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αCGRP-Induced Changes in Cerebral and Systemic Circulation; A TCD Study
Darja Visočnik1, Bojana Žvan1, Marjan Zaletel1
1Department of Neurology, University Medical Center Ljubljana, University of Ljubljana, Ljubljana, Slovenia.
Frontiers in Neurology
|November 26, 2020
Summary
Intravenous alpha CGRP (αCGRP) infusion significantly impacts cerebral and systemic circulation in healthy individuals. This study found αCGRP reduced cerebral blood flow velocity and mean arterial pressure, with a compensatory increase in heart rate.
Area of Science:
- Cardiovascular Physiology
- Neurovascular Regulation
- Pharmacology
Background:
- Calcitonin gene-related peptide (CGRP) is known to cause cerebral vasodilation when applied perivascularly.
- The effects of intravenous alpha CGRP (αCGRP) on cerebral and systemic hemodynamics remain largely uncharacterized.
Purpose of the Study:
- To investigate the hemodynamic effects of a continuous intravenous infusion of αCGRP in healthy human subjects.
- To assess changes in cerebral blood flow velocity and systemic parameters during αCGRP administration.
Main Methods:
- Twenty healthy volunteers received an intravenous infusion of αCGRP at 1.5 mcg/min for 20 minutes.
- Transcranial Doppler (TCD) was used to measure mean arterial velocity in the middle cerebral artery (vm MCA) and posterior cerebral artery (vm PCA).
- Mean arterial pressure (MAP), heart rate (HR), and end-tidal CO2 (Et-CO2) were also monitored.
Main Results:
- αCGRP infusion led to significant decreases in vm MCA (p < 0.001), vm PCA (p < 0.001), MAP (p < 0.001), and Et-CO2 (p = 0.030).
- Heart rate significantly increased during the infusion (p < 0.001).
- A positive correlation was observed between Et-CO2 and vm MCA (p = 0.001) and vm PCA (p = 0.043).
Conclusions:
- Intravenous αCGRP administration induces significant changes in both cerebral and systemic circulation in healthy volunteers.
- The findings suggest αCGRP may cause vasodilation in the MCA and PCA, potentially leading to a compensatory decrease in Et-CO2.
- Further research is warranted to elucidate the precise mechanisms and clinical implications of these hemodynamic alterations.

