title: Effects of different resuscitation fluids on pulmonary expression of aquaporin1 and aquaporin5 in a rat model of uncontrolled hemorrhagic shock and infection.
abstract: BACKGROUND
  To investigate the effects of fluids resuscitation on pulmonary expression of aquaporin1 and aquaporin5 in a rat model of uncontrolled hemorrhagic shock and infection.
  
  
  METHODS
  Sixty Sprague-Dawley rats were randomly assigned to five groups, sham operation group (Group C) and four treated groups: no fluid resuscitation group (Group NF), groups resuscitated with Lactated Ringer's (LR),7.5% NaCl (HTS) and Hydroxyl ethyl starch (HES) respectively. Three-phased uncontrolled hemorrhagic shock and infection model was used. Phase I: Massive hemorrhage with a mean arterial pressure of 35-40 mmHg for 60 min, and followed by infection of lipopolysaccharide. Then some animals were resuscitated with solutions mentioned above, until 90 min. Phase II: At hemorrhagic shock 90 minutes, phase II of 60 minutes began with hemostasis and returning of all the initial shed blood. Phase III: Observation phase for 3.5 hours. After phase III, arterial blood gas analysis and the survival rates of the rats were recorded, Wet-to-dry lung weight ratio, BALF protein, pulmonary permeability index, and expressions of aquaporin1 and aquaporin5 were tested.
  
  
  RESULTS
  The expressions of aquaporin1 and aquaporin5 were decreased in treatment groups comparing with sham operation group. Group HES and Group HTS decreased pulmonary vascular permeability and Wet-to-dry lung weight ratio, improved arterial blood gas analysis and survival rates, and attenuated the decreased pulmonary expression of aquaporin1 and aquaporin5 after the "two-hit", comparing with groups NF and LR,but these beneficial effects were blunted in group HTS.
  
  
  CONCLUSIONS
  The expression of aquaporin1 and aquaporin5 may play important roles in formation of pulmonary edema. Resuscitation with HTS and HES, especially HES can reduce lung injury after hemorrhagic shock, partly by up-regulating the expressions of aquaporin1 and aquaporin5.
authors.affiliation: Department of Anesthesiology, Subei People's Hospital (Clinical Medical College of Yangzhou University), Yangzhou, Jiangsu Province, People's Republic of China. happygezi81@163.com
authors.forename: Ju
authors.initials: J
authors.lastname: Gao
authors.forename: Luojing
authors.initials: L
authors.lastname: Zhou
authors.forename: Yali
authors.initials: Y
authors.lastname: Ge
authors.forename: Shunyan
authors.initials: S
authors.lastname: Lin
authors.forename: Jin
authors.initials: J
authors.lastname: Du
mesh_terms: D000818:Animals; D051398:Aquaporin 1 / Q000819:agonists / Q000235:genetics* / Q000378:metabolism; D051402:Aquaporin 5 / Q000819:agonists / Q000235:genetics* / Q000378:metabolism; D001784:Blood Gas Analysis; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002199:Capillary Permeability / Q000187:drug effects; D004195:Disease Models, Animal; D005440:Fluid Therapy; D015870:Gene Expression; D006895:Hydroxyethyl Starch Derivatives / Q000494:pharmacology*; D007552:Isotonic Solutions / Q000494:pharmacology*; D008070:Lipopolysaccharides; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D055370:Lung Injury / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D009929:Organ Size / Q000187:drug effects; D011654:Pulmonary Edema / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D000077325:Ringer's Lactate; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D012771:Shock, Hemorrhagic / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D016019:Survival Analysis
chemical_list: C496022:Aqp1 protein, rat; C496040:Aqp5 protein, rat; D051402:Aquaporin 5; D006895:Hydroxyethyl Starch Derivatives; D007552:Isotonic Solutions; D008070:Lipopolysaccharides; D000077325:Ringer's Lactate; D012462:Saline Solution, Hypertonic; D051398:Aquaporin 1