M. Nedergaard et Aj. Hansen, CHARACTERIZATION OF CORTICAL DEPOLARIZATIONS EVOKED IN FOCAL CEREBRAL-ISCHEMIA, Journal of cerebral blood flow and metabolism, 13(4), 1993, pp. 568-574
Cortical tissue surrounding acute ischemic infarcts undergoes repetiti
ve spontaneous depolarizations. It is unknown whether these events are
episodes of spreading depression (SD) elicited by the elevated inters
titial K+ ([K+]e) in the ischemic core or whether they are evoked by t
ransient decreases of the local blood flow. Electrophysiologically, de
polarization caused by SD or by ischemia (ID) can be distinguished by
their characteristic patterns of [K+]e rise: During SD, [K+]e rises ab
ruptly, while in ID, this fast rate of increase is preceded by a slow
rate lasting minutes. To characterize the depolarizations, we occluded
the right middle cerebral artery (MCA) in rats and inserted two K+-se
nsitive microelectrodes into the cortex surrounding the evolving infar
ct. Repeated increases in [K+]e arose spontaneously following MCA occl
usion. [K+]e increased during these transients from a resting level of
3-6 to 60 mM. One-third of these transient increases in [K+]e were bi
phasic, consisting of a slow initial increase to 10-12 mM, which laste
d for minutes, followed by an abrupt increase, a pattern characteristi
c of ID. The remaining two-thirds exhibited a steep monotonic increase
in [K+]e (<10 s), characteristic of SD. The duration of the transient
s was a function of the pattern of [K+]e increase: ID-like transients
lasted an average 10.7 +/- 5.1 min, whereas the duration of SD-like tr
ansients was 5.7 +/- 3.4 min. Both types of K+ transients occurred in
an apparently random fashion in individual animals. A K+ transient was
never observed solely at one electrode. In 40% of the cases, the K+ t
ransients occurred simultaneously at the two electrode sites, and in t
he remaining a temporal separation of 20-420 s was observed. Our data
suggest that the majority of the spontaneous depolarizations evoked by
focal ischemia are SD-like phenomena probably evoked by the high valu
es of [K+]e or glutamate in the ischemic focus, while the rest are eli
cited by independent foci of low blood flow within the ischemic border
areas.