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Transport of Lead‐203 at the Blood‐Brain Barrier During Short Cerebrovascular Perfusion with Saline in the Rat
Author(s) -
Deane R.,
Bradbury M. W. B.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb02337.x
Subject(s) - chemistry , bicarbonate , calcium , magnesium , blood–brain barrier , perfusion , medicine , central nervous system , organic chemistry
Lead transport at the blood‐brain barrier has been studied by short (< 1.5 min) vascular perfusion of one cerebral hemisphere of the rat with a buffered physiological salt solution at pH 7.4 without calcium, magnesium, or bicarbonate and containing 203 Pb‐labelled lead chloride. In the absence of complexing agents, 203 Pb uptake was rapid, giving a space of 9.7 ml/100 g of wet frontal cortex at 1 min. Lead‐203 influx was linear with lead concentration up to 4 μ M . Five percent albumin, 200 μ M cysteine, or 1 μ M EDTA almost abolished 203 Pb uptake. Lead‐203 entry into brain was uninfluenced by varying the calcium concentration or by magnesium or the calcium blocker methoxyverapamil. Similarly, 1 μ M bicarbonate or 50 μ M 4,4′‐diisothiocyanostilbene‐2,2′‐disulphonic acid was without effect. Increasing the potassium concentration reduced 203 Pb uptake. Vanadate at 2 μ M , 2 μ M carbonyl cyanide 4‐(trifluoromethoxy)phenylhydrazone (a metabolic uncoupler), or 2 μ M stannic chloride all markedly enhanced lead entry into brain, as did a more alkaline pH (7.80). In conclusion, there is a mechanism allowing rapid passive transport of 203 Pb at the brain endothelium, perhaps as PbOH + . Lead uptake into brain via this system is probably made less important by active transport of lead back into the capillary lumen by the calcium‐ATP‐dependent pump.