Splanchnic and systemic hemodynamic responses to portal vein endotoxin after resuscitation from hemorrhagic shock

T. J. Gavin, T. C. Fabian, J. D. Wilson, L. L. Trenthem, F. E. Pritchard, Martin Croce, R. M. Stewart, K. G. Proctor

Research output: Contribution to journalArticle

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Abstract

Background. Hemorrhagic shock and sepsis are usually studied separately or in rodents. This study combined the two insults in a large animal model. Methods. Anesthetized pigs were bled, held in shock for 1 hour, and then resuscitated with fluid. After 3 days, Escherichia coli endotoxin (LPS) was infused into the portal vein (150 μg/kg x 30 min) to mimic the effect of enteric substances breaching the mucosal barrier. Systemic and splanchnic hemodynamic, circulating leukocytes, and plasma levels of tumor necrosis factor (TNF) were measured in five groups: 40% hemorrhage plus fluid only resuscitation, 10% hemorrhage plus fluid-blood resuscitation, 50% hemorrhage plus fluid-blood resuscitation, sham, or sham plus 5 μg/kg LPS priming dose instead of hemorrhage. Results. On day 4 before infusion of LPS, there were no differences between groups in hemodynamics or O2 utilization, but systemic O2 delivery and O2 consumption were each reduced in the hemorrhaged groups because of the hemodilution associated with resuscitation. For 3 hours after infusion of LPS, all animals received aggressive fluid and respiratory support, but arterial blood pressure decreased, and systemic O2 utilization, splanchnic O2 utilization, and arterial lactate level increased; there were no differences between groups in the 50% group compared with sham, LPS-evoked decreases in cardiac index and stroke index were eliminated and LPS-evoked tachycardia, pulmonary and systemic vasoconstriction, and increases in hepatic and portal vein lactate levels were blunted. Despite similar leukocyte counts before infusion of LPS and similar leukopenia after LPS infusion, plasma LPS level was higher in the 50% group compared with sham. Furthermore, LPS evoked increases in portal and hepatic vein plasma TNF in the shams, but those changes were reduced in the 50% group. Conclusions. Most responses to LPS were similar after hemorrhagic shock or a sham operation, which is inconsistent with the concept of 'priming.' LPS-evoked increases in plasma TNF were blunted after shock, probably because of trauma-induced immune dysfunction. A combined shock plus septic challenge in a large animal model may be valuable for investigating the pathogenic mechanism in human beings.

Original languageEnglish (US)
Pages (from-to)310-324
Number of pages15
JournalSurgery
Volume115
Issue number3
StatePublished - 1994

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Viscera
Hemorrhagic Shock
Portal Vein
Endotoxins
Resuscitation
Hemodynamics
Hemorrhage
Hepatic Veins
Tumor Necrosis Factor-alpha
Shock
Lactic Acid
Animal Models
Hemodilution
Leukopenia
Septic Shock
Vasoconstriction
Leukocyte Count
Tachycardia
Rodentia
Sepsis

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Gavin, T. J., Fabian, T. C., Wilson, J. D., Trenthem, L. L., Pritchard, F. E., Croce, M., ... Proctor, K. G. (1994). Splanchnic and systemic hemodynamic responses to portal vein endotoxin after resuscitation from hemorrhagic shock. Surgery, 115(3), 310-324.

Splanchnic and systemic hemodynamic responses to portal vein endotoxin after resuscitation from hemorrhagic shock. / Gavin, T. J.; Fabian, T. C.; Wilson, J. D.; Trenthem, L. L.; Pritchard, F. E.; Croce, Martin; Stewart, R. M.; Proctor, K. G.

In: Surgery, Vol. 115, No. 3, 1994, p. 310-324.

Research output: Contribution to journalArticle

Gavin, TJ, Fabian, TC, Wilson, JD, Trenthem, LL, Pritchard, FE, Croce, M, Stewart, RM & Proctor, KG 1994, 'Splanchnic and systemic hemodynamic responses to portal vein endotoxin after resuscitation from hemorrhagic shock', Surgery, vol. 115, no. 3, pp. 310-324.
Gavin TJ, Fabian TC, Wilson JD, Trenthem LL, Pritchard FE, Croce M et al. Splanchnic and systemic hemodynamic responses to portal vein endotoxin after resuscitation from hemorrhagic shock. Surgery. 1994;115(3):310-324.
Gavin, T. J. ; Fabian, T. C. ; Wilson, J. D. ; Trenthem, L. L. ; Pritchard, F. E. ; Croce, Martin ; Stewart, R. M. ; Proctor, K. G. / Splanchnic and systemic hemodynamic responses to portal vein endotoxin after resuscitation from hemorrhagic shock. In: Surgery. 1994 ; Vol. 115, No. 3. pp. 310-324.
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abstract = "Background. Hemorrhagic shock and sepsis are usually studied separately or in rodents. This study combined the two insults in a large animal model. Methods. Anesthetized pigs were bled, held in shock for 1 hour, and then resuscitated with fluid. After 3 days, Escherichia coli endotoxin (LPS) was infused into the portal vein (150 μg/kg x 30 min) to mimic the effect of enteric substances breaching the mucosal barrier. Systemic and splanchnic hemodynamic, circulating leukocytes, and plasma levels of tumor necrosis factor (TNF) were measured in five groups: 40{\%} hemorrhage plus fluid only resuscitation, 10{\%} hemorrhage plus fluid-blood resuscitation, 50{\%} hemorrhage plus fluid-blood resuscitation, sham, or sham plus 5 μg/kg LPS priming dose instead of hemorrhage. Results. On day 4 before infusion of LPS, there were no differences between groups in hemodynamics or O2 utilization, but systemic O2 delivery and O2 consumption were each reduced in the hemorrhaged groups because of the hemodilution associated with resuscitation. For 3 hours after infusion of LPS, all animals received aggressive fluid and respiratory support, but arterial blood pressure decreased, and systemic O2 utilization, splanchnic O2 utilization, and arterial lactate level increased; there were no differences between groups in the 50{\%} group compared with sham, LPS-evoked decreases in cardiac index and stroke index were eliminated and LPS-evoked tachycardia, pulmonary and systemic vasoconstriction, and increases in hepatic and portal vein lactate levels were blunted. Despite similar leukocyte counts before infusion of LPS and similar leukopenia after LPS infusion, plasma LPS level was higher in the 50{\%} group compared with sham. Furthermore, LPS evoked increases in portal and hepatic vein plasma TNF in the shams, but those changes were reduced in the 50{\%} group. Conclusions. Most responses to LPS were similar after hemorrhagic shock or a sham operation, which is inconsistent with the concept of 'priming.' LPS-evoked increases in plasma TNF were blunted after shock, probably because of trauma-induced immune dysfunction. A combined shock plus septic challenge in a large animal model may be valuable for investigating the pathogenic mechanism in human beings.",
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T1 - Splanchnic and systemic hemodynamic responses to portal vein endotoxin after resuscitation from hemorrhagic shock

AU - Gavin, T. J.

AU - Fabian, T. C.

AU - Wilson, J. D.

AU - Trenthem, L. L.

AU - Pritchard, F. E.

AU - Croce, Martin

AU - Stewart, R. M.

AU - Proctor, K. G.

PY - 1994

Y1 - 1994

N2 - Background. Hemorrhagic shock and sepsis are usually studied separately or in rodents. This study combined the two insults in a large animal model. Methods. Anesthetized pigs were bled, held in shock for 1 hour, and then resuscitated with fluid. After 3 days, Escherichia coli endotoxin (LPS) was infused into the portal vein (150 μg/kg x 30 min) to mimic the effect of enteric substances breaching the mucosal barrier. Systemic and splanchnic hemodynamic, circulating leukocytes, and plasma levels of tumor necrosis factor (TNF) were measured in five groups: 40% hemorrhage plus fluid only resuscitation, 10% hemorrhage plus fluid-blood resuscitation, 50% hemorrhage plus fluid-blood resuscitation, sham, or sham plus 5 μg/kg LPS priming dose instead of hemorrhage. Results. On day 4 before infusion of LPS, there were no differences between groups in hemodynamics or O2 utilization, but systemic O2 delivery and O2 consumption were each reduced in the hemorrhaged groups because of the hemodilution associated with resuscitation. For 3 hours after infusion of LPS, all animals received aggressive fluid and respiratory support, but arterial blood pressure decreased, and systemic O2 utilization, splanchnic O2 utilization, and arterial lactate level increased; there were no differences between groups in the 50% group compared with sham, LPS-evoked decreases in cardiac index and stroke index were eliminated and LPS-evoked tachycardia, pulmonary and systemic vasoconstriction, and increases in hepatic and portal vein lactate levels were blunted. Despite similar leukocyte counts before infusion of LPS and similar leukopenia after LPS infusion, plasma LPS level was higher in the 50% group compared with sham. Furthermore, LPS evoked increases in portal and hepatic vein plasma TNF in the shams, but those changes were reduced in the 50% group. Conclusions. Most responses to LPS were similar after hemorrhagic shock or a sham operation, which is inconsistent with the concept of 'priming.' LPS-evoked increases in plasma TNF were blunted after shock, probably because of trauma-induced immune dysfunction. A combined shock plus septic challenge in a large animal model may be valuable for investigating the pathogenic mechanism in human beings.

AB - Background. Hemorrhagic shock and sepsis are usually studied separately or in rodents. This study combined the two insults in a large animal model. Methods. Anesthetized pigs were bled, held in shock for 1 hour, and then resuscitated with fluid. After 3 days, Escherichia coli endotoxin (LPS) was infused into the portal vein (150 μg/kg x 30 min) to mimic the effect of enteric substances breaching the mucosal barrier. Systemic and splanchnic hemodynamic, circulating leukocytes, and plasma levels of tumor necrosis factor (TNF) were measured in five groups: 40% hemorrhage plus fluid only resuscitation, 10% hemorrhage plus fluid-blood resuscitation, 50% hemorrhage plus fluid-blood resuscitation, sham, or sham plus 5 μg/kg LPS priming dose instead of hemorrhage. Results. On day 4 before infusion of LPS, there were no differences between groups in hemodynamics or O2 utilization, but systemic O2 delivery and O2 consumption were each reduced in the hemorrhaged groups because of the hemodilution associated with resuscitation. For 3 hours after infusion of LPS, all animals received aggressive fluid and respiratory support, but arterial blood pressure decreased, and systemic O2 utilization, splanchnic O2 utilization, and arterial lactate level increased; there were no differences between groups in the 50% group compared with sham, LPS-evoked decreases in cardiac index and stroke index were eliminated and LPS-evoked tachycardia, pulmonary and systemic vasoconstriction, and increases in hepatic and portal vein lactate levels were blunted. Despite similar leukocyte counts before infusion of LPS and similar leukopenia after LPS infusion, plasma LPS level was higher in the 50% group compared with sham. Furthermore, LPS evoked increases in portal and hepatic vein plasma TNF in the shams, but those changes were reduced in the 50% group. Conclusions. Most responses to LPS were similar after hemorrhagic shock or a sham operation, which is inconsistent with the concept of 'priming.' LPS-evoked increases in plasma TNF were blunted after shock, probably because of trauma-induced immune dysfunction. A combined shock plus septic challenge in a large animal model may be valuable for investigating the pathogenic mechanism in human beings.

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