Saperas E, Taché Y
CURE/Digestive Disease Center, VA Wadsworth Medical Center, Los Angeles, California 90073.
Dig Dis Sci. 1994 Jan;39(1):152-6. doi: 10.1007/BF02090075.
The underlying mechanisms involved in endotoxin-induced inhibition of gastric acid secretion were investigated in conscious rats with pylorus ligation for 2 hr. Intraperitoneal injection of endotoxin (0.1, 1, and 5 micrograms/rat) inhibited gastric acid output by 31%, 80%, and 84% respectively. Intraperitoneal endotoxin (1 microgram/rat) -induced inhibition of gastric acid secretion was not altered by pretreatment with the interleukin-1 receptor antagonist, IL-1RA, indomethacin, naloxone, or capsaicin. Treatments were injected peripherally at doses previously shown to antagonize the antisecretory effect of exogenous interleukin-1 beta, to inhibit prostaglandin synthesis in the stomach and brain, to block opiate receptors, and to alter functioning of unmyelinated afferent nerve fibers. These results indicate that the antisecretory effect of endotoxin can be expressed by factors other than interleukin-1, prostaglandins, or opioid peptides that do not require the integrity of capsaicin-sensitive afferent pathways.
在幽门结扎2小时的清醒大鼠中,研究了内毒素诱导胃酸分泌抑制的潜在机制。腹腔注射内毒素(0.1、1和5微克/只大鼠)分别使胃酸分泌量减少31%、80%和84%。腹腔注射内毒素(1微克/只大鼠)诱导的胃酸分泌抑制作用,不会因用白细胞介素-1受体拮抗剂(IL-1RA)、吲哚美辛、纳洛酮或辣椒素预处理而改变。这些药物以前述剂量经外周注射,分别用于拮抗外源性白细胞介素-1β的抗分泌作用、抑制胃和脑中前列腺素的合成、阻断阿片受体以及改变无髓传入神经纤维的功能。这些结果表明,内毒素的抗分泌作用可由白细胞介素-1、前列腺素或阿片肽以外的因素介导,且这些因素不需要辣椒素敏感传入通路的完整性。