Regional pH and electrolyte homeostasis of cat brain after prolonged ischemia.

Abstract

Following prolonged cerebral ischemia, primary electrophysiological recovery may be followed by secondary deterioration of the recovery process. It has been suggested that the secondary deterioration is caused by "late" cytotoxic brain edema. To test this hypothesis, adult normothermic cats were submitted to 1 h complete cerebral ischemia followed by 3 and 6 h recirculation, respectively. Postischemic recovery of energy metabolism was imaged by ATP-induced bioluminescence, and regional tissue pH and electrolyte content was measured in regions with and without metabolic recovery. In areas with postischemic restitution of metabolic activity, sodium gradually rose from 338 +/- 17 to 488 +/- 28 mumol/g protein and calcium from 8.81 +/- 0.35 to 18.24 +/- 0.97 mumol/g protein. Tissue potassium content decreased from 761 +/- 12 to 676 +/- 19 mumol/g protein and magnesium from 46.8 +/- 0.8 to 36.3 +/- 1.1 mumol/g protein. Tissue pH rose from 7.09 +/- 0.04 to 7.31 +/- 0.13 and 7.26 +/- 0.17 after 3 and 6 h recirculation, respectively. In areas without metabolic recovery, electrolyte disturbances were even more pronounced and pH--after transient alkalization--fell to 6.82 +/- 0.12. These data demonstrate that during the later phase of postischemic recirculation, progressive disturbances of electrolyte homeostasis create a preedematous situation that has to be considered for preventing delayed postischemic complications.