TY - JOUR
T1 - Immune function is more compromised after closed bone fracture and hemorrhagic shock than hemorrhage alone
AU - Wichmann, Matthias W.
AU - Zellweger, René
AU - DeMaso, Catherine M.
AU - Ayala, Alfred
AU - Williams, Christine
AU - Chaudry, Irshad H.
PY - 1996/9
Y1 - 1996/9
N2 - Objective: To determine whether closed bone fracture in conjunction with hemorrhagic shock compromises immune functions more severely than hemorrhagic shock alone. Design: In a randomized, controlled trial, closed bone fracture of the right lower leg and/or hemorrhagic shock (mean±SEM arterial blood pressure, 35±5 mm Hg for 90 minutes) were induced in male C3H/HeN mice (weight, 25 g). Animals subjected to hemorrhage were resuscitated with the shed blood and lactated Ringer solution. At 72 hours after the experiment, all animals were killed to obtain whole blood, splenocytes, and splenic and peritoneal macrophages. Macrophage interleukin-1 and splenocyte interleukin- 2 and interleukin-3 release were determined by bioassay, and splenocyte proliferation was measured by tritiated thymidine incorporation. Results: Closed bone fracture alone did not affect immune functions 72 hours after the trauma. Hemorrhagic shock, however, induced a significant depression of splenocyte and macrophage functions. Bone fracture followed by hemorrhagic shock further depressed splenocyte proliferation and splenocyte interleukin- 2 and interleukin-3 release as well as interleukin-1 release. Conclusion: Since bone injury coupled with hemorrhagic shock produces more severe depression of immune functions than hemorrhage alone, bone injury appears to play a contributory role in further depressing immune functions in trauma patients who experience major blood loss.
AB - Objective: To determine whether closed bone fracture in conjunction with hemorrhagic shock compromises immune functions more severely than hemorrhagic shock alone. Design: In a randomized, controlled trial, closed bone fracture of the right lower leg and/or hemorrhagic shock (mean±SEM arterial blood pressure, 35±5 mm Hg for 90 minutes) were induced in male C3H/HeN mice (weight, 25 g). Animals subjected to hemorrhage were resuscitated with the shed blood and lactated Ringer solution. At 72 hours after the experiment, all animals were killed to obtain whole blood, splenocytes, and splenic and peritoneal macrophages. Macrophage interleukin-1 and splenocyte interleukin- 2 and interleukin-3 release were determined by bioassay, and splenocyte proliferation was measured by tritiated thymidine incorporation. Results: Closed bone fracture alone did not affect immune functions 72 hours after the trauma. Hemorrhagic shock, however, induced a significant depression of splenocyte and macrophage functions. Bone fracture followed by hemorrhagic shock further depressed splenocyte proliferation and splenocyte interleukin- 2 and interleukin-3 release as well as interleukin-1 release. Conclusion: Since bone injury coupled with hemorrhagic shock produces more severe depression of immune functions than hemorrhage alone, bone injury appears to play a contributory role in further depressing immune functions in trauma patients who experience major blood loss.
UR - http://www.scopus.com/inward/record.url?scp=0029738469&partnerID=8YFLogxK
U2 - 10.1001/archsurg.1996.01430210093021
DO - 10.1001/archsurg.1996.01430210093021
M3 - Article
C2 - 8790172
AN - SCOPUS:0029738469
SN - 0004-0010
VL - 131
SP - 995
EP - 1000
JO - Archives of Surgery
JF - Archives of Surgery
IS - 9
ER -