title: Short-term, mild hypothermia can increase the beneficial effect of permissive hypotension on uncontrolled hemorrhagic shock in rats.
abstract: BACKGROUND
  Our previous and other studies have shown that hypotensive or hypothermic resuscitation have beneficial effects on uncontrolled hemorrhagic shock. Whether hypothermia can increase the beneficial effect of hypotensive resuscitation on hemorrhagic shock is not known.
  
  
  METHODS
  Two-hundred and twenty Sprague-Dawley rats were used to make uncontrolled hemorrhagic shock. Before bleeding was controlled, rats received normotensive or hypotensive resuscitation (target mean arterial pressure at 80 or 50 mmHg) in combination with normal (37°C) or mild hypothermia (34°C) (phase II). After bleeding was controlled, rats received whole blood and lactated Ringer's solution resuscitation for 2 h (phase III). The animal survival, blood loss, fluid requirement, cardiac output, and coagulation functions, as well as vital organ function, mitochondrial function, and energy metabolism of liver, kidney and intestines, were noted.
  
  
  RESULTS
  Short-term, mild hypothermia before bleeding was controlled increased the beneficial effect of hypotensive resuscitation. Hypothermia further decreased blood loss, oxygen consumption, and functional damage to the liver, kidney, and intestines during hypotensive resuscitation, protected mitochondrial function and energy metabolism (activity of Na(+)-K(+)-ATPase), and further improved survival time and survival rate (hypothermic/hypotensive combined group: survival rate, 9/10; survival time, 616 min; normothermic/normotensive group: 1/10, 256 min; hypothermic/normotensive group: 4/10, 293 min). Hypothermia slightly inhibited coagulation function.
  
  
  CONCLUSIONS
  Mild hypothermia before bleeding is controlled can increase the beneficial effect of hypotensive resuscitation on uncontrolled hemorrhagic shock. The mechanism underlying the benefits of short-term hypothermia may be related to the decrease in oxygen consumption and metabolism, and protection of mitochondrial and organ functions.
authors.affiliation: State Key Laboratory of Trauma, Burns and Combined Injury, Second Department of Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Li
authors.forename: Xiulai
authors.initials: X
authors.lastname: Lin
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhu
authors.forename: Lijie
authors.initials: L
authors.lastname: Li
authors.forename: Liangming
authors.initials: L
authors.lastname: Liu
mesh_terms: D000818:Animals; D001777:Blood Coagulation / Q000502:physiology; D001784:Blood Gas Analysis; D002302:Cardiac Output / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology; D005440:Fluid Therapy; D006439:Hemodynamics / Q000502:physiology; D007022:Hypotension / Q000503:physiopathology*; D007036:Hypothermia, Induced; D007413:Intestinal Mucosa / Q000378:metabolism; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology; D008930:Mitochondria, Liver / Q000378:metabolism; D010101:Oxygen Consumption / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000503:physiopathology / Q000628:therapy*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013534:Survival
chemical_list: D000254:Sodium-Potassium-Exchanging ATPase