Abstract
We investigated pathophysiology of a primate model eliciting spreading depression (SD), as well as a primate thromboembolic model, by using PET. Immediately after the first SD, focal cortical hyperemia was demonstrated without being followed by spreading or persistent hypoperfusion. Cyclooxygenase-2 (COX-2) induction was detected in SD animals by microarray analysis. Immunoreactive neurons were observed in SD animals. In the thromboembolic model, cerebral blood flow (CBF) following 24 h of ischemia reduced to 20–40% in the ischemic temporal cortex as well as ischemic basal ganglia, while the reduction was 40–60% in the ischemic parietal cortex. Upregulation of COX-2 mRNA expression was observed after 2 h of ischemia, but disappeared by 24 h in the ischemic temporal cortex. In the ischemic parietal cortex, where CMRglc was preserved, COX-2 expression persisted even after 24 h of ischemia. In conclusion, we showed unique features of CBF changes associated with SD in primates. Neuronal COX-2 induction was demonstrated in SD animals as well as within potentially viable hypoperfused brain areas in primates.
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