论文部分内容阅读
目的：探讨内皮素１（ＥＴ－１）在应激性溃疡形成与发展中的意义。方法：采用大鼠冷束缚应激溃疡模型（ＣＲＳ），动态检测应激前及应激后１，３，６，９，１２ｈ各时相血浆、胃粘膜组织ＥＴ－１含量、胃粘膜血流量（ＧＭＢＦ）及溃疡指数（ＵＩ）的变化。结果：应激后血浆、胃粘膜组织ＥＴ－１含量均较应激前明显升高，其中血浆ＥＴ－１含量于６ｈ达峰值，以后虽有所下降，但１２ｈ内仍高于正常（Ｐ＜０．０５）。而胃粘膜组织ＥＴ－１含量在应激后１２ｈ内持续显著上升（Ｐ＜０．０１）；同时ＧＭＢＦ明显降低（Ｐ＜０．０１），ＵＩ明显增加（Ｐ＜０．０１）。胃粘膜ＥＴ－１与ＵＩ呈显著正相关（ｒ＝０．９８４，Ｐ＜０．０１），与ＧＭＢＦ呈显著负相关（ｒ＝－０．８４２，Ｐ＜０．０５）。结论：内源性ＥＴ－１可能参与了应激性溃疡的形成与发展，其作用机制可能是通过减少ＧＭＢＦ，进而引起胃粘膜的缺血、糜烂与溃疡的形成
Objective: To investigate the significance of endothelin-1 (ET-1) in the formation and development of stress ulcer. Methods: Rat model of cold restraint stress ulcer (CRS) was used to detect the content of ET-1 in plasma and gastric mucosa before and after stress 1, 3, 6, 9 and 12 h, the gastric mucosal blood flow (GMBF) and ulcer index (UI) changes. Results: After stress, the content of ET-1 in plasma and gastric mucosa significantly increased compared with those before stress, and the content of ET-1 in plasma reached its peak at 6h after the stress, though still decreased after 12h, but still higher than normal within 12h (P < 0.05). However, the content of ET-1 in gastric mucosa continued to increase significantly within 12 hours after stress (P <0.01). Meanwhile, GMBF was significantly lower (P <0.01) and UI was significantly increased (P <0.01). There was a significant positive correlation between ET-1 and UI in gastric mucosa (r = 0.984, P <0.01), but negatively correlated with GMBF (r = -0.842, P <0.05). CONCLUSION: Endogenous ET-1 may be involved in the formation and development of stress ulcer. Its mechanism may be through the reduction of GMBF, which in turn leads to the formation of gastric mucosal ischemia, erosion and ulcer