1 It has been previously shown that spreading neuronal activation can generate a cortical spreading ischaemia (CSI) in rats. The purpose of the present study was to investigate whether vasodilators cause CSI to revert to a normal cortical spreading depression (CSD). 2 A KCl‐induced CSD travelled from an open cranial window to a closed window where the cortex was superfused with physiological artificial cerebrospinal fluid (ACSF). At the closed window, recordings revealed a short‐lasting negative slow potential shift accompanied by a variable, small and short initial hypoperfusion followed by hyperaemia and then oligaemia. 3 In contrast, spreading neuronal activation locally induced CSI at the closed window when ACSF contained a NO. synthase (NOS) inhibitor, NG‐nitro‐l‐arginine, and an increased K+ concentration ((K+)ACSF). CSI was characterised by a sharp and prolonged initial cerebral blood flow decrease to 29 ± 11 % of the baseline and a prolonged negative potential shift. 4 Co‐application of a NO. donor, S‐nitroso‐N‐acetylpenicillamine, and NOS inhibitor with high (K+)ACSF re‐established a short‐lasting negative potential shift and spreading hyperaemia typical of CSD. Similarly, the NO.‐independent vasodilator papaverine caused CSI to revert to a pattern characteristic of CSD. 5 In acute rat brain slices, NOS inhibition and high (K+)ACSF did not prolong the negative slow potential shift compared to that induced by high (K+)ACSF alone. 6 The data indicate that the delayed recovery of the slow potential was caused by vasoconstriction during application of high (K+)ACSF and a NOS inhibitor in vivo. This supports the possibility of a vicious circle: spreading neuronal activation induces vasoconstriction, and vasoconstriction prevents repolarisation during CSI. Speculatively, this pathogenetic process could be involved in migraine‐induced stroke.
The Journal of Physiology – Wiley
Published: Mar 1, 2001
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