Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Blood transfusion and the two-insult model of post-injury multiple organ failure
Autore:
Aiboshi, J; Moore, EE; Ciesla, CJ; Silliman, CC;
Indirizzi:
Univ Colorado, Hlth Sci Ctr, Bonfils Blood Ctr, Denver, CO 80204 USA Univ Colorado Denver CO USA 80204 Bonfils Blood Ctr, Denver, CO 80204 USA Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80204 USA Univ Colorado Denver CO USA 80204 Ctr, Dept Pediat, Denver, CO 80204 USA
Titolo Testata:
SHOCK
fascicolo: 4, volume: 15, anno: 2001,
pagine: 302 - 306
SICI:
1073-2322(200104)15:4<302:BTATTM>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLATELET-ACTIVATING-FACTOR; ACUTE LUNG INJURY; NEUTROPHIL ADHESION; PRIMES NEUTROPHILS; PHOSPHOLIPASE A(2); MAC-1 CD11B/CD18; TRAUMA; LIPIDS; ENDOTHELIUM; FIBRINOGEN;
Keywords:
platelet activating factor; lysophosphatidylcholines; superoxide anion; adherence; endothelial cell damage;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Moore, EE Univ Colorado, Hlth Sci Ctr, Denver Hlth Med Ctr, Dept Surg, 777Bannock St, Denver, CO 80204 USA Univ Colorado 777 Bannock St Denver CO USA 80204 r, CO 80204 USA
Citazione:
J. Aiboshi et al., "Blood transfusion and the two-insult model of post-injury multiple organ failure", SHOCK, 15(4), 2001, pp. 302-306

Abstract

Neutrophils (PMNs) have been implicated in the pathogenesis of multiple organ failure (MOF). The two-insult model of MOF is based on the fundamental concept that two sequential and independent insults that are individually innocuous against the host can cause overwhelming inflammation. The in vitroPMN priming/activation sequence simulates the two-insult model. Our work has demonstrated that transfusion is an early consistent risk factor for post-injury MOF and lysophosphatidylcholines (lyso-PCs) are generated in stored blood components. Additionally, platelet-activating factor (PAF) is a keyinflammatory agent produced in severely injured patients. We therefore hypothesize that two events, trauma and transfusion, enhance PMN cytotoxicity irrespective of the sequence. Superoxide (O-2(-)) production was measured by reduction of cytochrome c, adherence to fibrinogen was assessed by the radioactivity of adherent (Na2CrO4)-Cr-51 (Cr-51)-labeled PMNs, and endothelial cell (EC) damage by measuring the radioactivity released from Cr-51-labeled human umbilical vein endothelial cells monolayers. Isolated PMNs were primed with buffer, PAF (2 muM), or lyso-PCs (4.5, 15, and 30 muM) followed by activation with buffer, N-formyl-methionyl-leucyl-phenylalanine (fMLP)(1muM), PAF (2 CIM), or lyso-PCs (4.5, 15, and 30 muM). Neither PAF nor lyso-PCs alone stimulated O-2(-) production. While PAF alone caused PMN adherence, lyso-PCs alone did not allowed PMNs to adhere to fibrinogen. However, both combinations of PAF/lyso-PCs and lyso-PCs/PAF significantly augmented O-2(-) production and PMN adherence. Furthermore, these enhanced PMN cytotoxic responses significantly caused EC damage. These findings suggest that inthe scenario of the two-insult model, early or late transfusion administered following trauma can provoke PMN cytotoxicity via priming or activation,thereby increasing the risk of post-injury MOF.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 12:16:05