Michael Pollay

Transport of water and electrolytes between brain and ventricular fluid in the rabbit

Bidirectional sodium fluxes and net transfer of potassium, chloride, and water across the ventricular ependyma were studied in anesthetized rabbits by closed perfusion of the cerebral aqueduct and anterior fourth ventricle with solutions containing trace amounts of inulin-3H and 22Na. Inulin dilution and clearance from the perfusate indicated a bulk fluid accretion of 0.37 μl min−1 cm−2 of ependymal surface. The concurrent net sodium movement into ventricular fluid occurred at a rate of .0645 ± .0060 μEq min−1 cm−2 against typical ventriculo-vascular potential gradients of 5–10 mv. Potassium entered the perfusate at concentrations approximating that of normal cerebrospinal fluid (CSF). Chloride accumulated in the ventricular system at a rate of .0356 ± .0057 μEq min−1 cm−2 and its distribution between blood and ventricular fluids approached an electrochemical equilibrium. Water was transported at reduced rates into hypotonic perfusates without associated changes in sodium influx, whereas, both water and sodium movements were inhibited by acetazolamide or cardiac glycosides. These studies imply that movement of CSF across the blood-brain-CSF barrier is an isotonic flow coupled to sodium transport and represents one-third of the total intraventricular formation of CSF.

Diffusion of non-electrolytes in brain tissue

Abstract The diffusion of urea and creatinine in brain tissue was studied in rabbits using an aqueductal-fourth ventricular perfusion system. The movement of the test solutes in brain tissue conforms approximately to Ficks law of diffusion. It is believed that the computed diffusion coefficients in brain could be similar to their free diffusion coefficients if corrected for the tortuosity of the interstitial channels and the sink effect of the brain capillary bed. The experimental results suggest that there is a relatively open path between the cerebrospinal fluid and brain although the penetration of urea and creatinine molecules during short periods of time is limited to a distance of 100 μm or less from the ependymal surface.

Potassium transport across the choroidal ependyma

Abstract The transependymal flux of K + was studied in an extracorporeal perfusion system utilizing sheep choroid plexus. The movement of K + from blood to CSF appeared to be compatible with a Na-K pump in choroid plexus which saturated at a blood level of 3.3 meq/Kg and was adversely affected by ouabain (10 −5 M) in CSF or blood. The movement of K + from CSF appeared to be by a diffusionary process which was insensitive to ouabain. These results suggest that the homeostasis of CSF K + is in part due to a Na-K pump at the blood-CSF barrier (choroid plexus).

Cerebrovascular Flow and Glucose Transport in the Hydrocephalic Rat

This study evaluates regional cerebral perfusion flow and unidirectional glucose transport across the cerebral capillar in hydrocephalic rats. Perfusion flow and glucose influx were measured with 99mTc-ECD (Dupont Corp.) and 14C-(d)-Glucose, respectively. Perfusion flows for the control and hydrocephalic groups were 1.77ml/min per g and 1.53ml/min per g, respectively. The hydrocephalic perfusion flow was significantly lower than the control flow (P < .05). Maximal influx of glucose (Vmax) for the control group was 2.74 μm/min per g. The Vmax for the hydrocephalic group was 3.19 μm/min per g. Substrate concentration at half maximal transport (Km) was 8.02 mM for the controls and 11.5 mM for the hydrocephalies. There was no substantial difference between control and hydrocephalic groups for these kinetic parameters. These data suggest that reported changes in cerebral metabolism in hydrocephalus are due to derangements in utilization rather than to facilitated diffusion of glucose across the blood brain barrier.

Accumulation of Inorganic Sulfate by Choroid Plexus in Vitro

Summary The incubation of choroid plexus tissue with 35SO4 2- reveals that sulfate is accumulated in the tissue against a concentration gradient. The magnitude of tissue accumulation appears to depend on cellular metabolism as evidenced by the adverse effect of metabolic inhibitors. The inhibition of sulfate accumulation by thiosulfate and thiocyanate implies that these anions share a common carrier. These findings support the contention that the low concentration of sulfate in CSF is due to the active transport of this ion out of the CSF across the choroid plexus.