Bunker C B, Foreman J C, Dowd P M
Department of Dermatology, University College and Middlesex School of Medicine, London, UK.
Agents Actions. 1991 May;33(1-2):197-9. doi: 10.1007/BF01993166.
A defective histaminergic dilating system in the digital vasculature has been proposed for the pathophysiology of Raynaud's phenomenon but this is not supported by studies of digital intradermal responses to histamine or agents which cause histamine release. The vascular responses (measured by planimetry and laser Doppler flowmetry) of digital skin over the middle phalanx to intradermal histamine, compound 48/80 and Substance P have now been studied at low temperatures (because it is in the cold that Raynaud's phenomenon occurs) in normal controls and patients with primary Raynaud's phenomenon. A cold-related attenuation of mast cell histamine release by compound 48/80 was observed in both normal and Raynaud's subjects. These results do not support a major histaminergic defect in the pathogenesis of Raynaud's phenomenon.
有人提出，指端血管系统中组胺能舒张系统缺陷是雷诺现象病理生理学的原因，但对组胺或引起组胺释放的药物的指端皮内反应研究并不支持这一观点。现在，已在正常对照组和原发性雷诺现象患者中，于低温条件下（因为雷诺现象发生于寒冷环境）研究了中节指骨处指端皮肤对皮内注射组胺、化合物48/80和P物质的血管反应（通过平面测量法和激光多普勒血流仪测量）。在正常人和雷诺现象患者中均观察到，化合物48/80引起的肥大细胞组胺释放在低温时减少。这些结果不支持组胺能缺陷在雷诺现象发病机制中起主要作用的观点。
