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Titolo:
Evidence for reperfusion injury in cortical bone as a function of crush injury ischemia duration: A rabbit bone chamber study
Autore:
Hsieh, AS; Winet, H; Bao, JY; Glas, H; Plenk, H;
Indirizzi:
Univ Calif Los Angeles, Orthoped Hosp, Los Angeles, CA 90007 USA Univ Calif Los Angeles Los Angeles CA USA 90007 Los Angeles, CA 90007 USA Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA Univ So Calif Los Angeles CA USA 90089 ed Engn, Los Angeles, CA 90089 USA Univ So Calif, Dept Orthoped, Los Angeles, CA 90089 USA Univ So Calif LosAngeles CA USA 90089 rthoped, Los Angeles, CA 90089 USA Univ Vienna, Inst Histol & Embryol, A-1090 Vienna, Austria Univ Vienna Vienna Austria A-1090 stol & Embryol, A-1090 Vienna, Austria
Titolo Testata:
BONE
fascicolo: 1, volume: 28, anno: 2001,
pagine: 94 - 103
SICI:
8756-3282(200101)28:1<94:EFRIIC>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
TOURNIQUET ISCHEMIA; MICROCIRCULATION; MODEL; FLOW; RAT;
Keywords:
ischemia; reperfusion injury; osteonecrosis; angiogenesis; bone resorption; creeping substitution; bone chamber; intravital microscopy; histomorphology;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Winet, H Univ Calif Los Angeles, Orthoped Hosp, 2400 Flower St, Los Angeles, CA 90007 USA Univ Calif Los Angeles 2400 Flower St Los Angeles CA USA 90007 SA
Citazione:
A.S. Hsieh et al., "Evidence for reperfusion injury in cortical bone as a function of crush injury ischemia duration: A rabbit bone chamber study", BONE, 28(1), 2001, pp. 94-103

Abstract

A model for critical limb ischemia was produced by occluding femoral vessels in 24 rabbits with a pneumatic cuff for 0, 2, 4, or 6 hours. Immediate sequelae and subsequent creeping substitution of cortical bone were observedin vivo using an implanted tibial window, the optical bone chamber implant(with intravital microscopy), and then by light and fluorescence microscopy of fluorochrome-labeled and surface-stained ground sections of retrieved implants. Six rabbits were used as controls (0 h) for each ischemia treatment, and the animals were monitored for 5 weeks postocclusion. A subpopulation of 13 implants was retrieved after euthanization and then histologicallyassessed for bone necrosis and remodeling. The hypothesis tested was that reperfusion injury during the 24 h after occluder release (reperfusion phase), and vessel perfusion/caliber, angiogenesis, and net bone resorption during the 5 subsequent weeks (creeping substitution phase), would exhibit ischemia duration-dependent effects. All animals could bear weight on the affected limb to ambulate by 1 week posttreatment. Two-way analysis of variance(ANOVA) comparison of the resulting data confirmed a significant difference between control and ischemia-treated rabbits for: (1) vessel perfusion/reperfusion; (2) vessel caliber; and (3) net bone resorption. Vascular responses to 4 vs 6 h of ischemia were not significantly different, but net bone resorption was strictly ischemia duration-dependent. The conclusion that reperfusion injury was the mechanism spreading ischemia to more vessels was supported by a decrease in reperfusion and caliber of vessels, and an increase in vascular permeability and leukocyte adherence during the reperfusion phase. It is postulated that reperfusion injury produces a secondary ischemia that amplifies the occlusion-created primary ischemia and, in the present work, may have been succeeded by progressive episodes of ischemia, similar to the infarction pattern of ischemic hearts. (C) 2001 by Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 03:21:30