenuating both Ca2+ influx from the extracellular space and Ca2+ release from intracellular sites.

Acidosis↗
PubMed1994

Characterization of low pH-induced catecholamine secretion in the rat adrenal medulla.

Catecholamine (CA) secretion was evoked when the isolated rat adrenal gland was perfused with HEPES-buffered Krebs solution acidified by the addition of HCl or by gassing with 95% O2/5% CO2. The secretion was detectable at pH 7.0 and increased with decreasing pH until at approximately 6.4. The low pH-induced CA secretion consisted of two phases, an initial transient response followed by a sustained phase. An intracellular Ca2+ antagonist, 3,4,5-trimethoxybenzoic acid 8-(N,N-diethylamino)octyl ester, selectively inhibited the initial phase of secretion. Both of the responses were resistant to nifedipine, a blocker of voltage-gated Ca2+ channel, but were completely inhibited in Ca(2+)-free (1 mM EGTA containing) solution. Adrenaline was an exclusive component in CAs released by low pH. The time course and extent of intracellular acidification caused either by low pH in the external medium or by the offset of a transitory NH4Cl application had no correlation with those of the secretory responses in the corresponding period. These results suggest that extracellular acidification preferentially activates adrenaline secretive cells to evoke CA secretion and that this low pH-induced CA secretion may be mediated by dihydropyridine-insensitive Ca2+ influx. Furthermore, the initial transient phase of the low pH-induced CA secretion might be caused by a Ca2+ release from intracellular stores, which is also induced by the Ca2+ influx.

Acetylcholine↗
PubMed1994

Spinal cord potential recordings from the extradural space during scoliosis surgery.

For monitoring spinal cord functions during corrective surgery of scoliosis, we have recorded percutaneously from the posterior extradural space at the C5-7 levels the ascending conducted spinal cord potentials (ASCP) in response to extradural stimulation of the cauda equina in 134 patients. The ASCP consists of three spike-like components (C1, C2 and C3) followed by slow components. The extradurally recorded ASCP were not affected by anaesthetic agents. There were no significant differential effects of spinal distractions on each of the three spike potentials. There were no post-operative neurological abnormalities in patients whose ASCP showed no changes, amplitude increases, amplitude decreases of less than 50% or latency increases (> 0.2 ms) during spinal manipulations (no false negatives, but some false positives). Five patients who suffered postoperative neurological damage exhibited more than 50% changes in amplitude of the ASCP during surgery. All these neurological sequelae occurred in the first 80 patients. In the last 54 patients, in whom the distraction forces on the spine were controlled rapidly by observation of the amplitude changes in ASCP, there were no postoperative neurological abnormalities, except for one patient in whom an accidental spinal cord injury was produced by a hook. The results suggest that the distraction force on the spine must be reduced immediately when the amplitudes of the ASCP decrease by more than 50% of control values with or without latency increases.

Adolescent↗
PubMed1994

Differential regional effects of ketamine on spontaneous and glutamate-induced activities of single CNS neurones in rats.

Ketamine and L-glutamate were applied microiontophoretically to neurones of several central nervous system (CNS) structures in urethane anaesthetized Wistar rats. The spontaneous single-unit activities of all the hippocampal CA1 and CA3 neurones were suppressed by ketamine in an iontophoretic current-dependent manner. The spontaneous single-unit activities of eight of nine neurones in the thalamus were not affected by ketamine and suppressed in one. Spontaneous neurone activities in the midbrain reticular formation were not significantly affected by ketamine. Spontaneous activities of the cerebellar Purkinje cell were suppressed by ketamine in four of eight neurones. L-Glutamate excited all 13 hippocampal and nine thalamic neurones in a current-dependent manner. L-Glutamate-induced excitation of all CA1, CA3 and thalamic neurones was inhibited by ketamine. The inhibitory effects of ketamine on L-glutamate-induced excitation were dependent on the injection current intensity, although the sensitivity of thalamic neurones to the injection current was approximately three times that of hippocampal neurones. We conclude that the effects of ketamine on spontaneous activities of neurones vary according to the brain region, probably because of the distribution of NMDA receptors. Moreover, the actions of the drug on NMDA receptors appear to differ between the hippocampus and thalamus. These regionally differential actions of ketamine may reflect characteristics of anaesthesia induced by this drug.

Animals↗
PubMed1994

Erb's point stimulation produces slow positive potentials in the human lumbar spinal cord.

Evoked spinal cord potentials (SCPs) were recorded from the posterior epidural space (PES) at the cervical and lumbrosacral enlargements in response to electrical stimulation of the brachial plexus at Erb's point in 17 chronic pain patients. Erb's point stimulation produced slow positive potentials (heterosegmental slow positive potentials, HSPs) in the PES at the lumbrosacral enlargement in all 13 subjects without spinal cord lesions but not in 4 subjects with spinal cord lesions. The HSP1 with a central peak latency of 21 +/- 2 ms (mean +/- SE) was recorded at the stimulus intensity up to two to three times the threshold strength (T) of the initially positive spike (P1) of the segmental SCP, which was simultaneously recorded from the PES at the cervical enlargement. At the stimulus intensity of more than 3T, another slow positive potential (HSP2) with central peak latency of 71 +/- 6 ms was recorded. These slow positive potentials (HSP1 and HSP2) might be produced by a feedback loop via supraspinal structures, presumably primary afferent depolarizations, in comparison to the HSPs of our previous studies in the rat. Slow negative potentials were sometimes noted before (5 of 13) and/or after (2 of 13) the HSP1. These slow negative potentials probably reflect the activities of dorsal horn neurons producing the HSP1 and HSP2, respectively, also elicited by a feedback loop via supraspinal structures.

Adolescent↗
PubMed1994

Hypoxia modifies the vasodilatory effects of nitroglycerin, prostaglandin E1, and hydralazine on isolated porcine coronary arteries.

To evaluate the potency of vasodilatory drugs in hypoxia, we studied the effects of nitroglycerin (NTG), prostaglandin E1 (PGE1), and hydralazine on porcine coronary artery constricted with endothelin-1 (ET-1) in both oxygenated and hypoxic conditions. Removal of endothelium potentiated NTG-induced relaxation in oxygenated conditions. Hypoxia potentiated relaxation of endothelium-intact arteries induced by NTG, but not relaxation of endothelium-denuded arteries. These findings suggest that hypoxia may modify endothelial function in NTG-induced relaxation. The relaxation of endothelium-intact and -denuded arteries induced by PGE1 in hypoxia was significantly greater than that in the oxygenated condition. PGE1 significantly increased the content of cyclic AMP in the hypoxic condition; it was much greater than that in the oxygenated condition, suggesting that hypoxia may enhance PGE1-induced relaxation by increasing cyclic AMP levels. Hypoxia attenuated hydralazine-induced relaxation in both endothelium-intact and denuded arteries. Indomethacin and aspirin attenuated hydralazine-induced relaxation in the oxygenated condition, suggesting that cyclooxygenase-related eicosanoid(s) may be involved in hydralazine-induced relaxation. However, indomethacin did not alter relaxation of hypoxic arteries induced by hydralazine. These findings suggest that hypoxia may inactivate cyclooxygenase in hydralazine-induced relaxation. Hypoxia may greatly modify the action of vasodilators on porcine coronary smooth muscle.

Alprostadil↗
PubMed1994

Calcitonin inhibits production of immunoglobulins, rheumatoid factor and interleukin-1 by mononuclear cells from patients with rheumatoid arthritis.

OBJECTIVES: Elcatonin (eCT), an eel calcitonin derivative, is shown to considerably improve the clinical signs and symptoms, as well as laboratory data, in patients with rheumatoid arthritis (RA). The therapeutic efficacy of eCT, however, is reduced by preceding and/or concomitant use of corticosteroid. Thus the effects of eCT on the production of immunoglobulins, IgMRF and interleukin-1 (IL-1) by mononuclear cells (MNCs)/monocytes were studied, and compared among patients with RA that received three kinds of treatment and also normal volunteers (NV). METHODS: Ten patients with RA had been treated with a non-steroidal anti-inflammatory drug only (NSAID group), 11 with oral prednisolone (PSL group), and eight with intramuscular eCT (eCT group). MNCs/monocytes from these patients, and also 10 from the NV group, were collected and cultured. IgG, IgA, IgM, IgMRF, IL-1 alpha and IL-1 beta in the supernatants were measured by enzyme-linked immunosorbent assay (ELISA). In the NSAID, PSL and NV groups, eCT was added to the culture medium, and the effects of eCT on production of these substances were studied. RESULTS: Baseline production of IgM, IL-1 alpha and IL-1 beta by MNCs/monocytes in the eCT and NV groups was significantly lower than that in the NSAID group. Furthermore, addition of eCT to the culture medium significantly inhibited the productions of IgG, IgMRF, IL-1 alpha and IL-1 beta by MNCs/monocytes in the NSAID group, whereas production of neither IgG, IgA, IgM, IgMRF nor IL-1 by MNCs/monocytes in the PSL and NV groups was affected by eCT. CONCLUSION: eCT may regulate immune responses through MNC/monocyte function in patients with RA. The present results support our proposal that eCT is an effective agent for the treatment of RA.

Arthritis, Rheumatoid↗
PubMed1994

Changes in blood flow velocity in the middle cerebral artery during nonpulsatile hypothermic cardiopulmonary bypass.

BACKGROUND AND PURPOSE: We evaluated the utility of blood flow velocity measurements by transcranial Doppler ultrasonography as a tool to indirectly measure cerebral perfusion during cardiopulmonary bypass. METHODS: We simultaneously measured blood flow velocity in the middle cerebral artery and physiological variables in 18 patients undergoing cardiac surgery under hypothermic cardiopulmonary bypass in which pH and PaCO2 were managed with the alpha-stat acid-base strategy. We expressed blood flow velocity as a relative value of control obtained under normothermia and normocarbia before bypass. We also developed an original index, modified cerebral metabolic rate for oxygen, to estimate cerebral metabolic rate for oxygen. RESULTS: Relative velocity was significantly (P < .01) reduced during stable aortic cross-clamp compared with before bypass and was significantly (P < .01) increased during rewarming compared with at aortic cross-clamp. Modified cerebral metabolic rate for oxygen significantly correlated with nasopharyngeal temperature during cooling, aortic cross-clamp, and rewarming (r = .756, P < .0001; r = .4, P < .01; r = .725, P < .0005, respectively). Calculated temperature coefficient for modified cerebral metabolic rate of oxygen was 2.7 +/- 1.4 (mean +/- SD, n = 10) during cooling. Only nasopharyngeal temperature and PaCO2 were significant determinants of relative velocity during aortic cross-clamp. CONCLUSIONS: We can monitor cerebral perfusion and metabolism by measurements of relative velocity and modified cerebral metabolic rate for oxygen during hypothermic cardiopulmonary bypass.

Adolescent↗
PubMed1993

Phosphorylation of the carboxyl-terminal domain of the zeta 1 subunit is not responsible for potentiation by TPA of the NMDA receptor channel.

The carboxyl-terminal domain of the zeta 1 subunit of the mouse NMDA receptor channel produced as a fusion protein with GST was phosphorylated in vitro by PKC. A mutant of the zeta 1 subunit without serine or threonine residues in the carboxyl-terminal domain (zeta 1-2-NST) was constructed and was expressed alone or together with the epsilon 2 subunit in Xenopus oocytes. Current responses of the zeta 1-2-NST homomeric and epsilon 2/zeta 1-2-NST heteromeric NMDA receptor channels were enhanced by treatment with TPA, a PKC activator, and the extents of potentiation were comparable with the corresponding wild-type channels. These results suggest that the phosphorylation of the carboxyl-terminal domain of the zeta 1 subunit is not responsible for potentiation of NMDA receptor channels by the TPA treatment.

Amino Acid Sequence↗
PubMed1993

Modification by CO2 of endothelin-1-induced contraction of isolated guinea pig trachea.

To investigate the effect of changes in CO2 tension on airway smooth muscle tone induced by various agonists, contractile responses to acetylcholine, histamine and endothelin-1 (ET-1) were studied in isolated guinea pig tracheae at very low PCO2 (16 +/- 0 mmHg, n = 38), moderately low PCO2 (28 +/- 0 mmHg, n = 23), normal PCO2 (38 +/- 1 mmHg, n = 70) or high PCO2 (94 +/- 1 mmHg, n = 32). The minimum concentration of ET-1 (10(-10) M) needed to induce contractions was lower than that of acetylcholine (10(-7) M) and histamine (10(-7) M) at normal PCO2. Changes in PCO2 did not significantly affect acetylcholine- or histamine-induced contractions. In contrast, very low and moderately low PCO2 attenuated the contractions induced by ET-1, but high PCO2 potentiated those induced by a high concentration of ET-1. Very low PCO2 with normal pH and with high pH attenuated the contractions caused by ET-1, whereas normal PCO2 with high pH did not. These results suggest that ET-1-induced airway smooth muscle contraction can be modified by PCO2 per se. Aspirin and indomethacin potentiated the responses to ET-1 at very low PCO2 more than at normal PCO2, but attenuated the responses to low concentration of ET-1 at high PCO2. These results also suggest that cyclooxygenase-related eicosanoids are involved in the effects of PCO2 on ET-1-induced contractions.

Acetylcholine↗
PubMed1993

99mTc-DTPA activity in the azygos vein before and after sclerotherapy in patients with cirrhosis.

We determined the radioactivity of 99mTc-diethylene-triamine pentaacetic acid (99mTc-DTPA) from the azygos vein in 20 patients with cirrhosis to evaluate the hemodynamic relationship between esophageal varices and azygos venous blood flow before and after sclerotherapy. 99mTc-DTPA was injected into the splenic artery before and after sclerotherapy through a catheter in the right femoral artery. The patients were classified into three types. Type I consisted of nine patients who showed maximum levels of 99mTc-DTPA which were significantly lower (P < 0.01) than those determined before sclerotherapy. The Type II was composed of six patients who had far lower radioactivity levels than those of Type I, but also showed significantly lower maximum activity after sclerotherapy than before (P < 0.01). The five patients in Type III had significantly higher radioactivity after sclerotherapy than before (P < 0.05). Rupture of the esophageal varices occurred in one of the Type I (11.1%), none of the Type II, and four of Type III (80%) cases, among all of the patients followed for 40 months after sclerotherapy. The radioactivity in the azygos vein appeared later in Type I (P < 0.05) and Type II after sclerotherapy than before sclerotherapy, but in Type III there was no difference between pre- and post-sclerotherapy values. Type III patients in whom portography was performed showed short gastric and paraesophageal veins, whereas Type I and Type II patients did not. These data suggest that radioactivity in the azygos vein before and after sclerotherapy reflect the grade of shunting and estimate the recurrence of bleeding in patients with cirrhosis associated with esophageal varices.

Aged↗