INFLUENCE OF ISCHEMIA ON BLOOD-BRAIN AND BLOOD CSF CALCIUM-TRANSPORT

The objective was to explore whether the increased incorporation of Ca-45 into selectively vulnerable neurons, observed after transient ischemia, can be explained by enhanced blood-tissue and/or enhanced blood-CSF transfer. Anesthetized rats were subjected to 15 min of forebrain ischemia, with recirculation for 20 or 60 min, or 24 h. The transfer constants (K(in)) and unidirectional fluxes (J(in)) for calcium in tissue and CSF were determined following i.v. injection of Ca-45, integration of the curve for plasma-specific activity over 10 min, and sampling of cisternal CSF, and tissue (cortex, caudoputamen, hippocampus, and cerebellum). Predictably, values for K(in) and J(in) in control animals were much larger in CSF than in tissues, and hippocampus had higher values than the other areas, probably because of its closeness to the lateral ventricle. Ischemia failed to alter the K(in) and J(in) values, demonstrating that the low permeability of blood-brain and blood-CSF barriers to calcium is upheld both in the immediate recirculation period, and after 24 h of recirculation. The results support the contention that the increased Ca-45 incorporation during recovery is due to increased calcium cycling across functionally altered cell membranes.