摘要
目的探讨大鼠失血性休克复苏后的肠屏障功能,以及与肠道传输和血流量的关系方法 108只Wistar大鼠随机分为假休克(SS)组和失血性休克复苏(HS)组,染料法测定肠道传输,同位素标记生物微球法测量肠道血流量,应用荧光素异硫氢酸葡聚糖(FITC-D)和辣根过氧化酶(HRP)Ⅱ型两种分子探针测定小肠通透性,同时观察肠腔内细菌繁殖和细菌移位.结果 HS组1,2h时相点小肠传输速率为13.5％和24.6％,较SS组的51.5％和56.6％显著延迟(P<0.01)HS组1和2h空肠、回肠和结肠血流量显著降低,分别为0.52和0.47mL·min^1·g^1(SS组的1.13和1.04,P<0.05),0.43和0.41mL·min^(-1)·g^(-1)(SS组0.80和0.80,P<0.05),0.36和0.27mL·min^(-1)·g^(-1)(SS组0.62和0.64,P<0.01);HS组1,2h后肠腔内注射FITC-D门静脉血中含量显著升高,空肠内注射后分别为1.38和1.41mg·L^(-1)(SS组0.14和0.13,P<0.01),回肠内注射后分别为0.18和0.21mg·L^(-1)(SS组0.03和0.03,P<0.01);HS组1,2h后肠腔内注射HRP门静脉血中含量显著升高,空肠内注射后分别为6.25和8.16μg·L^(-1)(SS组3.18和2.88,P<0.01),回肠内注射后分别为3.15和3.08μg·L^(-1)(SS组1.59和1.57,P<0.01);HS组1,2和4h后小肠内细菌含量增加,空肠1,2h为58.0,82.0(×10~3CFU/cm^2)(SS组9.4,9.8,P<0.05).回肠2,4h为114.7,71.2(×10~3CFU/cm^2)(SS组10.2,20.4,P<0.05).伴随细菌移位的发生.结论失血性休克复苏后存在肠屏障功能损害,肠道传输延迟导致的肠道内细菌过度繁殖和肠道血流量下降引起的肠道通透性增加可能是肠源性细菌移位的重要机制.
AIM To investigate the gut barrier function disturbance after hemorrhagic shock resuscitation. METHODS A total of 108 Wistar rats were randomly divided into sham shock (SS) group and hemorrhagic shock resuscitation (HS) group. Small bowel transit was measured with coloring matter and the blood flow volume of intestinal tract were measured by isotope label biological microglobulin. The intestinal permeability of jejunum and ileum were determined by two molecular probing needle, FITC-D and HRP Ⅱ. RESULTS An obvious retarding of intestinal transit after hemorrhagic shock resuscitation was seen, the speed of intestinal transit at 1 and 2 h of HS was 13. 5% and 24. 6% (vs SS 51. 5% and 56. 6%, P<0. 01). The blood flow volume of intestinal tract after HS was decreased significantly, the blood flow volume at 1 and 2 h after HS of jejunum, ileum and colon was 0. 52 and 0. 47 mL·min^1. g^1(vs SS 1. 13 and 1. 04, P<0. 05), 0. 43 and 0. 41 mL· min^1·g^1(vs SS 0. 80 and 0. 80, P<0. 05), 0. 36 and 0. 27 mL·min^1·g^1(vs SS 0. 62 and 0. 64, P<0. 01). At the same time, the intestinal permeability of jejunum and ileum to FITC-D and HRP was increased. The level of FITC- D in portal vein 1 and 2 h HS after injecting FTIC-D into jejunum was 1. 38 and 1. 41 mg·L^(-1) (vs SS 0. 14 and 0. 13, P<0. 01), after into ileum was 0. 18 and 0. 21 mg·L^(-1)(vs SS 0. 03 and 0. 03, P<0. 01) hemorrhagic shock resuscitation; and after injecting HRP into jejunum was 6. 25 and 8. 16μg·L^1(vs SS 3. 18 and 2. 88, P<0. 01), into ileum was 3. 15 and 3. 08μg. L^(-1)(vs SS 1. 59 and 1. 57, P<0. 01). The bacteria in jejunum and ileum of HS were overgrowth, jejunum 1 and 2 h was 58. 0, 82. 0 (×10~3 CFU/ cm^2)(vs SS 9. 4 and 9. 8, P<0. 05), ileum 2 and 4 h was 114. 7 and 71. 2 (×10~3 CFU/cm^2) (vs SS 10. 2 and 20. 4, P<0. 05). And the bacterial translocation incidence in bacteremia, liver, spleen, kidney and mesenteric lymph nodes significantly increased. CONCLUSION After hemorrhagic shock resuscitation, there is gut barrier function disturbance. The overgrowth of bacteria in jejunum and ileum, caused by slow intestinal transit, and the increase of intestinal permeability of jejunum and ileum as a result of decrease of intestinal blood flow volume may play an important role on gut bacterial translocation.
出处
《世界华人消化杂志》
CAS
2001年第7期767-770,共4页
World Chinese Journal of Digestology
关键词
出血性休克
复苏术
病理生理
微生物
细菌移位
shock, hemorrhagic
resuscitation
intestines/physiopathology
intestines/microbiology
bacterial translocation
