Protective effect of dexmedetomidine on pulmonary edema with hemorrhagic shock in rats exposed to plateau environment

To investigate the protective effect of dexmedetomidine on pulmonary edema in rats with hemorrhagic shock after exposure to a plateau environment.

A total of 280 SD male rats（10 weeks old, 200~220 g）were randomly divided into 4 groups: the plateau control（sham）group, the hemorrhagic shock after exposure to the plateau environment（HS）group, the lactated Ringer's resuscitation（LR）group, and the dexmedetomidine + lactated Ringer's resuscitation（DEX+LR）group. Using a low-pressure hypoxic chamber to simulate 5 000 m altitude, the rats have stayed the chamber for 48 h to accept pretreatment, injecting oleic acid treatment via the tail vein. After 0.5 h of induction of oleic acid, the rats were slowly drawn blood via the femoral artery（40% to 50% of the blood volume）to establish a model of hemorrhagic shock after exposure to the plateau environment. The effect of dexmedetomidine on pulmonary vascular permeability was observed by changes in lung water content, pulmonary microvascular permeability and alveolar lavage fluid protein concentration after prophylactic administration of dexmedetomidine; The effect of dexmedetomidine on respiratory function was observed by measuring respiratory rate and tidal volume; Pathological changes of lung tissue was detected by HE staining; Blood gas analysis was used to detect the effect of dexmedetomidine on arterial blood gases and survival rate.

Compared with the sham group, the lung water content, pulmonary microvascular permeability and alveolar lavage fluid protein concentration of the rats in the HS group increased（P<0.05）. The respiratory rate increased（P<0.05）, and the tidal volume and minute ventilation decreased（P<0.05）. Results of HE staining showed that the alveolar wall was thickened, and the lumen of alveoli was partially narrowed, with infiltration of inflammatory cells. Results of arterial blood gas suggested there was acidosis, and rats were in a hypoxic state（P<0.05）. Compared with the HS group, the rats in the LR group had aggravated pulmonary oedema. HE staining showed there was a fusion of alveolar sacs, lung tissue structure was destroyed and appeared obvious inflammatory cell infiltration. Respiratory rate and tidal volume increased, and arterial blood gas got deteriorated（P<0.05）. Dexmedetomidine significantly improved the lung function of rats with hemorrhagic shock pulmonary oedema after exposure to the plateau environment, and there was a decreased in pulmonary microvascular permeability, lung water content and alveolar lavage fluid protein concentration, compared with the lactated Ringer's solution resuscitation group（P<0.05）. The tidal volume, respiratory rate and minute ventilation of the rats tended to be higher than that of the plateau control group（P<0.05）. HE staining results showed that the alveolar structure tended to be intact, and the exudation in the alveolar lumen was reduced or even disappeared. Arterial blood gas analysis suggested that the level of acidosis was improved（P<0.05）, which eventually improved the survival rate.

Pulmonary edema is more likely to be induced during the resuscitation of rats with hemorrhagic shock after exposure to the plateau environment, and prophylactic administration of dexmedetomidine（10 μg/kg）is effective in preventing the development of pulmonary oedema.