Dahlqvist A, Forsgren S, Hellström S
Department of Otorhinolaryngology, University of Umeå, Sweden.
Acta Otolaryngol. 1992;112(4):726-33. doi: 10.3109/00016489209137466.
We previously showed that long-term hypoxia increases the dopamine content in rat laryngeal nerve paraganglia. In the present study paraganglia of rats exposed to hypoxia (10 +/- 0.5% O2) for 14 days were examined immunohistochemically to detect changes in the expression of neuropeptides and catecholamine-synthesizing enzymes. Hypoxia induced an intense cellular substance P (SP)-like immunoreactivity (LI) in some paraganglia and an increase in the number of stromal nerve fibers showing SP-LI in others. The patterns of tyrosine hydroxylase-, dopamine-beta-hydroxylase-, phenylethanolamine-N-methyltransferase-, vasoactive intestinal polypeptide-, neuropeptide-Y and calcitonin gene-related peptide-LI were not changed in response to hypoxia. The results show that hypoxia induces changes in the pattern of SP immunoreactivity in laryngeal nerve paraganglia and may indicate that SP plays a role in the regulation of catecholamine metabolism in this tissue.
我们之前的研究表明,长期缺氧会增加大鼠喉神经节中的多巴胺含量。在本研究中,对暴露于缺氧环境(10±0.5% O₂)14天的大鼠神经节进行免疫组织化学检查,以检测神经肽和儿茶酚胺合成酶表达的变化。缺氧在一些神经节中诱导了强烈的细胞P物质(SP)样免疫反应性(LI),而在其他神经节中则增加了显示SP-LI的基质神经纤维数量。酪氨酸羟化酶、多巴胺-β-羟化酶、苯乙醇胺-N-甲基转移酶、血管活性肠多肽、神经肽Y和降钙素基因相关肽-LI的模式在缺氧反应中没有改变。结果表明,缺氧诱导了喉神经节中SP免疫反应性模式的变化,这可能表明SP在该组织中儿茶酚胺代谢的调节中发挥作用。