Sixty Sprague-Dawley (SD) rats were randomly assigned to the following five groups: control group (C group), no fluid
resuscitation group (NF group),
lactated Ringer's solution group (LRS group), 7.5%NaCl group (HS group) and hydroxyethyl
starch group (
hydroxyethyl starch 130/0.4, HES group). A four-phased uncontrolled
hemorrhagic shock model was reproduced. Uncontrolled
hemorrhagic shock phase began with blood withdrawal extended over 15 minutes, in which animals were subjected to massive
hemorrhage [mean arterial pressure (MAP)=40 mm Hg (1 mm Hg=0.133 kPa)] for 60 minutes and followed by intratracheal
lipopolysaccharide 2 mg/kg and continuous
bleeding with
amputation of the tail. Then, animals were partially resuscitated with LRS of 3 times the volume of shed blood (LRS group), followed by a bolus dose of 4 ml/kg
body weight of 7.5%NaCl (HS), or hydroxyethyl
starch (a volume equal to that of the shed blood), respectively, during different fluid
resuscitation regimes. After that, comprehensive
resuscitation phase of 60 minutes began with hemostasis, and transfusion of all the shed blood plus same amount of
normal saline. Observation phase was continued for 3.5 hours. At the end the experiment, the lung tissue was sampled to measure wet-to-dry lung weight ratio (W/D), and the expression of AQP1 and AQP5 were determined with immunohistochemistry. The
paraffin-embedded lungs were stained with
hematoxylin and
eosin for pathological analysis.
RESULTS: When compared with NF and LRS groups, the lung W/D ratio was significantly decreased, and the
shock induced decreased expression of AQP1 and AQP5 in lung tissue were attenuated in HES group, but these beneficial effects were blunted in the HS group.
CONCLUSION: Uncontrolled
hemorrhagic shock may induce
lung injury and
pulmonary edema as well as down regulation of the expression of AQP1 and AQP5 in rats.
Resuscitation with hypertonic fluids, especially with HES, can reduce lung damage and
pulmonary edema in this kind of
shock. The cause may be due in part to maintenance of the expression of AQP1 and/or AQP5 in the lung. Pulmonary AQP1 and AQP5 play an important role in fluid transportation.