论文部分内容阅读
目的 复制老年鼠多器官功能障碍综合征动物模型 ,为进一步探讨其发病机制奠定基础。方法 将 2 10只2 4月龄Wistar大鼠分为油酸 +脂多糖组 (O +LPS组 )、油酸组 (O组 )、脂多糖组 (LPS组 )。O +LPS组注射油酸 0 175ml/kg ,8h后再注射脂多糖 2 5ml/kg。O组和LPS组分别注射油酸 0 175ml/kg和脂多糖 2 5ml/kg。注射后持续 1 5L/min给氧4h(伤后 1h组除外 )。观测伤前及伤后 1、6、12、2 4、72、12 0h的肺、心、肝、肾、小肠功能变化、全身炎症反应发生率、多器官功能障碍综合征 (MODS)发生率及死亡率。结果 伤后 1~ 2 4h ,O +LPS组的动脉血氧分压 (PaO2 )低于 9 3kPa ,谷丙转氨酶、总胆红素、尿素氮、肌酐、谷草转氨酶、肌酸磷酸激酶、二胺氧化酶的最高值分别达 ( 2 83± 2 61 8)U/L、( 1 65± 0 97)μmol/L、( 18 5± 6 0 )mmol/L、( 76 7± 12 9)mmol/L、( 911 3± 5 16 8)U/L、( 1886± 1876)U/L、( 82 9 3± 3 14 2 10 3 )U/L ,均显著高于伤前自身对照值 (P <0 0 5 ,P <0 0 1)。伤后 6~ 2 4h ,MODS发生率分别为O +LPS组 70 %、LPS组 17 4%、O组15 4%;死亡率分别为O +LPS组 3 3 3 %、LPS组 2 3 3 %、O组 13 3 %。O +LPS组的MODS发生率和死亡率显著高于LPS组和O组 (P <0 0 1)。结论 本
Objective To copy the animal model of multiple organ dysfunction syndrome in old mice and lay a foundation for further exploring its pathogenesis. Methods Two hundred and twenty-two Wistar rats aged 24 months were divided into three groups: oleic acid + lipopolysaccharide group (O + LPS group), oleic acid group (O group) and lipopolysaccharide group (LPS group). O + LPS group injected oleic acid 0 175ml / kg, 8h and then injected lipopolysaccharide 25ml / kg. O group and LPS group were injected oleic acid 0 175ml / kg and lipopolysaccharide 25ml / kg respectively. Continuous injection of oxygen at 15 L / min for 4 h after injection (except 1 h after injury). The changes of lung, heart, liver, kidney and small intestine, the incidence of systemic inflammatory response and the incidence of multiple organ dysfunction syndrome (MODS) at 1, 6, 12, 24, mortality rate. Results The arterial partial pressure of oxygen (PaO2) in O + LPS group was lower than that of 93 kPa at 1 ~ 24 h after injury, and alanine aminotransferase, total bilirubin, urea nitrogen, creatinine, aspartate aminotransferase, creatine phosphokinase, The highest values of oxidase were (2 83 ± 2 61 8) U / L, (1 65 ± 0 97) μmol / L, (18 5 ± 60) mmol / L and L, (911 3 ± 5 16 8) U / L, (1886 ± 1876) U / L and (82 9 3 ± 3 14 2 10 3) U / L were significantly higher than pre-injury self-control value (P < 0 0 5, P <0 0 1). The incidence of MODS was 70% in O + LPS group, 17.4% in LPS group and 15.4% in O group after 6 ~ 24 hours after injury. The mortality rate was 33.3% in O + LPS group and 23.3% in LPS group, respectively , O group 13 3%. The MODS incidence and mortality in O + LPS group were significantly higher than those in LPS group and O group (P <0.01). Conclusion of this