PEROXYNITRITE: A MEDIATOR OF INCREASED MICROVASCULAR PERMEABILITY?
1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has inves...
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| Autor*in: |
Greenacre, S [verfasserIn] Ridger, V [verfasserIn] Wilsoncroft, P [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1997 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2007 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Clinical and experimental pharmacology and physiology - Oxford [u.a.] : Wiley-Blackwell, 1974, 24(1997), 11, Seite 0 |
| Übergeordnetes Werk: |
volume:24 ; year:1997 ; number:11 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1111/j.1440-1681.1997.tb02709.x |
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| 520 | |a 1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. | ||
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10.1111/j.1440-1681.1997.tb02709.x doi (DE-627)NLEJ242582613 DE-627 ger DE-627 rakwb Greenacre, S verfasserin aut PEROXYNITRITE: A MEDIATOR OF INCREASED MICROVASCULAR PERMEABILITY? Oxford, UK Blackwell Publishing Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| inducible nitric oxide synthase Ridger, V verfasserin aut Wilsoncroft, P verfasserin aut Brain, SD oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 24(1997), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:24 year:1997 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1997.tb02709.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 24 1997 11 0 |
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10.1111/j.1440-1681.1997.tb02709.x doi (DE-627)NLEJ242582613 DE-627 ger DE-627 rakwb Greenacre, S verfasserin aut PEROXYNITRITE: A MEDIATOR OF INCREASED MICROVASCULAR PERMEABILITY? Oxford, UK Blackwell Publishing Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| inducible nitric oxide synthase Ridger, V verfasserin aut Wilsoncroft, P verfasserin aut Brain, SD oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 24(1997), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:24 year:1997 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1997.tb02709.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 24 1997 11 0 |
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10.1111/j.1440-1681.1997.tb02709.x doi (DE-627)NLEJ242582613 DE-627 ger DE-627 rakwb Greenacre, S verfasserin aut PEROXYNITRITE: A MEDIATOR OF INCREASED MICROVASCULAR PERMEABILITY? Oxford, UK Blackwell Publishing Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| inducible nitric oxide synthase Ridger, V verfasserin aut Wilsoncroft, P verfasserin aut Brain, SD oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 24(1997), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:24 year:1997 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1997.tb02709.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 24 1997 11 0 |
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10.1111/j.1440-1681.1997.tb02709.x doi (DE-627)NLEJ242582613 DE-627 ger DE-627 rakwb Greenacre, S verfasserin aut PEROXYNITRITE: A MEDIATOR OF INCREASED MICROVASCULAR PERMEABILITY? Oxford, UK Blackwell Publishing Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| inducible nitric oxide synthase Ridger, V verfasserin aut Wilsoncroft, P verfasserin aut Brain, SD oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 24(1997), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:24 year:1997 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1997.tb02709.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 24 1997 11 0 |
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10.1111/j.1440-1681.1997.tb02709.x doi (DE-627)NLEJ242582613 DE-627 ger DE-627 rakwb Greenacre, S verfasserin aut PEROXYNITRITE: A MEDIATOR OF INCREASED MICROVASCULAR PERMEABILITY? Oxford, UK Blackwell Publishing Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. 2007 Blackwell Publishing Journal Backfiles 1879-2005 |2007|||||||||| inducible nitric oxide synthase Ridger, V verfasserin aut Wilsoncroft, P verfasserin aut Brain, SD oth In Clinical and experimental pharmacology and physiology Oxford [u.a.] : Wiley-Blackwell, 1974 24(1997), 11, Seite 0 Online-Ressource (DE-627)NLEJ243927150 (DE-600)2020033-X 1440-1681 nnns volume:24 year:1997 number:11 pages:0 http://dx.doi.org/10.1111/j.1440-1681.1997.tb02709.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 24 1997 11 0 |
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10.1111/j.1440-1681.1997.tb02709.x |
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verfasserin |
| title_sort |
peroxynitrite: a mediator of increased microvascular permeability? |
| title_auth |
PEROXYNITRITE: A MEDIATOR OF INCREASED MICROVASCULAR PERMEABILITY? |
| abstract |
1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. |
| abstractGer |
1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. |
| abstract_unstemmed |
1. Increased expression of inducible nitric oxide synthase (iNOS) and subsequent elevation of nitric oxide (NO) levels at inflammatory sites have led to the suggestion that peroxynitrite (the reaction product of superoxide and NO) is involved in proinflammatory processes. The present study has investigated the ability of peroxynitrite to induce oedema formation in the rat cutaneous microvasculature.2. Peroxynitrite was synthesized from hydrogen peroxide and acidified nitrite. Spectrophotometry was used to measure the concentration and breakdown of peroxynitrite. It was also used to determine maximum amounts of hydrogen peroxide and sodium nitrite remaining after synthesis.3. Oedema formation in response to intradermall. (i.d.) injected peroxynitrite, hydrogen peroxide and sodium nitrite was measured by the extra vascular accumulation of i.v. [125I]-albumin in the anaesthetized rat.4. Peroxynitrite (40,100 and 200 nmol/site) acted in a dose-dependent manner to cause a mean (± SEM) increase in plasma extravasation of 24 ± 2,55 ± 5 and 69 ± 6 μL, respectivel. (n= 4), with resulting inflammatory oedema. Peroxynitrite induced significantly larger plasma extravasation than equivalent vehicle controls at doses of 100 (P > 0.05) and 200 nmol (P > 0.001). This increased extravasation appears to be a direct microvascular response to peroxynitrite administration and not due to either a raised pH, necessary to stabilize the peroxynitrite, or contaminating concentrations of hydrogen peroxide or sodium nitrite from which peroxynitrite is formed.5. These results suggest that peroxynitrite acts to increase microvascular permeability and oedema formation. Therefore, peroxynitrite may mediate vascular pro-inflammatory effects in addition to its direct cytotoxic activity. |
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| title_short |
PEROXYNITRITE: A MEDIATOR OF INCREASED MICROVASCULAR PERMEABILITY? |
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| author2 |
Ridger, V Wilsoncroft, P Brain, SD |
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