Koyama T, Fujimoto K, Kang M, Yoshimatsu H, Sakata T, Tsunada S, Morita H, Iwakiri R, Sakai T
Department of Internal Medicine, Saga Medical School, Japan.
Proc Soc Exp Biol Med. 1995 May;209(1):27-31. doi: 10.3181/00379727-209-43873.
Our previous study suggested that histamine might enhance the increase of ornithine decarboxylase activity in injured intestinal mucosa. To test this hypothesis, we measured histamine content in mesenteric lymph and ornithine decarboxylase activity in intestinal mucosa after ischemia-reperfusion in the rat. We examined the effect of alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase, on ornithine decarboxylase activity after ischemia-reperfusion and compared this with its effect on the rat after refeeding. Ischemia-reperfusion was performed by 15-min occlusion of the superior mesenteric artery. After ischemia-reperfusion, histamine content in mesenteric lymph increased, and this increase was completely suppressed by alpha-fluoromethylhistidine pretreatment. In contrast to ischemia-reperfusion, histamine content in mesenteric lymph did not change after refeeding. Ornithine decarboxylase activity increased markedly 3 and 6 hr after ischemia-reperfusion and refeeding, whereas alpha-fluoromethylhistidine attenuated the increase in ornithine decarboxylase activity only in the ischemia-reperfusion group. These results indicate that increase in histamine synthesis in the intestinal mucosa plays an important role in the increase of ornithine decarboxylase activity after ischemia-reperfusion but that histamine is not related to the increase in ornithine decarboxylase activity after refeeding.
我们之前的研究表明，组胺可能会增强受损肠黏膜中鸟氨酸脱羧酶活性的增加。为了验证这一假设，我们测量了大鼠缺血再灌注后肠系膜淋巴中的组胺含量以及肠黏膜中的鸟氨酸脱羧酶活性。我们研究了组氨酸脱羧酶的自杀性抑制剂α-氟甲基组氨酸对缺血再灌注后鸟氨酸脱羧酶活性的影响，并将其与对再喂养大鼠的影响进行比较。通过阻断肠系膜上动脉15分钟来进行缺血再灌注。缺血再灌注后，肠系膜淋巴中的组胺含量增加，而这种增加被α-氟甲基组氨酸预处理完全抑制。与缺血再灌注不同，再喂养后肠系膜淋巴中的组胺含量没有变化。缺血再灌注和再喂养后3小时和6小时，鸟氨酸脱羧酶活性显著增加，而α-氟甲基组氨酸仅在缺血再灌注组中减弱了鸟氨酸脱羧酶活性的增加。这些结果表明，肠黏膜中组胺合成的增加在缺血再灌注后鸟氨酸脱羧酶活性的增加中起重要作用，但组胺与再喂养后鸟氨酸脱羧酶活性的增加无关。
