Originally, experiments in the 1920s showed that the blood–brain barrier (BBB) was still immature in newborns. The reason for this fallacy was a mistake in methodology (the osmotic pressure was too high and the delicate embryonal capillary vessels were partially damaged). It was later shown in experiments with a reduced volume of the injected liquids that the markers under investigation could not pass the BBB. It was reported that those natural substances such as albumin, α-1-fetoprotein or transferrin with elevated plasma concentration in the newborn could not be detected extracellular in the brain. The efflux-transporter P-glycoprotein exists already in the embryonal endothelium.
The measurement of brain uptake of acetamide, antipyrine, benzyl alcohol, butanol, caffeine, cytosine, diphenyl hydantoin, ethanol, ethylene glycol, heroin, mannitol, methanol, phenobarbital, propylene glycol, thiourea, and urea in ether-anesthetized newborn vs. adult rabbits shows that newborn rabbit and adult rat brain endothelia are functionally similar with respect to lipid-mediated permeability. These data confirmed no differences in permeability could be detected between newborn and adult BBB capillaries. No difference in brain uptake of glucose, amino acids, organic acids, purines, nucleosides, or choline was observed between adult and newborn rabbits. These experiments indicate that the newborn BBB has restrictive properties similar to the adult. In contrast to suggestions of an immature barrier in young animals, these studies indicate that a sophisticated, selective BBB is operative at birth.
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