Swine hemorrhagic shock model and pathophysiological changes in a desert dry-heat environment

Abstract

Background This study aimed to establish a traumatic hemorrhagic shock (THS) model in swine and examine pathophysiological characteristics in a dry-heat environment. Methods Forty 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. Results Survival, 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. Conclusions Our 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.

Monitoring the tissue perfusion during hemorrhagic shock and resuscitation: tissue-to-arterial carbon dioxide partial pressure gradient in a pig model

“…Additionally, etCO 2 can be decreased in shock states because of impaired pulmonary blood flow. Thus, tc-artPCO 2 adopted in our study might be more useful for detecting shock states in ventilated patients than NICO 2 G. Moreover, it was reported that an increase in arterial lactate occurred later than the decreases in CO and DO 2 in a pig model with hemorrhagic shock due to a time difference in the occurrence of tissue and circulating lactic acid [ 43 ]. Thus, DO 2 and/or CO could be more appropriate markers for shock than lactate levels.…”

Physiological and Pathological Evaluation of Mechanically Ventilated Anesthetized Pigs

“…The sympathetic nervous system initiates the mechanism of cardiovascular stabilization, which stimulates catecholamine release leading to positive inotropic cardiac function, increased heart rate (Schwertz et al 2004;De Backer and Foulon 2019), increased oxygen demand, and increased blood glucose level (Barth et al 2007;López Garcia de Lomana et al 2022). The hemodynamic balance of physiological activity depends on tissue oxygen metabolism (Shen et al 2021). If certain conditions that cause tissue and organ damage cannot be resolved, organ failure and death occur (McKinley et al 2016).…”

Monitoring the tissue perfusion during hemorrhagic shock and resuscitation: Tissue-to-arterial carbon dioxide partial pressure gradient in a pig model

“…Additionally, etCO 2 can be decreased in shock states because of impaired pulmonary blood ow. These facts suggest the superiority of tc-artPCO 2 for detecting shock in ventilated patients, compared to NICO 2 G. Moreover, it was reported that an increase in arterial lactate occurred later than the decreases in CO and DO 2 in a pig model with hemorrhagic shock, due to a time difference in the occurrence of tissue and circulating lactic acid [41]. Thus, DO 2 and/or CO could be more appropriate markers for shock than lactate level.…”