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Background <p>Hemorrhage remains the leading preventable cause of trauma mortality. Blast trauma combines primary blast effects with complex secondary and tertiary injuries, precipitating profound hemodynamic instability and microcirculatory disruption. While intramuscular (IM) arginine vasopressin (AVP) stabilizes arterial pressure in isolated hemorrhagic shock, vasopressin’s efficacy in blast-associated hemorrhagic shock is unknown.</p> Methods <p>In a randomized, blinded study, 22 swine underwent femoral blast injury and controlled class II hemorrhage. Animals received IM AVP 40 U (two doses 60&#xa0;min apart due to short half-life and transient effects; <i>n</i> = 5), IM terlipressin 2&#xa0;mg (<i>n</i> = 5), intravenous (IV) terlipressin 2&#xa0;mg (<i>n</i> = 5), or saline control (<i>n</i> = 7). All subjects received a 500 mL autologous whole blood transfusion and were observed for 120&#xa0;min. The primary outcome was systolic arterial pressure (SAP). Secondary outcomes included systemic vascular resistance index (SVRI), cardiopulmonary and metabolic variables, and serum AVP to assess IM uptake.</p> Results <p>IV terlipressin rapidly stabilized hemodynamics, increasing SAP (mean difference 24 mmHg, <i>p</i> = 0.01) and SVRI (mean difference 44593 dynes·s·cm⁻⁵·kg, <i>p</i> = 0.004) versus controls, and increased mixed venous oxygen saturation and urine output. Respiratory and metabolic variables were similar across groups. Neither IM AVP nor IM terlipressin generated a meaningful pressor response. IM AVP absorption was profoundly variable and did not reliably translate into hemodynamic stabilization; only one animal demonstrated both high systemic uptake and a sustained response.</p> Conclusions <p>In blast-associated hemorrhagic shock, IV terlipressin provided consistent hemodynamic stabilization, whereas IM vasopressin analogues were unreliable, highlighting a critical limitation of the IM route in blast pathophysiology.</p> Registry <p>Preclinicaltrials.eu, PCT ID: PCTE0000548, Registration date: 30 October 2024.</p>

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Hemodynamic rescue after blast injury: intravenous administration outperforms intramuscular vasopressin in a swine model

  • 期刊论文

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  • 发表日期：

    2026年3月24日

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  • Mattias Renberg,
  • Jenny Gustavsson,
  • Marius Rehn,
  • Mattias Günther

摘要

Background

Hemorrhage remains the leading preventable cause of trauma mortality. Blast trauma combines primary blast effects with complex secondary and tertiary injuries, precipitating profound hemodynamic instability and microcirculatory disruption. While intramuscular (IM) arginine vasopressin (AVP) stabilizes arterial pressure in isolated hemorrhagic shock, vasopressin’s efficacy in blast-associated hemorrhagic shock is unknown.

Methods

In a randomized, blinded study, 22 swine underwent femoral blast injury and controlled class II hemorrhage. Animals received IM AVP 40 U (two doses 60 min apart due to short half-life and transient effects; n = 5), IM terlipressin 2 mg (n = 5), intravenous (IV) terlipressin 2 mg (n = 5), or saline control (n = 7). All subjects received a 500 mL autologous whole blood transfusion and were observed for 120 min. The primary outcome was systolic arterial pressure (SAP). Secondary outcomes included systemic vascular resistance index (SVRI), cardiopulmonary and metabolic variables, and serum AVP to assess IM uptake.

Results

IV terlipressin rapidly stabilized hemodynamics, increasing SAP (mean difference 24 mmHg, p = 0.01) and SVRI (mean difference 44593 dynes·s·cm⁻⁵·kg, p = 0.004) versus controls, and increased mixed venous oxygen saturation and urine output. Respiratory and metabolic variables were similar across groups. Neither IM AVP nor IM terlipressin generated a meaningful pressor response. IM AVP absorption was profoundly variable and did not reliably translate into hemodynamic stabilization; only one animal demonstrated both high systemic uptake and a sustained response.

Conclusions

In blast-associated hemorrhagic shock, IV terlipressin provided consistent hemodynamic stabilization, whereas IM vasopressin analogues were unreliable, highlighting a critical limitation of the IM route in blast pathophysiology.

Registry

Preclinicaltrials.eu, PCT ID: PCTE0000548, Registration date: 30 October 2024.