Abstract
Previously we showed that platelets accumulate in areas of low CBF 4h after brain ischemia. Similarly, CSER and CBF recovery after brain ischemia was enhanced in dogs treated with either prostacyclin (PGI2) + indomethacin or the platelet-activating factor (PAF) receptor antagonist kadsurenone. Since these treatments inhibit platelet aggregation, we hypothesized that their beneficial effects were mediated via inhibition of platelet accumulation. To test this hypothesis, 22 dogs with 111In-labeled platelets were subjected to 1h of ischemia of the right hemisphere by air embolism. CSER in the right hemisphere was monitored during reperfusion, while CBF (autoradiography) and platelet accumulation (R-L ratio of 111In activity) were measured after 4h of reperfusion. 12 dogs served as controls, 6 were treated with PGI2 + indomethacin and 4 with kadsurenone.
Both treatments enhanced CSER recovery after Ih of reperfusion and eliminated neuron-disabling CBF at 4h (defined as <15ml/ 100g/min in gray matter and <6ml/100g in white). Despite this, platelet accumulation was not blocked by either treatment.
Anti-pfatelet aggregation therapy does not block postischemic platelet accumulation in the brain. Other effects of these treatments including improved CBF may contribute to enhanced recovery.
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Kochanek, P., Dutka, A. & Hallenbeck, J. BROAD SPECTRUM ANTI-PLATELET AGGREGATION THERAPY IMPROVES POSTISCHEMIC CEREBRAL BLOOD FLOW (CBF) AND CORTICAL SOMATOSENSORY EVOKED RESPONSE (CSER) RECOVERY, BUT FAILS TO BLOCK PLATELET ACCUMULATION IN THE DAMAGED HEMISPHERE. Pediatr Res 21 (Suppl 4), 202 (1987). https://doi.org/10.1203/00006450-198704010-00215
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DOI: https://doi.org/10.1203/00006450-198704010-00215