Caifu Shen1, Dunhong Wei1, Guangjun Wang1, Yan Kang2, Fan Yang1, Qin Xu1, Liang Xia1, Jiangwei Liu1. 1. Key Laboratory of Special Environmental Medicine of Xinjiang, General Hospital of Xinjiang Military Command of the Chinese People's Liberation Army, Urumqi, China. 2. The 69240 Army Hospital of the Chinese People's Liberation Army, Xinjiang, Urumqi, China.
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.
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.
Authors: Sam D Hutchings; David N Naumann; Philip Hopkins; Clare Mellis; Paul Riozzi; Stefano Sartini; Jasna Mamuza; Tim Harris; Mark J Midwinter; Julia Wendon Journal: Crit Care Med Date: 2018-09 Impact factor: 7.598
Authors: Elisabeth Knöller; Tatjana Stenzel; Friederike Broeskamp; Rouven Hornung; Angelika Scheuerle; Oscar McCook; Ulrich Wachter; Josef A Vogt; José Matallo; Martin Wepler; Holger Gässler; Michael Gröger; Martin Matejovic; Enrico Calzia; Lorenz Lampl; Michael Georgieff; Peter Möller; Pierre Asfar; Peter Radermacher; Sebastian Hafner Journal: Crit Care Med Date: 2016-05 Impact factor: 7.598