Enhanced brain opioid receptor activity precedes blood-brain barrier disruption.

We studied the effects of transient postischemic increased opioid receptors (OPR) binding (mu, delta, kappa) on blood-brain barrier (BBB), brain water content and brain mitochondrial oxidative enzymes system. Cats were exposed to temporary middle cerebral artery occlusion (MCAO). The significant increased OPR bindings observed 10 min after the release of MCAO (ischemic rCBF = 7 +/- 1 to 11 +/- 2 ml/100 g/min) preceded the early and late BBB disruptions, brain edema and postischemic impaired mitochondrial oxidative enzymes functions. Further, the study suggests indirectly that the latter process was irreversible and hence associated with subsequent ischemic cerebral infarction. In addition, the results revealed a possible viable therapeutic window in the early postischemic recirculation period, before the onset of impaired mitochondrial oxidative function.