Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone
Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to...
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1989 |
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| Umfang: |
6 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Acta neuropathologica - 1961, 77(1989) vom: Juni, Seite 576-581 |
| Übergeordnetes Werk: |
volume:77 ; year:1989 ; month:06 ; pages:576-581 ; extent:6 |
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NLEJ203600665 |
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| 520 | |a Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. | ||
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(DE-627)NLEJ203600665 DE-627 ger DE-627 rakwb eng Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. Springer Online Journal Archives 1860-2002 Schürer, L. oth Temesvari, P. oth Wahl, M. oth Unterberg, A. oth Baethmann, A. oth in Acta neuropathologica 1961 77(1989) vom: Juni, Seite 576-581 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:77 year:1989 month:06 pages:576-581 extent:6 http://dx.doi.org/10.1007/BF00687884 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 77 1989 6 576-581 6 |
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(DE-627)NLEJ203600665 DE-627 ger DE-627 rakwb eng Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. Springer Online Journal Archives 1860-2002 Schürer, L. oth Temesvari, P. oth Wahl, M. oth Unterberg, A. oth Baethmann, A. oth in Acta neuropathologica 1961 77(1989) vom: Juni, Seite 576-581 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:77 year:1989 month:06 pages:576-581 extent:6 http://dx.doi.org/10.1007/BF00687884 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 77 1989 6 576-581 6 |
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(DE-627)NLEJ203600665 DE-627 ger DE-627 rakwb eng Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. Springer Online Journal Archives 1860-2002 Schürer, L. oth Temesvari, P. oth Wahl, M. oth Unterberg, A. oth Baethmann, A. oth in Acta neuropathologica 1961 77(1989) vom: Juni, Seite 576-581 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:77 year:1989 month:06 pages:576-581 extent:6 http://dx.doi.org/10.1007/BF00687884 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 77 1989 6 576-581 6 |
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(DE-627)NLEJ203600665 DE-627 ger DE-627 rakwb eng Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. Springer Online Journal Archives 1860-2002 Schürer, L. oth Temesvari, P. oth Wahl, M. oth Unterberg, A. oth Baethmann, A. oth in Acta neuropathologica 1961 77(1989) vom: Juni, Seite 576-581 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:77 year:1989 month:06 pages:576-581 extent:6 http://dx.doi.org/10.1007/BF00687884 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 77 1989 6 576-581 6 |
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(DE-627)NLEJ203600665 DE-627 ger DE-627 rakwb eng Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. Springer Online Journal Archives 1860-2002 Schürer, L. oth Temesvari, P. oth Wahl, M. oth Unterberg, A. oth Baethmann, A. oth in Acta neuropathologica 1961 77(1989) vom: Juni, Seite 576-581 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:77 year:1989 month:06 pages:576-581 extent:6 http://dx.doi.org/10.1007/BF00687884 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 77 1989 6 576-581 6 |
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blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone |
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Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone |
| abstract |
Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. |
| abstractGer |
Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. |
| abstract_unstemmed |
Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide. |
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GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
| title_short |
Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone |
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http://dx.doi.org/10.1007/BF00687884 |
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Schürer, L. Temesvari, P. Wahl, M. Unterberg, A. Baethmann, A. |
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7.398587 |