Local cerebral blood flow following transient cerebral ischemia. I. Onset of impaired reperfusion within the first hour following global ischemia.
Using the hydrogen clearance technique, local cerebral blood flow (LCBF) in 22 dogs was estimated at 6 parietal sites prior to and following 5 min of total global ischemia. Ischemia was immediately followed by an initial reactive hyperemia during which the electrocorticogram (ECoG) usually began to recover, and within the first 30 min, most of the LCBF's decreased to subnormal values. This onset of hypoperfusion was accompanied by a concomitant decrease in ECoG activity. Two animals that maintained normal local perfusion after the initial hyperemia recovered ECoG activity quickly. These results suggest that the subsequent poor reperfusion was caused by an increased microvascular resistance rather than by blood aggregates, increased blood viscosity, or a variety of other mechanism which have been proposed. Increased vascular tonus was, at least, partly responsible for the increased vascular resistance. This report supports the hypothesis that impaired reperfusion (which occurs some time after an initial hyperemia) may be responsible for ultimate neuronal death, rather than the period of global ischemic hypoxia per se.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D002560:Cerebrovascular Circulation; D004285:Dogs; D004566:Electrodes; D004569:Electroencephalography; D006863:Hydrogen-Ion Concentration; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D010477:Perfusion; D013997:Time Factors
D002245:Carbon Dioxide