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目的 观察油酸 脂多糖致老年大鼠多器官功能障碍综合征 (multipleorgandysfunctionsyndromeintheelderlyrats ,MODSE)脏器损伤的规律 ,探讨肺损伤在这一过程中的作用 ,以及TNF α在MODSE发生、发展中的作用。方法 80只SD大鼠 (2 0月龄和 3月龄各 40只 )分为老年组及青年组 ,予油酸 (OA ,0 2 5ml kg)和脂多糖 (LPS ,3 5mg kg)分次静脉注射(间隔 4h) ,建立二次打击MODSE和青年MODS(MODSY)模型。观察对照组及伤后 2、6、2 4h ,重要器官 (肺、心、肝、肾 )病理及功能的变化 ,同时检测血清及肺、心、肝和肾组织中TNF α含量。结果 相同剂量的OA +LPS均能导致青年及老年鼠发生MODS。OA +LPS致伤后 2h ,老年组和青年组PaO2 即显著降低 [分别为 (67 5± 8 66)、(5 9 3± 7 41)mmHg ,P <0 0 1] ,提示肺脏损害出现最早、程度最重。伤后 6h ,心、肝、肾生化指标达峰值 (P <0 0 5 ) ,且老年组脏器损害较同时相点的青年组明显为重 (P <0 0 5 )。伤后 2h ,血清及肺、心、肝和肾组织中TNF α含量即达峰值 ,且持续高于正常对照组 (P <0 0 5 ) ,其中以肺脏中TNF α升高幅度最大。老年组TNF α含量均显著高于同时相点的青年组 (P <0 0 5 )。结论 油酸 +脂多糖所致老年鼠多器官功能障碍重于青年鼠 ,其中以肺损
Objective To observe the regularity of oleic acid lipopolysaccharide (LPS) -induced organ damage in aged rats with multiple organ dysfunction syndrome (MODSE), and to explore the role of lung injury in this process and the role of TNFα in the occurrence and development of MODSE. Methods Totally 80 SD rats (20 months old and 3 months old, 40 rats each) were divided into the elderly group and the young group. The animals were divided into three groups: oleic acid (025ml), lipopolysaccharide (LPS) Intravenous injection (interval 4h), the establishment of secondary attack MODSE and youth MODS (MODSY) model. The changes of pathology and function of vital organs (lung, heart, liver, kidney) at 2, 6, 24 h after injury were observed. TNFα levels in serum, lung, heart, liver and kidney tissues were also measured. Results The same dose of OA + LPS can cause MODS in young and old rats. 2h after OA + LPS injury, the PaO2 in the elderly group and the young group were significantly decreased [(67 5 ± 8 66), (59 3 ± 7 41) mmHg, respectively; P 0 01), suggesting that lung damage occurred the earliest , The most serious. Six hours after injury, the biochemical indexes of heart, liver and kidney reached the peak values (P <0.05), and the age-related visceral damage in the elderly group was significantly heavier than that in the young group (P <0.05). At 2h after injury, the content of TNFα in serum, lung, heart, liver and kidney reached the peak, which was consistently higher than that of the normal control group (P <0.05). The levels of TNFα in the elderly group were significantly higher than those in the young group (P <0.05). Conclusion The multi-organ dysfunction caused by oleic acid + lipopolysaccharide in aged mice is more severe than that in young mice,