Objective: To investigate the protective effect of ulinastatin on acute lung injury in mice with severe heat stroke.
Methods: 60 SPF male C57/BL6 mice were randomly divided into 6 groups (n=10): normal group, severe heatstroke model group, administration group before modeling, normal saline group before modeling, and administration after modeling The drug group and the normal saline group after modeling. The mice in the normal group were placed in an environment of (22±1) °C, and the mice in the other groups were placed in a heating chamber (temperature 37 °C, humidity 60%) for continuous heating. 10 min intraperitoneal injection of UTI 5×104 U/kg, while the two normal saline groups were intraperitoneally injected with the same amount of normal saline, the rectal temperature (Tc) was manually measured once every 30 min with a mercury thermometer for the first 1.5 h during the heating period, and then every The rectal temperature was measured once every 15 minutes, and when the Tc reached 42.7 °C (as a sign of severe heat stroke), the patients were evacuated from the high temperature chamber and transferred to room temperature for rewarming for 6 hours. The pathological changes of lung tissue in each group were observed, and the protein content, lung wet/dry ratio (W/D), lung water content, and pulmonary vascular permeability (Bronchial Alveolar Lavage Fluid, BALF) in each group were detected. Evans blue content).
RESULTS: Compared with the normal group, the severe heat stroke model group and the normal saline group before and after modeling had severe lung damage and obvious pathological changes. The permeability was significantly increased (P<0.05), and="" there="" was="" no="" significant="" difference="" between="" the="" groups="" p="">0.05). Compared with the severe heatstroke model group and the normal saline group before and after modeling, the lung cancer of the drug administration group after modeling The pathological changes in the lungs were significantly improved, and the lung W/D value, lung water content, protein content in BALF, and pulmonary vascular permeability were significantly reduced, but higher than those in the normal control group (all P<0.05), while the drug-administered group before modeling was significantly lower than the normal control group (P<0.05). Compared with other heat shock groups, the time of Tc≥42.7 ℃ in mice was significantly longer, but the above-mentioned lung injury indexes were not significantly improved.
Conclusion: Ulinastatin has inhibitory effect on pulmonary edema and inflammatory exudation caused by severe heat stroke, and can effectively fight against acute lung injury caused by severe heat stroke and play a protective role.