TY - JOUR

T1 - Regional cerebral blood flow during cortical spreading depression in rat brain

T2 - increased reactive hyperperfusion in low‐flow states

AU - Lauritzen, M.

PY - 1987/1/1

Y1 - 1987/1/1

N2 - The purpose of the present study was to characterize the initial vascular events accompanying cortical spreading depression (CSD) of the rat brain. Regional cerebral blood flow (rCBF) was measured during the first 1–2 min of CSD using 14C‐iodoantipyrine autoradiography. The material included a reference group, and 4 groups where rCBF was altered by indomethacin treatment, hypo‐ or hypercapnia, or one previous episode of CSD. rCBF did not change prior to, or during the onset of CSD. Thirty seconds later, rCBF increased depending on the pre‐existing level of blood flow, i.e. the rise of rCBF was pronounced at depressed flow levels, but small or absent at normal or high flow levels. The prevalent view that CSD is intimately associated with vasodilatation was accordingly not supported. The activated rCBF in normocapnic rats ranged between 93 and 175 ml/100g/min, supra normal values were the exception rather than the rule. The rCBF rise, when present, probably succeeds a period of brain hypoxia, and should be classified as a reactive hyperfusion. The results together with earlier clinical and experimental findings, support that CSD may serve as experimental migraine model.

AB - The purpose of the present study was to characterize the initial vascular events accompanying cortical spreading depression (CSD) of the rat brain. Regional cerebral blood flow (rCBF) was measured during the first 1–2 min of CSD using 14C‐iodoantipyrine autoradiography. The material included a reference group, and 4 groups where rCBF was altered by indomethacin treatment, hypo‐ or hypercapnia, or one previous episode of CSD. rCBF did not change prior to, or during the onset of CSD. Thirty seconds later, rCBF increased depending on the pre‐existing level of blood flow, i.e. the rise of rCBF was pronounced at depressed flow levels, but small or absent at normal or high flow levels. The prevalent view that CSD is intimately associated with vasodilatation was accordingly not supported. The activated rCBF in normocapnic rats ranged between 93 and 175 ml/100g/min, supra normal values were the exception rather than the rule. The rCBF rise, when present, probably succeeds a period of brain hypoxia, and should be classified as a reactive hyperfusion. The results together with earlier clinical and experimental findings, support that CSD may serve as experimental migraine model.

KW - cerebral blood flow

KW - migraine

KW - spreading depression

UR - http://www.scopus.com/inward/record.url?scp=0023146640&partnerID=8YFLogxK

U2 - 10.1111/j.1600-0404.1987.tb07881.x

DO - 10.1111/j.1600-0404.1987.tb07881.x

M3 - Review

C2 - 3107334

AN - SCOPUS:0023146640

VL - 75

SP - 1

EP - 8

JO - Acta Neurologica Scandinavica, Supplement

JF - Acta Neurologica Scandinavica, Supplement

SN - 0065-1427

IS - 1

ER -