Changes in vascular and metabolic reactivity as indices of ischaemia in the penumbra.
The reactivities of cerebral cortical blood flow (hydrogen clearance) and of compensated NADH fluorescence to local cortical electrical stimulation were examined on the marginal gyrus before and after transorbital occlusion of the middle cerebral artery in cats. Prestimulus cerebral blood flow (CBF) was 38.2 +/- 12.9 (SD) ml 100 g-1 min-1 and fell to 19.8 +/- 11.1 following occlusion (p less than 0.02). Peak hydrogen clearance rate (percent increase above prestimulus clearance) was 81.6 +/- 53.6 and fell to 19.9 +/- 29.8 after middle cerebral artery occlusion (p less than 0.01). Steady-state NADH fluorescence rose from 33.5 +/- 10.7 to 40.5 +/- 17.6% full-scale deflection following MCAO (p less than 0.01). Latency from stimulus to maximal fluorescence depression in response to cortical stimulation increased from 12.2 +/- 8.2 to 22.1 +/- 11.9 s (p less than 0.01). Hyperaemic responses at anteromedial sites on the marginal gyrus significantly exceeded those at posterolateral sites. The results are interpreted as indicating early ischaemic metabolic change; however, the presence of residual vasodilator responses to stimulation suggests that flow reduction and early ischaemic change in the territory studied are not simply due to inadequate collateral input, but may also reflect deafferentation or functional suppression. The possible significance of diminished vascular reactivity in the penumbra as a cause of increased vulnerability to extracellular release of excitatory amino acids is discussed.
Strong
A J
AJ
Department of Surgery (Neurosurgery), University of newcastle upon Tyne, U.K.
Gibson
G
G
Miller
S A
SA
Venables
G S
GS
D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002415:Cats; D002536:Cerebral Arteries / Q000502:physiology; D002540:Cerebral Cortex / Q000098:blood supply* / Q000503:physiopathology; D003250:Constriction; D004558:Electric Stimulation; D005260:Female; D005453:Fluorescence; D006859:Hydrogen / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D009243:NAD / Q000378:metabolism*; D010084:Oxidation-Reduction
D009243:NAD; D006859:Hydrogen