CHARACTERIZATION OF CORTICAL DEPOLARIZATIONS EVOKED IN FOCAL CEREBRAL-ISCHEMIA

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.