Abstract
Occlusion of both common carotid arteries of the Mongolian gerbil results consistently in bilateral ischemia of the cerebral cortex permitting investigation of the effects of short-term ischemia of cerebral energy reserves. Biochemical evidence in the present study confirms cerebral ischemia in all gerbils subjected to bilateral carotid occlusion. The changes in metabolites during recirculation may reflect the intensity of the ischemic insult more accurately than alterations which occur during ischemia. To ensure the assessment of short periods of ischemia without ambiguity, the metabolites and cyclic nucleotides were measured after 1, 5, 20, 30 and 60 min of ischemia; and 1, 5, 30, 60 and 360 min after circulation was reestablished. The major part of changes in metabolites and cyclic nucleotides due to ischemia occurred during the first minute, ischemia of longer duration had little further effect. However, the restoration of the metabolic profile was altered by the duration of the ischemic period. In general, the longer the period of ischemia, the slower the replenishment of high-energy phosphate compounds and energy sources. Cyclic AMP increased 5 to 13 times during ischemia; cyclic GMP decreased to as little as 1/5 of control values 60 min after occlusion. During recirculation, cyclic AMP increased as much as 100-fold, while cyclic GMP increased up to 6-fold. The temporal derangements in cyclic nucleotide concentrations coincide with the loss and restoration of cortical activity; a possible mechanism has been suggested.
