摘要
探讨应激性溃疡的发病机制，通过建立家兔应激性溃疡模型，并观察其血清血栓素Ａ２（ＴＸＡ２）水平变化及胃粘膜和粘膜下层微循环结构的病理改变。结果显示：应激性溃疡家兔血清血栓素Ｂ２（ＴＸＢ２）的水平显著升高，胃组织微循环障碍。作者认为：血清ＴＸＡ２的显著升高及其所介导的胃组织微循环障碍是家兔应激性溃疡发生、发展的重要发病机制之一；联合应用环氧化酶抑制剂和Ｈ２受体阻滞剂对预防和治疗应激性溃疡的发生具有理想效果。
To explore the pathogenesis of stress ulcer,stress ulcer model was established in rabbits,and changes in serum thromboxane(TXA 2)and the structure of microcirculation in the gastric mucosa and submucosa were observed.The results showed that serum TXA 2 in the rabbits with stress ulcer was markedly increased and the microcirculation in the gastric tissues was disordered.It is suggested that the significant increase in serum TXA 2 and the subsequently induced microciruculatory disorder of the gastric tissues is one of the important pathogenetic factors in the emergence and evolution of stress ulcer in the rabbits.Combined use of cycloxidase inhibitor and H 2receptor blocker had obviously preventive and curative effectiveness on the emergence of stress ulcer.
出处
《中国危重病急救医学》
CAS
CSCD
1996年第9期516-518,共3页
Chinese Critical Care Medicine
