TY - JOUR
T1 - Furosemide inhibits regenerative cortical spreading depression in anaesthetised cats
AU - Read, S.J.
AU - Smith, M.I.
AU - Benham, C.D.
AU - Hunter, A.J.
AU - Parsons, A.A.
N1 - ‘The definitive version is available at www.blackwell-synergy.com '. Copyright Blackwell Publishing. DOI: 10.1046/j.1468-2982.1997.1708826.x [Full text of this article is not available in the UHRA]
PY - 1997
Y1 - 1997
N2 - Ionic perturbations occur during cortical spreading depression (SD), a phenomenon implicated in migraine pathophysiology. We studied the effect of 0.2,2 and 20 mg kg-1 iv (n=4) furosemide on cortical direct current (d.c.) potential, cerebrovascular laser Doppler flux (rCBFLDF), artery diameter and NO concentration in the parietal cortex of the anaesthetized cat during repetitive SD. In vehicle treated animals (n=4), SD activity was sustained for 50 1.8 min. However, duration of SD activity was significantly reduced when compared to vehicle to 39 6.6 (n=4), 3.1 8.3 (n = 4) and 27.3 11.3 min (n=4), at 0.2, 2 and 20 mg kg-1 iv furosemide respectively. It is hypothesized that the mechanism of inhibition of SD d.c. activity by furosemide may be through alterations in cortica ion buffering capacity or inhibition of cell swelling in neurones or glia. These mechanisms may represent potential novel drug targets in future migraine therapy.
AB - Ionic perturbations occur during cortical spreading depression (SD), a phenomenon implicated in migraine pathophysiology. We studied the effect of 0.2,2 and 20 mg kg-1 iv (n=4) furosemide on cortical direct current (d.c.) potential, cerebrovascular laser Doppler flux (rCBFLDF), artery diameter and NO concentration in the parietal cortex of the anaesthetized cat during repetitive SD. In vehicle treated animals (n=4), SD activity was sustained for 50 1.8 min. However, duration of SD activity was significantly reduced when compared to vehicle to 39 6.6 (n=4), 3.1 8.3 (n = 4) and 27.3 11.3 min (n=4), at 0.2, 2 and 20 mg kg-1 iv furosemide respectively. It is hypothesized that the mechanism of inhibition of SD d.c. activity by furosemide may be through alterations in cortica ion buffering capacity or inhibition of cell swelling in neurones or glia. These mechanisms may represent potential novel drug targets in future migraine therapy.
U2 - 10.1046/j.1468-2982.1997.1708826.x
DO - 10.1046/j.1468-2982.1997.1708826.x
M3 - Article
SN - 0333-1024
VL - 17
SP - 826
EP - 832
JO - Cephalalgia
JF - Cephalalgia
IS - 8
ER -