Bacterial priming increases lung injury in gram-negative sepsis.
Am J Respir Crit Care Med
; 158(2): 610-9, 1998 Aug.
Article
em En
| MEDLINE
| ID: mdl-9700142
ABSTRACT
Sepsis syndrome is a leading cause of acute respiratory distress syndrome (ARDS), but the development of acute lung injury is highly variable for reasons that are poorly understood. We hypothesized that nonlethal systemic exposure to gram-negative bacteria, with its consequent activation of inflammatory processes, would increase functional and structural lung injury on a second exposure to live organisms, as compared with exposure of naive animals. Sixteen adult baboons received 1 to 2 x 10(10) colony-forming-units (cfu)/kg Escherichia coli by intravenous infusion. Eight animals received live bacteria as a single infusion, whereas the other eight received 10% of the total dose as heat-killed organisms (priming dose) 12 h before the live infusion. Pulmonary gas exchange and hemodynamics were monitored for 48 h or until blood pressure could not be maintained. The animals were killed and one lung was processed for electron microscopy and morphometry. Group data were compared through analysis of variance (ANOVA). The systemic circulatory responses to the bacterial challenge were similar, although less severe shock occurred in primed animals. In contrast, primed animals had increased structural damage involving lung epithelium and endothelium, and showed increased cellularity of the interstitium. The morphologic evidence of increased lung injury in septic animals with prior exposure to heat-killed bacteria suggests that prior activation of systemic inflammatory responses is a contributing factor in the pathogenesis of ARDS.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Síndrome do Desconforto Respiratório
/
Infecções por Bactérias Gram-Negativas
/
Síndrome de Resposta Inflamatória Sistêmica
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Revista:
Am J Respir Crit Care Med
Assunto da revista:
TERAPIA INTENSIVA
Ano de publicação:
1998
Tipo de documento:
Article
País de afiliação:
Estados Unidos