摘要

Current antimigraine drugs are believed, besides their direct vasoconstrictive effect, to inhibit calcitonin gene-related peptide (CGRP) release from trigeminal nerve endings during migraine. Objective: The objective of this report is to establish a biomarker for the CGRP-interfering effect of antimigraine drugs. Methods: We quantified the effect of sumatriptan on the trigeminal nerve-mediated rise in forehead dermal blood flow (DBF), induced by capsaicin application (0.6 mg/ml) and electrical stimulation (0.2-1.0 mA), in a randomised, double-blind, placebo-controlled, crossover study in healthy male (n = 11, age +/- SD: 29 +/- 8 years) and female (n = 11, 32 +/- 7 years) individuals. Results: DBF responses to capsaicin were attenuated by sumatriptan (Delta DBF, mean +/- SEM: 82 +/- 18 AU, p = 0.0002), but not by placebo (Delta DBF: 21 +/- 12 AU, p = 0.1026). Conclusion: We demonstrated that sumatriptan inhibits increases in DBF, induced by the release of, most likely, CGRP. Thus, our model may be used as a biomarker to establish the trigeminovascular effects of (potential) antimigraine drugs, such as CGRP receptor antagonists or antibodies directed against CGRP or its receptor.

  • 出版日期2017-1