Effect Of Ulinastatin On The Inflammatory Mediators Of Rats With Severe Pneumonia

Background:Severe pneumonia fatality rate remained high ,despite of effective antibiotic treatment and other supportive care measures. At present, studies have shown that severe pneumonia resulting from systemic inflammatory response (SIR) caused by multiple organ dysfunction syndrome (MODS) are the body defense mechanism caused by the excessive activation of the outcome of its own destruction, not bacteria or toxins, such as a direct injury. The body is at the role of proinflammatory factors that produce pro-inflammatory cytokines,which promote inflammation, stimulate cell defense response ,eliminate invading micro-organisms, promote tissue repair; at the same time ,the body release anti-inflammatory media, confrontation inflammatory mediators, reduce the generation of inflammatory mediators, so to confine inflammation, control systemic inflammatory response at the appropriate range. If the pro-inflammatory and anti-inflammatory are balance, environmental stability; If any party to gain advantage, there will be SIRS or CARS, and further damage caused by the body itself. How to effectively promote the in vivo pro-inflammatory / anti-inflammatory balance, to maintain stability within the environment has become a new hot spot for the treatment of severe pneumonia.Objective:To duplicate the severe pneumonia animal model of SD rats.To investigate the effection of ulinastatin on the inflammatory mediators and anti-inflammatory mediators,to explore ulinastatin on the protective effect of severe pneumonia. Methods:A rat model of severe pneumonia was caused by intratracheal instillation of Klebsiella pneumoniae (0.25ml 1.2×109CFU/ml). 54 SD rats were randomly divided into control group(18), model group(18), ulinastatin group(18). The control group were injected with normal saline by tracheal.The model group and ulinastatin group were induced by intratracheal instillation of Klebsiella pneumoniae to be severe pneumonia.From the 6th day ,the control group and model group were intraperitoneal injection of saline for 5 days, the ulinastatin group intraperitoneal injection of UTI (5×104U/kg). At 7th,9th and 11th day, 6 rats of each group were measurement of serum IL-6, IL-8, IL-10,and lung tissues pathology.Results:1,The clinical symptoms of the model group and ulinastatin group was significantly worse than the control group.2,At 7th,9th,11th day after inoculation,the model group and ulinastatin serum IL-6,IL-8,IL-10 were significantly higher than the control group(P <0.01).UTI can decrease the serum IL-6,IL-8.The 11th IL-6 and 9th,11th IL-8 levels of the ulinastatin group were lower than the model group ,and has statistically significant difference (P <0.05). UTI can increase serum IL -10 levels. The level of the 7th,9th,11th day between the ulinastatin group and model group has statistically significant difference (P <0.01).Conclusion:1,Intratracheal instillation of Klebsiella pneumoniae can successfully make the rat model of severe pneumonia.2,UTI can regulate the inflammatory mediators in rats with severe pneumonia ,and have a therapeutic effect.