Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
ROLE OF MAC-1 AND ICAM-1 IN ISCHEMIA-REPERFUSION INJURY IN A MICROCIRCULATION MODEL OF BALB C MICE/
Autore:
NOLTE D; HECHT R; SCHMID P; BOTZLAR A; MENGER MD; NEUMUELLER C; SINOWATZ F; VESTWEBER D; MESSMER K;
Indirizzi:
UNIV MUNICH,INST SURG RES,MARCHIONINISTR 15 D-80366 MUNICH GERMANY UNIV MUNICH,INST VET ANAT D-80366 MUNICH GERMANY MAX PLANCK INST IMMUNBIOL,HANS SPEMANN LABS FREIBURG GERMANY
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 4, volume: 36, anno: 1994,
pagine: 80001320 - 80001328
SICI:
0363-6135(1994)36:4<80001320:ROMAII>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLATELET-ACTIVATING FACTOR; POSTISCHEMIC SKELETAL-MUSCLE; MONOCLONAL-ANTIBODY; INTERCELLULAR-ADHESION; LEUKOCYTE ADHESION; HEMORRHAGIC-SHOCK; MYOCARDIAL INJURY; STRIATED-MUSCLE; FREE-RADICALS; NO-REFLOW;
Keywords:
INTRAVITAL FLUORESCENCE MICROSCOPY; STRIATED MUSCLE; LEUKOCYTE-ENDOTHELIUM INTERACTION; MACROMOLECULAR LEAKAGE; ADHESION PROTEINS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
D. Nolte et al., "ROLE OF MAC-1 AND ICAM-1 IN ISCHEMIA-REPERFUSION INJURY IN A MICROCIRCULATION MODEL OF BALB C MICE/", American journal of physiology. Heart and circulatory physiology, 36(4), 1994, pp. 80001320-80001328

Abstract

The leukocyte beta(2)-integrin Mac-1 (CD11b/CD18) and its endothelialligand intercellular adhesion molecule 1 (ICAM-1) are involved in leukocyte adhesion to and macromolecular leakage from postcapillary venules during inflammatory reactions. Both events are also encountered after ischemia-reperfusion of striated muscle, suggesting a central role of both adhesion proteins in reperfusion injury. Using intravital fluorescence microscopy and a microcirculation model in awake BALB/C mice,we investigated the effects of monoclonal antibodies (MAb) and Fab fragments to Mac-1 and MAb to ICAM-1 on leukocyte-endothelium interaction and macromolecular leakage of fluorescein isothiocyanate-dextran (1.5 x 10(5) mol wt) in striated skin muscle after 3 h of ischemia followed by reperfusion. We demonstrate that administration of MAb and Fab to Mac-1 before reperfusion was as effective as administration of MAb to ICAM-1, which was found to be significantly upregulated in the postischemic tissue by immunohistochemical analysis, in preventing postischemic leukocyte adhesion to and macromolecular leakage from postcapillary venules, whereas postischemic leukocyte rolling was not affected after MAb administration. Postischemic capillary perfusion was efficiently preserved in animals treated with anti-Mac-1 and anti-ICAM-1 MAb compared with animals receiving the isotype-matched control antibodies. Likewise, delayed infusion of anti-Mac-1 or anti-ICAM-1 MAb at 0.5 h of reperfusion effectively prevented the further increase of postischemic leukocyte adhesion and macromolecular leakage compared with controls. Transmission electron-microscopic analysis of the postischemic tissue revealed marked endothelial cell swelling in control animals, whichwas absent in animals treated with anti-Mac-1 or anti-ICAM-1 MAb before onset of reperfusion. These results demonstrate the pathophysiological role of Mac-1/ICAM-1-mediated leukocyte adhesion in the development of postischemic reperfusion injury of striated muscle in vivo and indicate the therapeutic relevance of antiadhesive strategies against these adhesion molecules before and after onset of reperfusion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 19:54:14