Fitzpatrick D W, Fisher H
Surgery. 1982 Apr;91(4):430-4.
The relationships among anserine (beta-alanyl-1-methyl-L-histidine), carnosine (beta-alanyl-L-histidine), free histidine, and histamine metabolism were examined in rats wounded by dorsal skin incision. Following wounding, rats were treated with either a histamine liberator (compound 48/80) or a histidine decarboxylase inhibitor (4-imidazolyl-3-amino-2-butanone). The liberator greatly enhanced wounded skin-breaking strength and collagen deposition at the wound site, while the histidine decarboxylase inhibitor reduced skin-breaking strength and collagen deposition. In the second experiment of this study, histamine or histidine treatment was shown to prevent trauma-induced reductions of tissue carnosine but was less effective in ameliorating tissue anserine loss. The results illustrate an interaction between imidazole dipeptides and stress and suggest that carnosine acts as a histidine reserve in relation to histamine synthesis during trauma.
在背部皮肤切开致伤的大鼠中,研究了鹅肌肽(β-丙氨酰-1-甲基-L-组氨酸)、肌肽(β-丙氨酰-L-组氨酸)、游离组氨酸和组胺代谢之间的关系。致伤后,给大鼠注射组胺释放剂(化合物48/80)或组氨酸脱羧酶抑制剂(4-咪唑基-3-氨基-2-丁酮)。释放剂显著增强了伤口皮肤的抗张强度和伤口部位的胶原蛋白沉积,而组氨酸脱羧酶抑制剂则降低了皮肤抗张强度和胶原蛋白沉积。在本研究的第二个实验中,结果表明组胺或组氨酸处理可防止创伤引起的组织肌肽减少,但在改善组织鹅肌肽损失方面效果较差。这些结果说明了咪唑二肽与应激之间的相互作用,并表明在创伤期间,肌肽作为组胺合成相关的组氨酸储备发挥作用。