Regional hypothermia improves gastric microcirculatory oxygenation during hemorrhage in dogs.

Richard Truse,Jan Schulz,Inge Bauer,Christian Vollmer,Michael Smyk,Andreas P M Weber,Tabea Mettler-Altmann,Anna Herminghaus,Olaf Picker,Aleksandar R Zivkovic

doi:10.1371/journal.pone.0226146

Abstract

Mild systemic hypothermia increases gastric mucosal oxygenation (μHbO2) during hemorrhagic shock in dogs. In the context of critical blood loss hypothermia might be fatal due to adverse side effects. Selective regional hypothermia might overcome these limitations. The aim of our study was to analyze the effects of regional gastric and oral mucosal hypothermia on μHbO2 and perfusion (μflow). In a cross-over study six anesthetized dogs were subjected to local oral and gastric mucosal hypothermia (34°C), or maintenance of local normothermia during normovolemia and hemorrhage (-20% blood volume). Macro- and microcirculatory variables were recorded continuously. During normovolemia, local hypothermia increased gastric microcirculatory flow (μflow) without affecting oxygenation (μHbO2) or oral microcirculation. During mild hemorrhagic shock gastric μHbO2 decreased from 72±2% to 38±3% in the normothermic group. This was attenuated by local hypothermia, where μHbO2 was reduced from 74±3% to 52±4%. Local perfusion, oral microcirculation and macrocirculatory variables were not affected. Selective local hypothermia improves gastric μHbO2 during hemorrhagic shock without relevant side effects. In contrast to systemic hypothermia, regional mucosal hypothermia did not affect perfusion and oxygen supply during hemorrhage. Thus, the increased μHbO2 during local hypothermia rather indicates reduced mucosal oxygen demand.

Highlights

Acute blood loss and ensuing circulatory shock after trauma continues to be a major cause of death
An a priori power analysis (G Power Version 3.1.9.2) [33] revealed a power of 0.85 for detection of differences between the different groups with n = 6 in 4 groups, repeated measurements, α < 0.05 and η2 of 0.5. Both the oral and gastric mucosa were rapidly cooled down in the non-shock group (HT-N) from 37.7 ± 0.2 ̊C to 33.9 ± 0.2 ̊C and from 38.1 ± 0.3 ̊C to 34.0 ± 0.1 ̊C respectively, whereas the mucosal temperature remained normothermic in the control group (NT-N)
In the normothermic control group mucosal temperature remained unchanged throughout the experiment (NT-H)

Summary

Introduction

Acute blood loss and ensuing circulatory shock after trauma continues to be a major cause of death. An estimated 5 million people die worldwide as a result of severe injuries [1]. With the exception of the traumatic event itself, exsanguination is the most frequent cause of immediate death followed in the first 24 hours by CNS injury [2]. Multi organ dysfunction syndrome (MODS) is the leading cause of death among patients who die in intensive.

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