Abstract
BackgroundTo investigate the effects of fluids resuscitation on pulmonary expression of aquaporin1 and aquaporin5 in a rat model of uncontrolled hemorrhagic shock and infection.MethodsSixty 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.ResultsThe 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.ConclusionThe 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.
Highlights
Traumatic injury, often accompanied by hemorrhagic shock (HS), continues to be the most common cause of death for young people, as well as a significant source of morbidity and mortality for all ages [1,2].Infusions of crystalloid and colloid solutions are often the mainstay for the prehospital and inhospital treatments of severe HS
The arterial blood gases of group HTS were better than group NF, but there was no difference in the Lactate level and base excess when compared with group Lactated Ringer (LR)
-2.0060.63 -21.6763.01g -19.1763.66g -14.6763.07g+ -10.1762.47g+m transport rate was associated with the downward regulation of AQP1 and AQP5 [17].Our present study showed that there was significantly decreased expression of AQP1 and AQP5 in the rat lungs after ‘‘two-hit’’ model, which was consistent with the increased W/D ratio, as well as the obvious histological alterations
Summary
Often accompanied by hemorrhagic shock (HS), continues to be the most common cause of death for young people, as well as a significant source of morbidity and mortality for all ages [1,2].Infusions of crystalloid and colloid solutions are often the mainstay for the prehospital and inhospital treatments of severe HS. Intensive experiment works are needed to find the more appropriate fluid for resuscitation.The acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS) are the major causes of morbidity and mortality following hemorrhagic shock [4]. Pulmonary edema resulting from injury or infection is one of the pathological conditions of the lung, which is characterized by disrupted fluid transport [5]. Several lines of recent evidence suggest that aquaporins (AQPs) may play a critical role in the pathophysiology of ALI/ARDS. The observed decrease in permeability in AQP1-knockout mice support a role for AQP1 in the pathophysiology of the lung [8,9]. Recent studies demonstrated that the expression levels of AQP1 and AQP5 in the lung decreased in viral infection model of pulmonary edema [10,11]. To investigate the effects of fluids resuscitation on pulmonary expression of aquaporin and aquaporin in a rat model of uncontrolled hemorrhagic shock and infection
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