Hernandez D E, Arredondo M E, Xue B G
Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.
Neurosci Lett. 1990 Apr 6;111(3):339-43. doi: 10.1016/0304-3940(90)90285-h.
Increasing evidence indicates that thyrotropin-releasing hormone (TRH), and endogenous brain-gut peptide may play a role in experimental ulcerogenesis. Potential interactions between TRH and imipramine (a typical tricyclic antidepressant (TCA] on the development of TRH-induced gastric lesions have not been investigated. Imipramine (0.05, 0.5 and 5 mg/kg, i.p.) dose-dependently inhibited gastric lesion formation induced by intracisternal (i.c.) administration of TRH (1 micrograms). In addition, imipramine (5 mg/kg, i.p.) significantly decreased gastric acid secretion in response to i.c. TRH (1 microgram) in rats with pyloric ligation. These findings suggest the TCAs may be effective drug agents against centrally initiated gastric ulcerations. The mechanism of this response probably involves blockade of cholinergic (muscarinic) and H2 histamine receptors.
越来越多的证据表明,促甲状腺激素释放激素(TRH)和内源性脑肠肽可能在实验性溃疡形成中起作用。TRH与丙咪嗪(一种典型的三环类抗抑郁药(TCA))之间对TRH诱导的胃部病变发展的潜在相互作用尚未得到研究。丙咪嗪(0.05、0.5和5mg/kg,腹腔注射)剂量依赖性地抑制了脑池内(i.c.)注射TRH(1微克)诱导的胃部病变形成。此外,丙咪嗪(5mg/kg,腹腔注射)显著降低了幽门结扎大鼠对脑池内注射TRH(1微克)的胃酸分泌。这些发现表明三环类抗抑郁药可能是对抗中枢引发的胃溃疡的有效药物。这种反应的机制可能涉及胆碱能(毒蕈碱)和H2组胺受体的阻断。