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Titolo:
ENDOTOXIN-INDUCED PULMONARY DYSFUNCTION IS PREVENTED BY C1-ESTERASE INHIBITOR
Autore:
GUERRERO R; VELASCO F; RODRIGUEZ M; LOPEZ A; ROJAS R; ALVAREZ MA; VILLALBA R; RUBIO V; TORRES A; DELCASTILLO D;
Indirizzi:
HOP UNIV REINA SOFIA,SERV CUIDAD INTENS,UNIDAD INVEST,AVDA MENENDEZ PIDAL S-N E-14004 CORDOBA SPAIN HOSP UNIV REINA SOFIA,SERV HEMATOL & NEFROL E-14004 CORDOBA SPAIN UNIV CORDOBA,DEPT BIOQUIM & BIOL MOLEC E-14004 CORDOBA SPAIN
Titolo Testata:
The Journal of clinical investigation
fascicolo: 6, volume: 91, anno: 1993,
pagine: 2754 - 2760
SICI:
0021-9738(1993)91:6<2754:EPDIPB>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
RESPIRATORY-DISTRESS SYNDROME; GRAM-NEGATIVE BACTEREMIA; PLASMA KALLIKREIN; SEPTIC SHOCK; BLOOD-COAGULATION; CONTACT PHASE; SYNDROME ARDS; ACTIVATION; COMPLEMENT; SEPSIS;
Keywords:
ACUTE RESPIRATORY DISTRESS SYNDROME; C1-ESTERASE INHIBITOR; COAGULATION; ENDOTOXINS; HYPOXEMIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
53
Recensione:
Indirizzi per estratti:
Citazione:
R. Guerrero et al., "ENDOTOXIN-INDUCED PULMONARY DYSFUNCTION IS PREVENTED BY C1-ESTERASE INHIBITOR", The Journal of clinical investigation, 91(6), 1993, pp. 2754-2760

Abstract

In septic shock, hypotension, disseminated intravascular coagulation,and neutrophil activation are related to the activation of the blood coagulation contact system. This study evaluates in dogs the effect ofthe C1-esterase inhibitor (C1-INH), a main inhibitor of the blood coagulation contact system, on the cardiovascular and respiratory dysfunction associated with endotoxic shock. Two groups were included: controls, which received Escherichia coli endotoxin, and a C1-1 NH group in which C1-INH was infused before E. coli endotoxin administration. In both groups, endotoxin produced hypodynamic shock; however, the decrease in the systolic index and the ventricular systolic work indexes weregreater in controls than the C1-INH group. In controls, the arterial O2 partial pressure decreased by 30% and the alveolo-arterial O2 difference increased by 625%, these parameters remained unchanged in the C1-INH group. Hypoxemia was associated with increased intrapulmonary shunt, decreased blood coagulation contact factors, and decreased C3c. Incontrast, C1-INH administration prevented endotoxin-induced hypoxemia, the increase in intrapulmonary shunt, and the decrease in blood coagulation contact factors. This study shows that, in dogs with endotoxicshock, pulmonary dysfunction is associated with an activation of the blood coagulation contact phase system. An inhibition of this system by C1-INH prevented the hypoxemia induced by endotoxic shock.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 06:26:28