The amount of circumscribed brain edema and the degree of post-ischemic neuronal recovery do not correlate well.

Fifty-four dogs were exposed to multi-focal ischemia sufficient to maintain suppression of the P1--N1 amplitude of the cortical sensory-evoked response (CSER) for 60 minutes. Subsequently, the P1--N1 amplitude recovery of the CSER was followed for an additional 15, 60, or 120 min while the dogs were treated or left untreated. The combination of PGI2, indomethacin, and heparin promoted a statistically significant augmentation of CSER amplitude return relative to: 1) no treatment; 2) PGI2 alone; 3) indomethacin alone; 4) PGI2 and heparin; 5) indomethacin and heparin; 6) PGI2 and indomethacin. Percentage gray matter water by the wet weight/dry weight technique was significantly elevated in all embolized groups compared to ten non-embolized controls, but the percentage recovery of the CSER did not correlate with the presence or degree of gray matter edema among embolized animals followed for 1 hour. Separation of embolized animals by the presence or absence of "neuron-disabling" flows (defined as 0-15 ml/100 gm/min for gray matter and 0-6 ml/100 gm/min for white matter) did produce significantly different mean CSER percentage recoveries but percentage gray matter water in the two groups was comparable. A proposed explanation of the data is that brain ischemia engenders two parallel processes which may become uncoupled. Ischemia creates metabolic conditions that lead to increased cellular imbibition of water and produces increased vascular leakiness. These perturbations increase brain water content. Concomitantly, there is an occurrence of further metabolic derangements and multifactorial interaction at the blood-endothelial interface which have a direct influence on neuronal function and recovery.