TY - JOUR
T1 - Effect of corticotropin releasing factor on acid-base alterations and bacterial translocation in a murine model of thermal injury
AU - Zapata-Sirvent, R. L.
AU - Hansbrough, J. F.
AU - Steinsapir, S.
AU - Greenleaf, G. E.
AU - Brown, M.
PY - 1993/8
Y1 - 1993/8
N2 - Corticotropin-releasing factor (CRF) is a 41 amino acid polypeptide produced by the hypothalamus which has been shown to decrease inflammation and tissue oedema when administered following burns, cold and acid injuries in some animal models, and to increase mesenteric blood flow. We determined whether systemic administration of CRF to burned mice would decrease metabolic acidosis and protect the gastrointestinal (GI) tract from ischaemic injury leading to bacterial translocation (BT). Synthetic CRF was administered by intraperitoneal injection in doses of 20 and 200 μg/kg to mice immediately following 25 and 32 per cent TBSA burn injuries; the doses were repeated at 8 and 16 h postburn. Severe metabolic acidosis, measured 12 h after burn injury, was not improved in mice which received CRF treatment. Bacterial translocation, measured by quantifying bacteria in mesenteric lymph nodes harvested from animals 48 h postburn, was also not decreased with CRF treatment. CRF does not improve general tissue perfusion nor decrease GI derangements leading to bacterial translocation in this animal model of burn injury.
AB - Corticotropin-releasing factor (CRF) is a 41 amino acid polypeptide produced by the hypothalamus which has been shown to decrease inflammation and tissue oedema when administered following burns, cold and acid injuries in some animal models, and to increase mesenteric blood flow. We determined whether systemic administration of CRF to burned mice would decrease metabolic acidosis and protect the gastrointestinal (GI) tract from ischaemic injury leading to bacterial translocation (BT). Synthetic CRF was administered by intraperitoneal injection in doses of 20 and 200 μg/kg to mice immediately following 25 and 32 per cent TBSA burn injuries; the doses were repeated at 8 and 16 h postburn. Severe metabolic acidosis, measured 12 h after burn injury, was not improved in mice which received CRF treatment. Bacterial translocation, measured by quantifying bacteria in mesenteric lymph nodes harvested from animals 48 h postburn, was also not decreased with CRF treatment. CRF does not improve general tissue perfusion nor decrease GI derangements leading to bacterial translocation in this animal model of burn injury.
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U2 - 10.1016/0305-4179(93)90117-Q
DO - 10.1016/0305-4179(93)90117-Q
M3 - Article
C2 - 8357477
AN - SCOPUS:0027291806
SN - 0305-4179
VL - 19
SP - 302
EP - 305
JO - Burns
JF - Burns
IS - 4
ER -