Open AccessDifferential Pathophysiology of Bacterial Translocation After Thermal Injury and Sepsis
Author(s) -
William G. Jones,
Annabel Barber,
Joseph P. Minei,
Thomas J. Fahey,
G. Tom Shires
Publication year - 1991
Publication title -
annals of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.153
H-Index - 309
eISSN - 1528-1140
pISSN - 0003-4932
DOI - 10.1097/00000658-199107000-00005
Subject(s) - medicine , sepsis , lipid peroxidation , pathophysiology , xanthine oxidase , resuscitation , allopurinol , ischemia , gastroenterology , pharmacology , immunology , anesthesia , oxidative stress , biochemistry , biology , enzyme
Bacterial translocation (BT) occurs transiently after thermal injury and may result from an ischemic intestinal insult. To evaluate continued intestinal ischemia in the ongoing BT associated with sepsis after injury, rats were randomized to (1) 30% burn injury with Pseudomonas wound infection (BI), (2) BI + fluid resuscitation (BI + Fluid), (3) BI after allopurinol pretreatment to inhibit xanthine oxidase (BI + Allo), or (4) BI after azapropazone pretreatment to inhibit neutrophil degranulation (BI + Aza). On postburn days (PBD) 1, 4, and 7, animals were studied for evidence of BT and intestinal lipid peroxidation. BI + Fluid, BI + Allo, and BI + Aza significantly (p less than 0.05) reduced rates of BT and ileal lipid peroxidation acutely after thermal injury (PBD 1) compared to BI. All four groups had equally high rates of BT associated with the onset of sepsis (PBDs 4 and 7), without evidence of further intestinal lipid peroxidation. These data indicate that the chronic gut barrier failure associated with sepsis after injury occurs independently of continued intestinal ischemia.