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H Shiomi

Publications and source records attributed to H Shiomi.

At least 37 records · Page 2Linked to original sources
PubMed1997

Bacterial translocation as a cause of septic shock in humans: a report of two cases.

While bacterial translocation has been reported to occur under numerous conditions in animal models, there has been no paper to date focusing on bacterial translocation as a direct cause of septic shock in humans. We present herein the cases of two patients who developed septic shock believed to have been directly caused by bacterial translocation. Neither of the patients had a focus of infection, the intestinal walls were intact in gross appearance, and the peritoneal cavity had not been contaminated by surgery. Moreover, in both patients, the same organisms were detected in the blood, ascites fluid, and mesenteric lymph nodes, and bacilli were found in the intestinal wall.

Aged↗
PubMed1996

Involvement of endogenous nitric oxide in the mechanism of bradykinin-induced peripheral hyperalgesia.

1. When NG-nitro-L-arginine methyl ester (L-NAME, 0.1-10 nmol) or NG-monomethyl-L-arginine (L-NMMA, 10 nmol-1 mumol) was intradermally administered with bradykinin (BK, 3 nmol) into the instep of rat hind-paws, a dose-related suppression of BK-induced hyperalgesia, assessed by the paw-pressure test, was produced. 2. L-Arginine (1 mumol) but not D-arginine (1 mumol) reversed the suppressive effects of L-NAME (10 nmol) and L-NMMA (1 mumol) on BK-induced hyperalgesia. 3. Concomitant intradermal administration of BK (3 nmol) with haemoglobin (1 nmol) significantly suppressed BK-induced hyperalgesia in the paw-pressure test. The BK-induced hyperalgesia was abolished by concomitant intradermal administration of either a guanylate cyclase inhibitor, methylene blue (10 nmol), or LY83583 (1 nmol). In addition, KT5823 (1 nmol) or Rp-8-bromoguanosine-3':5'-cyclic monophosphothioate (Rp-8-Br-cGMPS; 1 nmol), an inhibitor of cyclic GMP-dependent protein kinase, also significantly suppressed BK-induced hyperalgesia. 4. The carrageenin-induced hyperalgesia was significantly attenuated by L-NAME in a dose-dependent manner. 5. L-Arginine (1 mumol), sodium nitroprusside (1 mumol), dibutyryl cyclic GMP (1 mumol) or 8-bromo cyclic GMP (1 mumol) all failed to produce any significant relieving effect on the nociceptive threshold of rodent hind-paws. Concomitant administrations of each agent with a sub-threshold dose (0.1 nmol) of BK induced significant hyperalgesia. 6. Rp-adenosine 3':5'-cyclic monophosphothioate (Rp-cAMPS; 1 nmol), an inhibitor of cyclic AMP-dependent protein kinase, significantly suppressed BK-induced mechanical hyperalgesia. Concomitant administration of forskolin (1 nmol) with 8-bromo cyclic GMP (100 nmol) induced significant hyperalgesia. 7. In the superfusion experiment of a blister base on the instep of rodent hind-paws, intradermally administered BK (3 nmol) significantly increased the outflow of both cyclic GMP and cyclic AMP from the blister base. Concomitant administrations of L-NAME (10 nmol) with BK significantly reduced the BK-induced outflow of cyclic GMP without affecting the cyclic AMP content. 8. These results suggest that the NO-cyclic GMP pathway is involved in the mechanism of BK-induced hyperalgesia, and an activation of both cyclic GMP-and cyclic AMP-second messenger system plays an important role in the production of peripherally induced mechanical hyperalgesia.

Animals↗
PubMed1995

Purification and characterization of a major kyotorphin-hydrolyzing peptidase of rat brain.

We purified a major kyotorphin (L-Tyr-L-Arg)-hydrolyzing peptidase (KTPase) from the rat brain, to electrophoretic homogeneity using conventional chromatographic techniques. KTPase was purified 1,660-fold with a specific activity of 161 mumol/min/mg protein and 6.8% recovery. The purified enzyme was composed of a single polypeptide with a molecular mass of 67 kDa and an isoelectric point (pI) of 5.5. KTPase has the ability to hydrolyze a variety of natural dipeptides. It also liberated NH2-terminal tyrosine from Tyr-Gly-Gly and Tyr-Tyr-Leu. Bestatin and arphamenine B were potent inhibitors of this enzyme, while amastatin and puromycin had little effect. An excess of anti-KTPase antibody raised in a white rabbit precipitated approximately 80% of the kyotorphin-hydrolyzing activity in the cytosol of rat brain. These data suggested that 67 kDa KTPase has a role in the degradation of kyotorphin within neuronal cells of the rat brain.

Amino Acid Sequence↗
PubMed1995

Suppressive effect of anti-alpha 1-antichymotrypsin serum on pulmonary fibrosis induced by phorbol myristate acetate in vivo.

BACKGROUND: PMA induces pulmonary fibrosis in the rabbit (1). Pulmonary fibrosis induced by PMA occurs in the alveolar wall and has the same pattern as idiopathic pulmonary fibrosis (IPF)(2), so this system can be used as an animal model for IPF. PMA also increases the content of alpha-1-antichymotrypsin (ACT) in cultured alveolar macrophages of bronchoalveolar lavages (BAL), and dexamethasone inhibits this PMA-induced increase (3). Here we investigated the role of ACT in pulmonary fibrosis induced by PMA. EXPERIMENTAL DESIGN: Rabbits were treated intratracheally for 6 days with saline, dimethyl sulphoxide (DMSO) used as a solvent of PMA, PMA dissolved in DMSO or PMA plus anti-ACT rabbit serum. BAL samples were obtained. ACT in cell pellet and cell-free fluid of BAL were assayed by radioimmunoassay. Sections of the lung were examined histologically by a point count method. The ratio of fibrosis to elastosis (fibrotic ratio) was evaluated for each rabbit by the ratio of total points of collagen stained by the Azan-Mallory method to those of elastic fiber stained by the Elastica van Gieson method. Hydroxyproline (HP) was assayed biochemically, and the amount of HP in the alveolar wall for each rabbit was calculated using the assayed values of HP and the ratio of histologic collagen points in the alveolar wall to those in the lung tissue by a point count method. RESULTS: The fibrotic ratio of the PMA group increased fourfold compared with that of the saline group. The ratio of the PMA plus anti-ACT group decreased and was similar to that of the saline group. The ratio of the DMSO group was about two times as much as that of the saline or the PMA plus anti-ACT groups. The calculated amount of hydroxyproline in the alveolar wall of the PMA group increased and was approximately 1.5-fold compared with that of the saline group. The amount of HP of the PMA plus anti-ACT group decreased and was similar to that of the saline group. In the BAL, the amount and the percentage of ACT in cell pellet per macrophage of the PMA group increased more than those of the saline and DMSO groups. The amount and percentage of the PMA plus anti-ACT group were significantly less than those of the PMA group. Those of the DMSO group were similar to those of the saline group. CONCLUSIONS: These findings suggest that anti-ACT has a suppressive effect on pulmonary fibrosis induced by PMA and that ACT is important in the PMA model of pulmonary fibrosis.

Animals↗
PubMed1994

Prostaglandin E2 protects cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.

The effects of prostaglandin (PG) E2 on glutamate-induced cytotoxicity were examined using primary cultures of rat cortical neurons. The cell viability was significantly reduced when cultures were briefly exposed to either glutamate or N-methyl-D-aspartate (NMDA) then incubated with normal medium for 1 h. Similar cytotoxicity was observed with the brief application of ionomycin, a calcium ionophore, and S-nitrosocysteine, a nitric oxide (NO)-generating agent. PGE2 at concentrations of 0.01-1 microM dose-dependently ameliorated the glutamate-induced cytotoxicity. PGE1, butaprost, an EP2 receptor agonist, and 8-bromo-cAMP were also effective in protecting cultures against glutamate cytotoxicity. By contrast, neither 17-phenyl-omega-trinor-PGE2, an EP1 receptor agonist, nor M&B 28767, an EP3 receptor agonist, affected glutamate-induced cytotoxicity. NMDA-induced cytotoxicity was ameliorated by PGE2, butaprost, MK-801, N-omega-nitro-L-arginine, a NO synthase inhibitor, and hemoglobin, which binds NO. These agents excluding MK-801 ameliorated the ionomycin-induced cytotoxicity. The cytotoxicity induced by S-nitrosocysteine was prevented only by hemoglobin but not by the other agents including PGE2. These findings indicate that PGE2 protects cultured cortical neurons against NMDA receptor-mediated glutamate neurotoxicity via EP2 receptors. EP2 receptor stimulation may suppress a step in NO formation triggered by Ca(2+)-influx through NMDA receptors.

Animals↗
PubMed1993

Characterization of the release and metabolism of delta sleep-inducing peptide (DSIP) in the rat brain.

In the present study, we examined whether delta sleep-inducing peptide (DSIP) was (1) secreted from neurons on depolarization and (2) degraded by membrane-associated peptidases. Incubation of DSIP with rat brain membrane resulted in the degradation of DSIP with liberation of tryptophan, an N-terminal amino acid of DSIP. Bestatin and puromycin, aminopeptidase inhibitors, significantly inhibited the degradation of DSIP and release of tryptophan. The releases of immunoreactive DSIP-like substance (irDSIP) from rat brain slices and synaptosomes were significantly stimulated by high K(+)-evoked depolarization. The released irDSIP was coeluted with native DSIP on gel filtration chromatography. High K(+)-evoked release of irDSIP did not show extracellular Ca(2+)-dependency. This Ca(2+)-independency suggests that the secretory pathway of DSIP may be different from that of other neurotransmitters. These results demonstrate that DSIP is released from nerve endings on depolarization and inactivated by membrane-associated puromycin-sensitive aminopeptidase. Therefore, DSIP may serve as a neuropeptide-like material in the central nervous systems.

Amino Acid Sequence↗
PubMed1992

Mechanisms of cholecystokinin-induced protection of cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.

The protective effects of cholecystokinin (CCK) against glutamate-induced cytotoxicity were examined using cultured neurons obtained from the rat cerebral cortex. Cell viability was significantly reduced when the cultures were briefly exposed to glutamate or N-methyl-D-aspartate (NMDA) and then incubated with normal medium for 60 min. A 60-min exposure to kainate also reduced cell viability. CCK protected cortical neurons against glutamate-, NMDA- and kainate-induced cytotoxicity. Glutamate- and NMDA-induced cytotoxicity was also reduced by N omega-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor. However, CCK did not prevent the cytotoxic effects of sodium nitroprusside (SNP) which spontaneously releases NO. Moreover, CCK did not affect NMDA-induced Ca2+ influx measured with rhod-2, a fluorescent Ca2+ indicator. Therefore, release of a NO-like factor from the cerebral cortex was assayed using the thoracic artery in vitro. When the artery was incubated with minced cerebral tissues, glutamate elicited marked relaxation. SNP also elicited relaxation of the smooth muscle. CCK inhibited glutamate-induced relaxation but did not affect that induced by SNP. These results indicate that CCK prevents NMDA receptor-mediated cytotoxicity without reducing the Ca2+ influx. It is suggested that CCK inhibits NO-formation triggered by NMDA receptor activation.

Amino Acids↗
PubMed1991

Identification and characterization of two distinct kyotorphin-hydrolyzing enzymes in rat brain.

We identified and characterized two kyotorphin-hydrolyzing peptidases (KTPases) in a soluble fraction of rat brain. When the soluble fraction was chromatographed with DEAE-Sephacel, the enzyme activity was resolved into two peaks, which were designated as KTPases I and II in their order of elution. KTPases I and II accounted for 95% and 5% of the KTPase activity in the soluble fraction, respectively. KTPases I and II hydrolyzed kyotorphin with Km values of 22 microM and 110 microM, respectively. By gel filtration, Mr values of KTPases I and II were determined to be 55,000 and 98,000, respectively. Immunological analyses of KTPase II with an anti-enkephalin aminopeptidase antibody indicated that KTPase II was identical to an enkephalin aminopeptidase with Mr = 98,000. However, KTPase I was a novel peptidase responsible for the major kyotorphin-degrading activity in the soluble fraction of rat brain.

Aminopeptidases↗
PubMed1991

Characterization of delta-sleep-inducing peptide-evoked release of Met-enkephalin from brain synaptosomes in rats.

Delta-sleep-inducing peptide (DSIP) stimulates the release of Met-enkephalin (Met-ENK) from superfused slices of the rodent lower brainstem in vitro. In our present study, DSIP (10(-10)-10(-9) M) induced a significant release of Met-ENK from medullary synaptosomes of rats. This DSIP-evoked release of Met-ENK was Ca2+ dependent and tetrodotoxin (TTX) insensitive. Furthermore, DSIP (10(-11)-10(-9) M) significantly increased 45Ca2+ uptake in medullary synaptosomes. These results demonstrate that DSIP acts directly on the nerve endings of Met-ENK-containing neurons to release this pentapeptide by generating a Ca2+ influx into these neurons. Effects of DSIP on Met-ENK release in other discrete brain regions were also studied. Significant DSIP-evoked Met-ENK release from synaptosomes was observed in the cortex, hypothalamus, and midbrain (at concentrations of 10(-10) and 10(-9) M) and in the hippocampus and thalamus (only at 10(-9) M), but not in the striatum. In the hypothalamus, the release of Leu-enkephalin from its synaptosomes was slightly, but not significantly, enhanced by DSIP (10(-10)-10(-8) M). Our findings demonstrate that DSIP triggered a Ca2+ influx in nerve endings to induce a subsequent release of Met-ENK from neurons in only certain brain regions.

Animals↗
PubMed1991

Prognostic significance of long ventricular pauses in athletes.

The long-term prognosis of athletes with long ventricular pauses has been unknown. In this study, thirty highly-trained cross-country skiers and 24 age-matched controls underwent 24 h Holter monitoring to detect the duration of the longest ventricular pause (LVP), and we followed the athletes for more than 3 years to evaluate prognostic significance of prolonged LVP. The LVPs of the athletes averaged 2.2 +/- 0.6 sec (range 1.3-3.4), which were significantly longer than those, 1.6 +/- 0.3 sec, of the controls. In the athletes, 20 cases (66.7%) had LVPs more than 2 sec, and 5 (16.7%) showed LVPs longer than 3 sec. During 3 years follow-up, no athletes had symptoms of near syncope, syncope or death under continued heavy training. Our study suggested that athlete with prolonged ventricular pause, even of 3 sec or more, did not have a different clinical risk than those without long pauses.

Adult↗
PubMed1989

Delta-sleep-inducing peptide (DSIP) stimulates the release of immunoreactive Met-enkephalin from rat lower brainstem slices in vitro.

We studied whether delta-sleep-inducing peptide (DSIP) acted on opioid receptor directly or indirectly. DSIP did not have binding activity to any subtype of opioid receptors. DSIP at doses of 1 pM-1 nM significantly stimulated the release of immunoreactive Met-enkephalin (iME) from superfused slices of the rat lower brainstem. The DSIP-induced release of iME was calcium-dependent. These results show that DSIP acts on opioid receptor indirectly by stimulating the release of iME in producing antinociceptive effects.

Animals↗
PubMed1989

Involvement of spinal noradrenergic system in the mechanism of an antinociceptive effect of delta-sleep-inducing peptide (DSIP).

We studied whether the antinociceptive effect produced by intracerebroventricular injection of delta-sleep-inducing peptide (DSIP) to mice involved the monoaminergic pathways that descended from brainstem to spinal cord (the descending inhibitory systems). In the tail-pinch test, the antinociceptive effect of DSIP was significantly reduced by the pretreatment with reserpine (3 mg/kg i.p.) which depleted endogenous monoamines. Moreover, the intrathecal injections of monoamine antagonists were performed to evaluate the roles of the spinal noradrenergic and/or serotonergic systems in the production of the DSIP antinociception. In both tail-pinch and hot plate tests, the antinociceptive effect of DSIP was significantly antagonized by the previous intrathecal administration of phentolamine (an alpha-adrenergic blocker) or yohimbine (an alpha 2-adrenergic blocker), but was unaffected by the pretreatment with methysergide (a serotonin antagonist). These results demonstrate that the activation of the descending inhibitory systems, mainly spinal noradrenergic systems, is involved in the elicitation of DSIP antinociception.

Adrenergic Fibers↗
PubMed1989

[A case of schwannoma of intrathoracic right phrenic nerve].

A 22-year old man was admitted because of an abnormal shadow on his chest X-ray film. Radiographic findings revealed that the tumor was located in the right middle mediastinum. At operation a smooth round tumor was found arising from the right phrenic nerve. The tumor was removed with phrenic nerve. Pathohistological examination revealed this tumor was benign schwannoma. Intrathoracic schwannoma usually arise from intercostal and sympathetic nerve and that arising from phrenic nerve is very rare. We removed the tumor by means of cutting his right phrenic nerve because of complete resection. Postoperatively he did well without any respiratory distress. And his respiratory function studies recovered normal 9 months after the operation. We think that schwannoma arising from phrenic nerve should be removed completely and in such a case cutting of the one side phrenic nerve is at ease if the patient have normal respiratory function.

Adult↗
PubMed1988

Potent antinociceptive effect of centrally administered delta-sleep-inducing peptide (DSIP).

The effect of central administration of delta-sleep-inducing peptide (DSIP) on nociceptive responses was evaluated in mice and rats. DSIP, administered intracerebroventricularly or intracisternally to mice, produced a significant dose-dependent antinociceptive effect in the tail-pinch and hot-plate tests. Intrathecal administration of DSIP did not produce such an effect. The antinociceptive effect of DSIP was blocked by pretreatment with the opioid antagonist, naloxone. Moreover, DSIP did not produce an antinociceptive effect in morphine-tolerant mice. Similar antinociceptive effects of DSIP were observed in rats. These results suggest that DSIP produces an antinociceptive effect by acting at the supraspinal level and that this effect is mediated via the opioid receptor, either directly or indirectly. DSIP may play an important role in pain regulation in the central nervous system.

Analgesics↗
PubMed1987

Kyotorphin (tyrosine-arginine) synthetase in rat brain synaptosomes.

Kyotorphin (Tyr-Arg) is a unique neuropeptide which produces analgesia by releasing Met-enkephalin from slices of the brain and spinal cord. Recent studies revealed that kyotorphin possesses the properties of neurotransmitter/neuroregulator. In the present study, we identified a kyotorphin synthetase in the soluble fraction of rat brain synaptosomes (synaptosol) and characterized it. The enzyme partially purified with Sephacryl S-300 showed an absolute requirement for ATP, MgCl2, tyrosine, and arginine. The optimal pH was 7.5-9.0 and the pI was determined to be 6.1-6.2 by isoelectric focusing. The Km was 25.6 microM for tyrosine, 926 microM for arginine, 294 microM for ATP, and 442 microM for MgCl2. The Vmax was 34.0 pmol/mg of protein/h. The apparent molecular size of this "kyotorphin synthetase" further purified by the DE52 column was 240,000-245,000 daltons, estimated using TSKgel G4000SW column chromatography. The enzyme reaction is represented by the following equation: Tyr + Arg + ATP + MgCl2 + kyotorphin synthetase----Tyr-Arg (kyotorphin) + AMP + PPi + MgCl2 + kyotorphin synthetase. The regional distribution and subcellular localization of the synthetase showed a close correlation to that of kyotorphin levels in the rat brain. The amounts of kyotorphin formed from amino acids by the synthetase in the dialyzed synaptosol was 3.0-4.0 times higher than that from precursor proteins by processing enzymes within the 30 min incubation.

Analgesics↗
PubMed1986

Pretranslational and posttranslational mechanisms for regulating beta-endorphin-adrenocorticotropin of the anterior pituitary lobe.

Stress-induced activation of secretion of ACTH and beta-endorphin (beta-END) from anterior lobe corticotrophs leads to both short term and longer term perturbation of the system. Immediately following an acute stress session, the rate of translation of the ACTH/beta-END precursor proopiomelanocortin appears accelerated by 50% and the rate of conversion of the precursor into products is doubled. These changes appear to take place at the translational and posttranslational level and reflect a better use of the preformed messenger RNA which compensates for the stress-induced peptide depletion. When the animal is subjected daily to the stress session, longer term mechanisms appear to emerge. The ACTH/beta-END stores in the gland are increased, apparently owing to an increase in transcription, as reflected by a small but significant increase in proopiomelanocortin messenger RNA. The posttranslational processing is no longer accelerated after further stress. This longer term mechanism appears to be pretranslational and to supplant the posttranslational mechanisms observed after acute stress. These two levels of control may represent different points in the regulation of this critical peptide system.

Adrenocorticotropic Hormone↗