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An Evolving Uncontrolled Hemorrhage Model Using Cynomolgus Macaques.

Benjamin A Bograd1, Jason S Radowsky, Diego A Vicente

  • 1*Department of Surgery, Walter Reed National Military Medical Center, Bethesda; and †Department of Regenerative Medicine, Naval Medical Research Center, Silver Spring; ‡Department of Surgery, Uniformed Services, University of the Health Sciences, Bethesda, Maryland.

Shock (Augusta, Ga.)
|January 8, 2015
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Summary
This summary is machine-generated.

This study developed a nonhuman primate model of hemorrhagic shock from liver trauma, demonstrating its potential to cause systemic inflammation and organ dysfunction. The model shows promise for studying critical injury responses and developing new treatments.

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Area of Science:

  • Trauma and Injury Research
  • Hemorrhagic Shock Pathophysiology
  • Primate Models in Medicine

Background:

  • Trauma-induced hemorrhagic shock can lead to systemic inflammation, multiple organ failure, and death.
  • Evaluating the pathophysiology of uncontrolled hemorrhagic shock in nonhuman primates is crucial for developing effective treatments.
  • This study aimed to create an acute systemic inflammatory syndrome response and a reproducible hemorrhage model.

Purpose of the Study:

  • To evaluate the pathophysiology of a nonhuman primate uncontrolled hemorrhagic shock model.
  • To establish a reproducible model of hemorrhage and systemic inflammatory response.
  • To investigate the physiological responses and outcomes following liver trauma-induced hemorrhagic shock.

Main Methods:

  • Nonhuman primates underwent laparoscopic left hepatectomy (60% or 80%) to induce uncontrolled hemorrhage.
  • Resuscitation involved saline bolus, followed by warming, hemostasis, and packed red blood cell transfusion.
  • Animals were observed for 14 days with necropsy for histopathology.

Main Results:

  • Group B (80% hepatectomy) showed higher survival (75%) than Group A (57%).
  • Group B maintained significantly lower hematocrit post-injury.
  • Nonsurvivors exhibited kidney tubular degeneration, indicating organ dysfunction.

Conclusions:

  • Nonhuman primates exhibited physiological responses to hemorrhagic shock and liver trauma, including systemic inflammatory response syndrome.
  • The model demonstrated multiple organ dysfunction syndrome, leading to either early death or recovery.
  • Future work will focus on a clinically applicable polytrauma model for critical injury research.