CORTICAL ACTIVITY, IONIC HOMEOSTASIS, AND ACIDOSIS DURING RAT-BRAIN REPETITIVE ISCHEMIA

Recent data strongly suggest that repetitive ischemic episodes have an adverse cumulative effect on development of edema and tissue damage. We wanted to assess further whether special risks such as exacerbation of extracellular acidification reflecting progressive exhaustion of the capacity to buffer H+in the extracellular space are associated with repeated short ischemic insults. We monitored spontaneous electrical activity, extracellular direct-current potential, extracellular H+ activity, and tissue Pco2 in the cerebral cortex of rats subjected to four cycles of 3-minute ischemia produced by four-vessel occlusion with 27-minute reperfusion after each insult. Except for electrical activity, which failed to recover fully from the first ischemic insult, all parameters returned to a level close to normal after each reperfusion. Changes during ischemia did not evolve with repetition of the insult. Electrical silence occurred within approximately 20 seconds after the onset of each ischemic episode and always preceded the steep drop of direct-current potential, indicating ischemic depolarization. Each four-vessel occlusion immediately initiated a steep rise of tissue Pco2 and extracellular H+ activity, with extracellular H+ activity reaching a maximum within approximately 145 seconds. Changes in extracellular Ht activity during each recirculation period consistently included an additional and short-lasting increase associated with repolarization, a rapid decrease closely related to that of tissue Pco2, and a slow progressive return to normal. These results suggest that short, repetitive ischemic episodes severe enough to produce cell membrane depolarization and maximum acidosis of the neuronal microenvironment do not have a deleterious cumulative effect on the studied parameters, in particular, on interstitial acidosis. © 1990 American Heart Association, Inc.