Savage M V, Brengelmann G L, Buchan A M, Freund P R
Department of Physiology and Biophysics, University of Washington, Seattle 98195.
J Appl Physiol (1985). 1990 Dec;69(6):2149-54. doi: 10.1152/jappl.1990.69.6.2149.
The transmitter substance for the active cutaneous vasodilation that accompanies sweating during hyperthermia in humans is unknown. Hökfelt et al. (Nature Lond. 284: 515-521, 180) hypothesized that it is vasoactive intestinal polypeptide (VIP) that is cotransmitted with acetylcholine. Heinz-Erian et al. (Science Wash. DC 229: 1407-1408, 1985) reported that VIP innervation is sparse in the skin of persons with cystic fibrosis (CF). A corresponding attenuation of active vasodilation in these subjects would be evidence that VIP is involved in this effector mechanism of human thermor-regulation. Immunocytochemical analysis of skin biopsies from four men with CF confirmed that VIP innervation was sparse. We also analyzed immunoreactivity for calcitonin gene-related peptide (CGRP; normal), substance P (normal), and neuropeptide Y (low). VIP-immunoreactive Merkel cells were abnormal. Despite sparse VIP-immunoreactive innervation, our CF subjects' cutaneous vascular responses to hyperthermia were normal. Because VIP was not completely absent, this evidence is insufficient to rule out VIP as the vasodilator transmitter. However, the CGRP and substance P innervation we observed could mean that release of one or both of these peptides was the mechanism of the fully developed active cutaneous vasodilation.
在人类体温过高时出汗所伴随的主动性皮肤血管舒张的递质尚不清楚。霍克费尔特等人（《自然》伦敦版，284卷：515 - 521页，1980年）推测，与乙酰胆碱共同传递的是血管活性肠肽（VIP）。海因茨 - 埃里安等人（《科学》华盛顿特区版，229卷：1407 - 1408页，1985年）报告称，囊性纤维化（CF）患者皮肤中的VIP神经支配稀疏。这些受试者中相应的主动性血管舒张减弱将证明VIP参与了人类体温调节的这一效应机制。对四名CF男性患者的皮肤活检进行免疫细胞化学分析证实，VIP神经支配稀疏。我们还分析了降钙素基因相关肽（CGRP；正常）、P物质（正常）和神经肽Y（低）的免疫反应性。VIP免疫反应性的默克尔细胞异常。尽管VIP免疫反应性神经支配稀疏，但我们的CF受试者对体温过高的皮肤血管反应正常。由于VIP并未完全缺失，这一证据不足以排除VIP作为血管舒张递质的可能性。然而，我们观察到的CGRP和P物质神经支配可能意味着这两种肽中的一种或两种的释放是完全发展的主动性皮肤血管舒张的机制。
