Abstract
Coupling between local perfusion and metabolism was examined in Mongolian gerbils during the development of delayed neuronal death using a combination of double-tracer autoradiography and imaging of local energy state. Animals were anesthetized with 1.5% halothane and forebrain ischemia was produced by occluding both common carotid arteries. After 5 min of ischemia, brains were recirculated for 6 h and 1, 2, or 4 days. At the end of the experiment, regional cerebral blood flow (CBF) and glucose utilization (CMRglc) were determined in identical brain sections with [131I]iodoantipyrine and [14C]deoxyglucose, respectively. Adjacent sections were taken for imaging of ATP and glucose using substratespecific bioluminescence reactions. In the CA1 subfield of control animals, CBF and CMRglc amounted to 81 ± 8 ml 100g−1 min−1 and 69 ± 2 μmol 100 g−1 min-1, respectively, and the calculated CBF/CMRglc ratio was 1.18 ± 0.12 ml/μmol (mean ± SD). After ischemia, the CBF/CMRglc ratio increased to 1.31 ± 0.14, 1.43 ± 0.16, 1.45 ± 0.16, and 1.56 ± 0.18 ml/μmol following 6 h and 1, 2, or 4 days recirculation, respectively. Glucose levels did not change during the 6 h to 4 day recirculation period in the hippocampal CA1 subfield. In the same region, ATP levels were unchanged during 6 h to 2 day postischemic recovery but reduced to about 70% after 4 days of recirculation. The results indicate that a mismatch of the flow-metabolism couple following transient ischemia does not appear to contribute to the postischemic maturation of delayed neuronal death in selectively vulnerable brain regions.