Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia
Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperam...
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1992 |
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| Umfang: |
13 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Metabolic brain disease - 1986, 7(1992) vom: Feb., Seite 63-75 |
| Übergeordnetes Werk: |
volume:7 ; year:1992 ; month:02 ; pages:63-75 ; extent:13 |
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NLEJ198075332 |
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| 245 | 1 | 0 | |a Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia |
| 264 | 1 | |c 1992 | |
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| 520 | |a Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. | ||
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| 700 | 1 | |a Suzuki, Kenji |4 oth | |
| 700 | 1 | |a Matsuo, Nobuaki |4 oth | |
| 700 | 1 | |a Moriguchi, Tetsuya |4 oth | |
| 700 | 1 | |a Takeyama, Naoshi |4 oth | |
| 700 | 1 | |a Kitazawa, Yasuhide |4 oth | |
| 700 | 1 | |a Tanaka, Takaya |4 oth | |
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(DE-627)NLEJ198075332 DE-627 ger DE-627 rakwb eng Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia 1992 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. Springer Online Journal Archives 1860-2002 Suzuki, Kenji oth Matsuo, Nobuaki oth Moriguchi, Tetsuya oth Takeyama, Naoshi oth Kitazawa, Yasuhide oth Tanaka, Takaya oth in Metabolic brain disease 1986 7(1992) vom: Feb., Seite 63-75 (DE-627)NLEJ188990275 (DE-600)2018067-6 1573-7365 nnns volume:7 year:1992 month:02 pages:63-75 extent:13 http://dx.doi.org/10.1007/BF01000146 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 7 1992 2 63-75 13 |
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(DE-627)NLEJ198075332 DE-627 ger DE-627 rakwb eng Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia 1992 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. Springer Online Journal Archives 1860-2002 Suzuki, Kenji oth Matsuo, Nobuaki oth Moriguchi, Tetsuya oth Takeyama, Naoshi oth Kitazawa, Yasuhide oth Tanaka, Takaya oth in Metabolic brain disease 1986 7(1992) vom: Feb., Seite 63-75 (DE-627)NLEJ188990275 (DE-600)2018067-6 1573-7365 nnns volume:7 year:1992 month:02 pages:63-75 extent:13 http://dx.doi.org/10.1007/BF01000146 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 7 1992 2 63-75 13 |
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(DE-627)NLEJ198075332 DE-627 ger DE-627 rakwb eng Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia 1992 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. Springer Online Journal Archives 1860-2002 Suzuki, Kenji oth Matsuo, Nobuaki oth Moriguchi, Tetsuya oth Takeyama, Naoshi oth Kitazawa, Yasuhide oth Tanaka, Takaya oth in Metabolic brain disease 1986 7(1992) vom: Feb., Seite 63-75 (DE-627)NLEJ188990275 (DE-600)2018067-6 1573-7365 nnns volume:7 year:1992 month:02 pages:63-75 extent:13 http://dx.doi.org/10.1007/BF01000146 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 7 1992 2 63-75 13 |
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(DE-627)NLEJ198075332 DE-627 ger DE-627 rakwb eng Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia 1992 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. Springer Online Journal Archives 1860-2002 Suzuki, Kenji oth Matsuo, Nobuaki oth Moriguchi, Tetsuya oth Takeyama, Naoshi oth Kitazawa, Yasuhide oth Tanaka, Takaya oth in Metabolic brain disease 1986 7(1992) vom: Feb., Seite 63-75 (DE-627)NLEJ188990275 (DE-600)2018067-6 1573-7365 nnns volume:7 year:1992 month:02 pages:63-75 extent:13 http://dx.doi.org/10.1007/BF01000146 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 7 1992 2 63-75 13 |
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(DE-627)NLEJ198075332 DE-627 ger DE-627 rakwb eng Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia 1992 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. Springer Online Journal Archives 1860-2002 Suzuki, Kenji oth Matsuo, Nobuaki oth Moriguchi, Tetsuya oth Takeyama, Naoshi oth Kitazawa, Yasuhide oth Tanaka, Takaya oth in Metabolic brain disease 1986 7(1992) vom: Feb., Seite 63-75 (DE-627)NLEJ188990275 (DE-600)2018067-6 1573-7365 nnns volume:7 year:1992 month:02 pages:63-75 extent:13 http://dx.doi.org/10.1007/BF01000146 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 7 1992 2 63-75 13 |
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changes in brain ecf amino acids in rats with experimentally induced hyperammonemia |
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Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia |
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Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. |
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Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. |
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Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ198075332</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506144918.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070527s1992 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ198075332</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Changes in brain ECF amino acids in rats with experimentally induced hyperammonemia</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1992</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">13</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Using microdialysis, we studied brain extracellular fluid (ECF) amino acid metabolism in rats with experimentally induced hyperammonemia and regional elevation of brain ECF ammonia levels. The total brain ECF amino acid level was increased by an elevation of the blood ammonia level. Hyperammonemia elevated brain ECF aromatic amino acids and reduced arterial blood branched chain amino acids. When rats with hyperammonemia were intravenously administered norleucine, the brain ECF norleucine level rose markedly, suggesting increased permeability of the blood-brain barrier. When rats with hyperammonemia were infused with a branched chain amino acid-rich preparation, the elevated brain ECF aromatic amino acids level was not suppressed. Following local intracerebral ammonia infusion, only glutamate levels showed a marked elevation. These results suggest that impairment of the blood-brain barrier related to hyperammonemia increases the inflow of low molecular weight substances including amino acids. Furthermore, the ammonia-induced increase of glutamate in the cerebral ECF suggests that high ammonia levels may increase the excitability of the brain. Thus, ammonia may serve as a key factor in the onset of hepatic encephalopathy.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Suzuki, Kenji</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Matsuo, Nobuaki</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Moriguchi, Tetsuya</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Takeyama, Naoshi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kitazawa, Yasuhide</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tanaka, Takaya</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Metabolic brain disease</subfield><subfield code="d">1986</subfield><subfield code="g">7(1992) vom: Feb., Seite 63-75</subfield><subfield code="w">(DE-627)NLEJ188990275</subfield><subfield code="w">(DE-600)2018067-6</subfield><subfield code="x">1573-7365</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:7</subfield><subfield code="g">year:1992</subfield><subfield code="g">month:02</subfield><subfield code="g">pages:63-75</subfield><subfield code="g">extent:13</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF01000146</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">7</subfield><subfield code="j">1992</subfield><subfield code="c">2</subfield><subfield code="h">63-75</subfield><subfield code="g">13</subfield></datafield></record></collection>
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