摘要
目的 :探讨严重腹腔感染状态下大鼠胃粘膜Na+ -K+ -ATPase活性变化对胃粘膜电位差 (GTPD)的影响。方法 :利用大鼠盲肠结扎穿孔造成腹腔严重感染动物模型 ,应用电生理记录仪检测穿孔前和穿孔后 3h、6h、12h、2 4h、4 8hGTPD变化 ;应用生化法测定了各时相大鼠胃粘膜Na+ -K+ -ATPase活性。结果 :盲肠穿孔后 3hNa+ -K+ -ATPase活性显著降低 (P <0 .0 5 ) ,12h降至最低 (P <0 .0 1) ,仅为对照组的 4 8.5 % ,4 8h仍未恢复正常。GTPD伤后 6h显著下降 (P <0 .0 5 ) ,12h降至最低 (P <0 .0 1) ,2 4h和 4 8h仍显著低于对照组(P <0 .0 5 ,P <0 .0 5 )。结论 :严重腹腔感染状态下胃粘膜Na+ -K+ -ATPase活性降低可能是引起胃粘膜屏障功能受损的主要原因。
Objective:To investigate the effect of gastric mucosal Na +-K +-ATPase activity on gastric transmucosal potential difference during severe intraperitoneal infection in rats.Methods: The intraperitoneal infection rat model was established by cecal ligation and puncture(CLP). The electric-physiological recorder meter was used to measure gastric mucosal potential difference. Assay of Na +-K +-ATPase activity in gastric mucosal tissue was conducted by biochemistry method. Results:The activity of Na +-K +-ATPase was markedly decreased in infected group at 3h after perforation, compared with the control group ( P <0.05) . There was a minimum of Na +-K +-ATPase activity at 12h post-perforation in infected group ( P <0.01), only about 46.6% matched to the control group. Gastric transmucosal potential difference (GTPD) of infected group decreased significantly compared with the control group ( P <0.05) at 6h after perforation, and rapidly dropped to the lowest at 12h post-perforation ( P <0.01). At 24h and 48h after perforation, GTPD was lower in infected group than that in the control group ( P <0.05, P <0.05). Conclusion:The reduce of Na +-K +- ATPase activity might be play an important role in gastric mucosal barrier damage following severe abdominal infection induced by CLP.
出处
《中国现代医学杂志》
CAS
CSCD
2003年第11期34-36,共3页
China Journal of Modern Medicine