{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T13:18:04Z","timestamp":1753881484233,"version":"3.41.2"},"reference-count":21,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,4,24]],"date-time":"2021-04-24T00:00:00Z","timestamp":1619222400000},"content-version":"vor","delay-in-days":113,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"University Medical Center Ljubljana","award":["20160033"],"award-info":[{"award-number":["20160033"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["BioMed Research International"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p><jats:italic>Background<\/jats:italic>. Calcitonin gene\u2010related peptide (CGRP) is regarded as an important molecule in trigeminovascular sensitization (TVS). CGRP\u2010induced headaches (CGRP\u2010IH) are evoked by intravascular administration of CGRP in nonmigraine and migraine subjects. CGRP might be associated with vasodilatation of the middle cerebral artery (MCA). It is unclear whether CGRP\u2010induced hemodynamic changes relate to CGRP\u2010IH in nonmigraine subjects. <jats:italic>Methods<\/jats:italic>. Twenty healthy subjects participated in our study. Polymodal recording of mean arterial velocity in MCA (vm MCA), end\u2010tidal carbon dioxide partial pressure (Et\u2010CO<jats:sub>2<\/jats:sub>), mean arterial pressure (MAP), and heart rate (HR) was employed using transcranial Doppler (TCD) sonography. During the experiment, we administered intravenous infusion of CGRP at a rate of 1.5\u2009mcg\/min. The vm MCA, Et\u2010CO<jats:sub>2<\/jats:sub>, HR, and MAP were determined at time points <jats:italic>T<\/jats:italic><jats:sub>0<\/jats:sub>, <jats:italic>T<\/jats:italic><jats:sub>1<\/jats:sub>, <jats:italic>T<\/jats:italic><jats:sub>2<\/jats:sub>, and <jats:italic>T<\/jats:italic><jats:sub>3<\/jats:sub>. We calculated the responses at different time points and combined them into a single response vm MCA<jats:sub>tot<\/jats:sub>, Et\u2010CO<jats:sub>2tot<\/jats:sub>, HR<jats:sub>tot<\/jats:sub>, and MAP<jats:sub>tot<\/jats:sub>. <jats:italic>Results<\/jats:italic>. We found significant differences along the time points in vm MCA (<jats:italic>p<\/jats:italic> = &lt;0.001), Et\u2010CO<jats:sub>2<\/jats:sub> (<jats:italic>p<\/jats:italic> = 0.003), MAP (<jats:italic>p<\/jats:italic> &lt; 0.001), and HR (<jats:italic>p<\/jats:italic> &lt; 0.001). The relationship between vm MCA<jats:sub>tot<\/jats:sub> and Et\u2010CO<jats:sub>2tot<\/jats:sub> was significant and positive (<jats:italic>p<\/jats:italic> = 0.005). The <jats:italic>t<\/jats:italic>\u2010test showed significant differences between CGRP\u2010IH and non\u2010CGRP\u2010IH subjects in vm MCA<jats:sub>tot<\/jats:sub> (<jats:italic>p<\/jats:italic> = 0.021) but not in Et\u2010CO<jats:sub>2tot<\/jats:sub> (<jats:italic>p<\/jats:italic> = 0.838), MAP<jats:sub>tot<\/jats:sub> (<jats:italic>p<\/jats:italic> = 0.839), and HR<jats:sub>tot<\/jats:sub> (<jats:italic>p<\/jats:italic> = 0.198). Only vm MCA<jats:sub>tot<\/jats:sub> showed a significant relationship with CGRP\u2010IH (<jats:italic>p<\/jats:italic> = 0.028). <jats:italic>Conclusions<\/jats:italic>. Our study provides evidence for vasodilatation of MCA in relation to CGRP\u2010IH due to intravascular CGRP detected by multimodal TCD. In the context of TVS induced by CGRP, MCA vasodilatation seems to represent an epiphenomenon of the underlying TVS.<\/jats:p>","DOI":"10.1155\/2021\/5540254","type":"journal-article","created":{"date-parts":[[2021,4,24]],"date-time":"2021-04-24T18:22:28Z","timestamp":1619288548000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["The Influence of Calcitonin Gene\u2010Related Peptide on Cerebral Hemodynamics in Nonmigraine Subjects with Calcitonin Gene\u2010Related Peptide\u2010Induced 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