Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison
Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which...
Ausführliche Beschreibung
Autor*in: |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
1996 |
---|
Umfang: |
8 |
---|
Reproduktion: |
Springer Online Journal Archives 1860-2002 |
---|---|
Übergeordnetes Werk: |
in: Neurosurgical review - 1978, 19(1996) vom: Apr., Seite 253-260 |
Übergeordnetes Werk: |
volume:19 ; year:1996 ; month:04 ; pages:253-260 ; extent:8 |
Links: |
---|
Katalog-ID: |
NLEJ206358156 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | NLEJ206358156 | ||
003 | DE-627 | ||
005 | 20210706200659.0 | ||
007 | cr uuu---uuuuu | ||
008 | 070528s1996 xx |||||o 00| ||eng c | ||
035 | |a (DE-627)NLEJ206358156 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
245 | 1 | 0 | |a Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison |
264 | 1 | |c 1996 | |
300 | |a 8 | ||
336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
337 | |a nicht spezifiziert |b z |2 rdamedia | ||
338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
520 | |a Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. | ||
533 | |f Springer Online Journal Archives 1860-2002 | ||
700 | 1 | |a Zumkeller, Matthias |4 oth | |
700 | 1 | |a Dietz, Hermann |4 oth | |
773 | 0 | 8 | |i in |t Neurosurgical review |d 1978 |g 19(1996) vom: Apr., Seite 253-260 |w (DE-627)NLEJ188987444 |w (DE-600)1474861-7 |x 1437-2320 |7 nnns |
773 | 1 | 8 | |g volume:19 |g year:1996 |g month:04 |g pages:253-260 |g extent:8 |
856 | 4 | 0 | |u http://dx.doi.org/10.1007/BF00314841 |
912 | |a GBV_USEFLAG_U | ||
912 | |a ZDB-1-SOJ | ||
912 | |a GBV_NL_ARTICLE | ||
951 | |a AR | ||
952 | |d 19 |j 1996 |c 4 |h 253-260 |g 8 |
matchkey_str |
article:14372320:1996----::lrsrcuacagsnhbodribrirnasfetetetihioi |
---|---|
hierarchy_sort_str |
1996 |
publishDate |
1996 |
allfields |
(DE-627)NLEJ206358156 DE-627 ger DE-627 rakwb eng Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison 1996 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Dietz, Hermann oth in Neurosurgical review 1978 19(1996) vom: Apr., Seite 253-260 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:19 year:1996 month:04 pages:253-260 extent:8 http://dx.doi.org/10.1007/BF00314841 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 19 1996 4 253-260 8 |
spelling |
(DE-627)NLEJ206358156 DE-627 ger DE-627 rakwb eng Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison 1996 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Dietz, Hermann oth in Neurosurgical review 1978 19(1996) vom: Apr., Seite 253-260 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:19 year:1996 month:04 pages:253-260 extent:8 http://dx.doi.org/10.1007/BF00314841 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 19 1996 4 253-260 8 |
allfields_unstemmed |
(DE-627)NLEJ206358156 DE-627 ger DE-627 rakwb eng Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison 1996 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Dietz, Hermann oth in Neurosurgical review 1978 19(1996) vom: Apr., Seite 253-260 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:19 year:1996 month:04 pages:253-260 extent:8 http://dx.doi.org/10.1007/BF00314841 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 19 1996 4 253-260 8 |
allfieldsGer |
(DE-627)NLEJ206358156 DE-627 ger DE-627 rakwb eng Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison 1996 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Dietz, Hermann oth in Neurosurgical review 1978 19(1996) vom: Apr., Seite 253-260 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:19 year:1996 month:04 pages:253-260 extent:8 http://dx.doi.org/10.1007/BF00314841 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 19 1996 4 253-260 8 |
allfieldsSound |
(DE-627)NLEJ206358156 DE-627 ger DE-627 rakwb eng Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison 1996 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Dietz, Hermann oth in Neurosurgical review 1978 19(1996) vom: Apr., Seite 253-260 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:19 year:1996 month:04 pages:253-260 extent:8 http://dx.doi.org/10.1007/BF00314841 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 19 1996 4 253-260 8 |
language |
English |
source |
in Neurosurgical review 19(1996) vom: Apr., Seite 253-260 volume:19 year:1996 month:04 pages:253-260 extent:8 |
sourceStr |
in Neurosurgical review 19(1996) vom: Apr., Seite 253-260 volume:19 year:1996 month:04 pages:253-260 extent:8 |
format_phy_str_mv |
Article |
institution |
findex.gbv.de |
isfreeaccess_bool |
false |
container_title |
Neurosurgical review |
authorswithroles_txt_mv |
Zumkeller, Matthias @@oth@@ Dietz, Hermann @@oth@@ |
publishDateDaySort_date |
1996-04-01T00:00:00Z |
hierarchy_top_id |
NLEJ188987444 |
id |
NLEJ206358156 |
language_de |
englisch |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ206358156</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210706200659.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s1996 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ206358156</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">Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1996</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">8</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 The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels.</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">Zumkeller, Matthias</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dietz, Hermann</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Neurosurgical review</subfield><subfield code="d">1978</subfield><subfield code="g">19(1996) vom: Apr., Seite 253-260</subfield><subfield code="w">(DE-627)NLEJ188987444</subfield><subfield code="w">(DE-600)1474861-7</subfield><subfield code="x">1437-2320</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:19</subfield><subfield code="g">year:1996</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:253-260</subfield><subfield code="g">extent:8</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF00314841</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">19</subfield><subfield code="j">1996</subfield><subfield code="c">4</subfield><subfield code="h">253-260</subfield><subfield code="g">8</subfield></datafield></record></collection>
|
series2 |
Springer Online Journal Archives 1860-2002 |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)NLEJ188987444 |
format |
electronic Article |
delete_txt_mv |
keep |
collection |
NL |
remote_str |
true |
illustrated |
Not Illustrated |
issn |
1437-2320 |
topic_title |
Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
zu |
author2_variant |
m z mz h d hd |
hierarchy_parent_title |
Neurosurgical review |
hierarchy_parent_id |
NLEJ188987444 |
hierarchy_top_title |
Neurosurgical review |
isfreeaccess_txt |
false |
familylinks_str_mv |
(DE-627)NLEJ188987444 (DE-600)1474861-7 |
title |
Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison |
spellingShingle |
Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison |
ctrlnum |
(DE-627)NLEJ206358156 |
title_full |
Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison |
journal |
Neurosurgical review |
journalStr |
Neurosurgical review |
lang_code |
eng |
isOA_bool |
false |
recordtype |
marc |
publishDateSort |
1996 |
contenttype_str_mv |
zzz |
container_start_page |
253 |
container_volume |
19 |
physical |
8 |
format_se |
Elektronische Aufsätze |
title_sort |
ultrastructural changes in the blood-brain barrier in rats after treatment with nimodipine and flunarizine. a comparison |
title_auth |
Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison |
abstract |
Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. |
abstractGer |
Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. |
abstract_unstemmed |
Abstract The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels. |
collection_details |
GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
title_short |
Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison |
url |
http://dx.doi.org/10.1007/BF00314841 |
remote_bool |
true |
author2 |
Zumkeller, Matthias Dietz, Hermann |
author2Str |
Zumkeller, Matthias Dietz, Hermann |
ppnlink |
NLEJ188987444 |
mediatype_str_mv |
z |
isOA_txt |
false |
hochschulschrift_bool |
false |
author2_role |
oth oth |
up_date |
2024-07-06T06:52:48.885Z |
_version_ |
1803811573084454912 |
fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ206358156</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210706200659.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s1996 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ206358156</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">Ultrastructural changes in the blood-brain barrier in rats after treatment with Nimodipine and Flunarizine. A comparison</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1996</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">8</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 The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150–180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p<0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels.</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">Zumkeller, Matthias</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dietz, Hermann</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Neurosurgical review</subfield><subfield code="d">1978</subfield><subfield code="g">19(1996) vom: Apr., Seite 253-260</subfield><subfield code="w">(DE-627)NLEJ188987444</subfield><subfield code="w">(DE-600)1474861-7</subfield><subfield code="x">1437-2320</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:19</subfield><subfield code="g">year:1996</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:253-260</subfield><subfield code="g">extent:8</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF00314841</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">19</subfield><subfield code="j">1996</subfield><subfield code="c">4</subfield><subfield code="h">253-260</subfield><subfield code="g">8</subfield></datafield></record></collection>
|
score |
7.400462 |