Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia
Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cer...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2000 |
|---|
| Umfang: |
7 |
|---|
| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
|---|---|
| Übergeordnetes Werk: |
in: Acta neurochirurgica - 1950, 142(2000) vom: März, Seite 333-339 |
| Übergeordnetes Werk: |
volume:142 ; year:2000 ; month:03 ; pages:333-339 ; extent:7 |
| Links: |
|---|
| Katalog-ID: |
NLEJ208104496 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLEJ208104496 | ||
| 003 | DE-627 | ||
| 005 | 20210707004850.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 070528s2000 xx |||||o 00| ||eng c | ||
| 035 | |a (DE-627)NLEJ208104496 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 245 | 1 | 0 | |a Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia |
| 264 | 1 | |c 2000 | |
| 300 | |a 7 | ||
| 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 Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. | ||
| 533 | |f Springer Online Journal Archives 1860-2002 | ||
| 700 | 1 | |a Abels, C. |4 oth | |
| 700 | 1 | |a Röhrich, F. |4 oth | |
| 700 | 1 | |a Corvin, S. |4 oth | |
| 700 | 1 | |a Meyermann, R. |4 oth | |
| 700 | 1 | |a Baethmann, A. |4 oth | |
| 700 | 1 | |a Schürer, L. |4 oth | |
| 773 | 0 | 8 | |i in |t Acta neurochirurgica |d 1950 |g 142(2000) vom: März, Seite 333-339 |w (DE-627)NLEJ188985085 |w (DE-600)1464215-3 |x 0942-0940 |7 nnns |
| 773 | 1 | 8 | |g volume:142 |g year:2000 |g month:03 |g pages:333-339 |g extent:7 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1007/s007010050043 |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a ZDB-1-SOJ | ||
| 912 | |a GBV_NL_ARTICLE | ||
| 951 | |a AR | ||
| 952 | |d 142 |j 2000 |c 3 |h 333-339 |g 7 | ||
| matchkey_str |
article:09420940:2000----::ekctedteimneatoipavsesolwngo |
|---|---|
| hierarchy_sort_str |
2000 |
| publishDate |
2000 |
| allfields |
(DE-627)NLEJ208104496 DE-627 ger DE-627 rakwb eng Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. Springer Online Journal Archives 1860-2002 Abels, C. oth Röhrich, F. oth Corvin, S. oth Meyermann, R. oth Baethmann, A. oth Schürer, L. oth in Acta neurochirurgica 1950 142(2000) vom: März, Seite 333-339 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:142 year:2000 month:03 pages:333-339 extent:7 http://dx.doi.org/10.1007/s007010050043 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 142 2000 3 333-339 7 |
| spelling |
(DE-627)NLEJ208104496 DE-627 ger DE-627 rakwb eng Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. Springer Online Journal Archives 1860-2002 Abels, C. oth Röhrich, F. oth Corvin, S. oth Meyermann, R. oth Baethmann, A. oth Schürer, L. oth in Acta neurochirurgica 1950 142(2000) vom: März, Seite 333-339 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:142 year:2000 month:03 pages:333-339 extent:7 http://dx.doi.org/10.1007/s007010050043 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 142 2000 3 333-339 7 |
| allfields_unstemmed |
(DE-627)NLEJ208104496 DE-627 ger DE-627 rakwb eng Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. Springer Online Journal Archives 1860-2002 Abels, C. oth Röhrich, F. oth Corvin, S. oth Meyermann, R. oth Baethmann, A. oth Schürer, L. oth in Acta neurochirurgica 1950 142(2000) vom: März, Seite 333-339 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:142 year:2000 month:03 pages:333-339 extent:7 http://dx.doi.org/10.1007/s007010050043 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 142 2000 3 333-339 7 |
| allfieldsGer |
(DE-627)NLEJ208104496 DE-627 ger DE-627 rakwb eng Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. Springer Online Journal Archives 1860-2002 Abels, C. oth Röhrich, F. oth Corvin, S. oth Meyermann, R. oth Baethmann, A. oth Schürer, L. oth in Acta neurochirurgica 1950 142(2000) vom: März, Seite 333-339 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:142 year:2000 month:03 pages:333-339 extent:7 http://dx.doi.org/10.1007/s007010050043 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 142 2000 3 333-339 7 |
| allfieldsSound |
(DE-627)NLEJ208104496 DE-627 ger DE-627 rakwb eng Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. Springer Online Journal Archives 1860-2002 Abels, C. oth Röhrich, F. oth Corvin, S. oth Meyermann, R. oth Baethmann, A. oth Schürer, L. oth in Acta neurochirurgica 1950 142(2000) vom: März, Seite 333-339 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:142 year:2000 month:03 pages:333-339 extent:7 http://dx.doi.org/10.1007/s007010050043 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 142 2000 3 333-339 7 |
| language |
English |
| source |
in Acta neurochirurgica 142(2000) vom: März, Seite 333-339 volume:142 year:2000 month:03 pages:333-339 extent:7 |
| sourceStr |
in Acta neurochirurgica 142(2000) vom: März, Seite 333-339 volume:142 year:2000 month:03 pages:333-339 extent:7 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| isfreeaccess_bool |
false |
| container_title |
Acta neurochirurgica |
| authorswithroles_txt_mv |
Abels, C. @@oth@@ Röhrich, F. @@oth@@ Corvin, S. @@oth@@ Meyermann, R. @@oth@@ Baethmann, A. @@oth@@ Schürer, L. @@oth@@ |
| publishDateDaySort_date |
2000-03-01T00:00:00Z |
| hierarchy_top_id |
NLEJ188985085 |
| id |
NLEJ208104496 |
| 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">NLEJ208104496</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707004850.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s2000 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ208104496</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">Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2000</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</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">Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia.</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">Abels, C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Röhrich, F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Corvin, S.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Meyermann, R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Baethmann, A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schürer, L.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Acta neurochirurgica</subfield><subfield code="d">1950</subfield><subfield code="g">142(2000) vom: März, Seite 333-339</subfield><subfield code="w">(DE-627)NLEJ188985085</subfield><subfield code="w">(DE-600)1464215-3</subfield><subfield code="x">0942-0940</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:142</subfield><subfield code="g">year:2000</subfield><subfield code="g">month:03</subfield><subfield code="g">pages:333-339</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/s007010050043</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">142</subfield><subfield code="j">2000</subfield><subfield code="c">3</subfield><subfield code="h">333-339</subfield><subfield code="g">7</subfield></datafield></record></collection>
|
| series2 |
Springer Online Journal Archives 1860-2002 |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)NLEJ188985085 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| collection |
NL |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
0942-0940 |
| topic_title |
Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
c a ca f r fr s c sc r m rm a b ab l s ls |
| hierarchy_parent_title |
Acta neurochirurgica |
| hierarchy_parent_id |
NLEJ188985085 |
| hierarchy_top_title |
Acta neurochirurgica |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)NLEJ188985085 (DE-600)1464215-3 |
| title |
Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia |
| spellingShingle |
Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia |
| ctrlnum |
(DE-627)NLEJ208104496 |
| title_full |
Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia |
| journal |
Acta neurochirurgica |
| journalStr |
Acta neurochirurgica |
| lang_code |
eng |
| isOA_bool |
false |
| recordtype |
marc |
| publishDateSort |
2000 |
| contenttype_str_mv |
zzz |
| container_start_page |
333 |
| container_volume |
142 |
| physical |
7 |
| format_se |
Elektronische Aufsätze |
| title_sort |
leukocyte-endothelium-interaction in pial vessels following global, cerebral ischaemia |
| title_auth |
Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia |
| abstract |
Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. |
| abstractGer |
Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. |
| abstract_unstemmed |
Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia. |
| collection_details |
GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
| title_short |
Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia |
| url |
http://dx.doi.org/10.1007/s007010050043 |
| remote_bool |
true |
| author2 |
Abels, C. Röhrich, F. Corvin, S. Meyermann, R. Baethmann, A. Schürer, L. |
| author2Str |
Abels, C. Röhrich, F. Corvin, S. Meyermann, R. Baethmann, A. Schürer, L. |
| ppnlink |
NLEJ188985085 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth |
| up_date |
2024-07-06T11:15:36.121Z |
| _version_ |
1803828106228662272 |
| 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">NLEJ208104496</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707004850.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s2000 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ208104496</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">Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2000</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</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">Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p<0.001) and a smaller increase of the venular diameters (p<0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia.</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">Abels, C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Röhrich, F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Corvin, S.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Meyermann, R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Baethmann, A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schürer, L.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Acta neurochirurgica</subfield><subfield code="d">1950</subfield><subfield code="g">142(2000) vom: März, Seite 333-339</subfield><subfield code="w">(DE-627)NLEJ188985085</subfield><subfield code="w">(DE-600)1464215-3</subfield><subfield code="x">0942-0940</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:142</subfield><subfield code="g">year:2000</subfield><subfield code="g">month:03</subfield><subfield code="g">pages:333-339</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/s007010050043</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">142</subfield><subfield code="j">2000</subfield><subfield code="c">3</subfield><subfield code="h">333-339</subfield><subfield code="g">7</subfield></datafield></record></collection>
|
| score |
7.399908 |