Abstract

BackgroundThis study aimed to establish a traumatic hemorrhagic shock (THS) model in swine and examine pathophysiological characteristics in a dry-heat environment.MethodsForty domestic Landrace piglets were randomly assigned to four study groups: normal temperature non-shock (NS), normal temperature THS (NTHS), desert dry-heat non-shock (DS), and desert dry-hot THS (DTHS) groups. The groups were exposed to either normal temperature (25°C) or dry heat (40.5°C) for 3 h. To induce THS, anesthetized piglets in the NTHS and DTHS groups were subjected to liver trauma and hypovolemic shock until death, and piglets in the NS and DS groups were euthanized at 11 h and 4 h, respectively. Body temperature, blood gas, cytokine production, and organ function were assessed before and after environmental exposure at 0 h and at every 30 min after shock to death. Hemodynamics was measured post exposure and post-shock at 0 h and at every 30 min after shock to death.ResultsSurvival, body temperature, oxygen delivery, oxygen consumption, and cardiac output were significantly different for traumatic hemorrhagic shock in the dry-heat groups compared to those in the normal temperature groups. Lactic acid and IL-6 had a marked increase at 0.5 h, followed by a progressive and rapid increase in the DTHS group.ConclusionsOur findings suggest that the combined action of a dry-heat environment and THS leads to higher oxygen metabolism, poorer hemodynamic stability, and earlier and more severe inflammatory response with higher mortality.

Highlights

  • Trauma hemorrhagic shock (THS) is a type of hypovolemic shock involving massive blood loss that results in a pathologic state in which intravascular volume and oxygen delivery (DO2) are impaired

  • To induce THS, anesthetized piglets in the normal temperature THS (NTHS) and dry-hot THS (DTHS) groups were subjected to liver trauma and hypovolemic shock until death, and piglets in the NS and dry-heat non-shock (DS) groups were euthanized at 11 h and 4 h, respectively

  • Body temperature, oxygen delivery, oxygen consumption, and cardiac output were significantly different for traumatic hemorrhagic shock in the dry-heat groups compared to those in the normal temperature groups

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Summary

Introduction

Trauma hemorrhagic shock (THS) is a type of hypovolemic shock involving massive blood loss that results in a pathologic state in which intravascular volume and oxygen delivery (DO2) are impaired. This can lead to inadequate tissue perfusion along with cellular hypoxia and metabolic disorders [1, 2]. Iraq has an extremely hot and dry climate, with variations in temperature and intense ultraviolet radiation [6], and our experimental team’s previous research showed that the post-traumatic mortality rate of rats in the dry-heat desert environment is high [7]. We speculated that the high mortality rate in the Iraq war was related to the dry-heat environment.

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