摘要
目的 探讨严重腹腔感染状态下大鼠胃粘膜血流量 (gastricmucosalbloodflow ,GMBF)和胃粘膜内pH值 (pHi)的变化及意义。方法 利用大鼠盲肠结扎穿孔造成腹腔严重感染动物模型 ,应用激光多普勒微循环血流计测定穿孔前和穿孔后 3、6、12、2 4、48h各时相大鼠GMBF ,用玻璃电极法测定粘膜内pHi的变化。结果 感染组GMBF在盲肠穿孔后 3h与对照组相比明显降低 (P <0 0 5 ) ,12h降至最低 (P <0 .0 1) ,2 4h开始回升 ,48h仍低于对照组。胃粘膜内pHi穿孔后 3h即有下降 ,6h明显低于对照组 (P <0 0 5 ) ,12h下降至最低 (P <0 0 1)。 2 4h有所恢复 ,但显著低于对照组。
Objective To investigate the changes of gastric mucosal blood flow and intramucosal pH value (pHi) during severe intraperitoneal infection in rats and the related significance. Methods The intraperitoneal infection rat model was established by cecal ligation and puncture (CLP). Laser Doppler blood flow meter on micro circulation and the vitreous electrode were used to examine the gastric mucosal blood flow and the gastric mucosal pH value, respectively. Results The gastric mucosal blood flow (GMBF) in the infected group was significantly lower than that in the control group ( P <0.05) at 3 h after CLP, and rapidly dropped to the lowest ( P <0.01) at 12 h after perforation, but began to increase at 24 h. At 48 h following CLP, GMBF still remained lower in the infected group than that in the control group. Compared with that in the control group, gastric mucosal pH in the infected group decreased significantly ( P <0.05) at 6 h after perforation, and rapidly dropped to the lowest at 12 h after perforation ( P <0.01). At 24 h after perforation, pHi was still significantly lower in the infected group than that in the control group ( P <0.01). Conclusion The decrease of GMBF and pHi might be the major reason for gastric mucosal barrier damage following severe abdominal infection induced by CLP.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2004年第7期614-616,共3页
Journal of Third Military Medical University