Objective To establish a rat model of traumatic hemorrhagic shock in dry-hot desert environment. Methods Ninety male SD rats were randomly equally divided into three groups (n=30): the normal temperature environment traumatic hemorrhagic shock group (normal temperature group) (temperature 25℃, humidity 35%), dry-hot traumatic hemorrhagic shock group I (dry heat group I) and dry-hot traumatic hemorrhagic shock group Ⅱ(dry heat group II)(temperature 40℃, humidity 10%). The rats were anesthetized, fixed, and intravenous indwelling needles were inserted into the right carotid artery, vein and the right femoral artery so as to make bleeding, and at the same time, fracture of the left hindlimb femur was made from the dropped steel wheel. The wounds were quickly bounded after injury. The mean arterial pressure was kept at 35±5 mmHg. The rats of group I was transferred into normal environment. The rats of group II were kept in the dry-hot environment continuously. The 3h-survival rates were calculated, and all the rats were sacrificed at 3 hours after the traumatic injury. Heart, lung and liver tissue samples were taken for histopathological examination using HE staining. Results In the normal environment group, one rat died within less than 2 hours and 2 rats died within 2-3 hours after injury. In the dry-hot environment group I, 2 rats died within 1 hour and 3 rats died within 2-3 hours. In the dry-hot environment group II, 5 rats died within 1 hour and all the rest 27 rats died within 2.5 hours. The survival rates of the normal temperature group, dry-hot groups I and II were 90%, 83.3%, and 0, respectively. There were no significant difference between the normal temperature group and the dry hot group I (P>0.05), but significant difference between the normal temperature group and dry-hot group I and the dry-hot group II (P<0.01). The pathological observation showed that the heart, lung and liver of the dead rats of the normal temperature group, dry hot groups I and in the dry hot group II had more severe edema, degeneration, leukocyte infiltration, wide-spread hemorrhage, and cell necrosis. Conclusions We have successfully established a rat model of traumatic hemorrhagic shock in dry-hot desert environment. The results of this study indicate that the hot desert environment may seriously decrease the survival rate of traumatic hemorrhagic shock rats. It suggests that in dry-hot environment, the traumatic hemorrhagic shock patients should be transported to a normal temperature and humidity environment as soon as possible.