Calkins Casey M, Bensard Denis D, Partrick David A, Karrer Frederick M, McIntyre Robert C
Division of General Surgery, Department of Surgery, University of Colorado Health Sciences Center and The Children's Hospital of Denver, Denver, CO 80262, USA.
J Pediatr Surg. 2002 Jul;37(7):1042-7; discussion 1042-7. doi: 10.1053/jpsu.2002.33841.
BACKGROUND/PURPOSE: Neutrophils (PMNs) are well known effectors of lung injury after sepsis. The accumulation of PMNs into the lung is dependent on a complex cascade of events that includes the local production of chemokines. Interestingly, neonates are protected from lung injury after zymosan-induced sepsis. The authors hypothesized that this protection was caused by either altered PMN function or diminished lung chemokine production compared with the adult.
Sepsis was induced in neonatal and adult rats by an intraperitoneal injection of zymosan. Animals were killed 24 hours later and lungs examined for PMN accumulation and function, chemokine production, and lung injury.
Septic neonates (SN) were protected from pulmonary edema when compared with septic adults (SA). Lung PMN number and chemokine (MIP-2) production increased in both septic neonates and adults when compared with vehicle (V) treated animals. Conversely, PMN function was decreased significantly in neonates when compared with adults.
Despite equivalent lung PMN accumulation and chemotactic protein production, PMN function and lung injury in septic neonates was diminished when compared with that of adults. These findings suggest that neonates may be relatively protected from sepsis-induced lung injury caused by immature PMN function.
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