RESUMO
Blood-brain barrier (BBB) function was assessed in 19-21-day-old rats exposed to low level lead from birth. Newborn rats received lead via milk from lactating dams given drinking water containing 0.1% lead acetate [Pb(Ac)2]. The treatment regime produced lead levels in the neonates within the range 20-80 micrograms dl-1 blood, without affecting growth. Cerebrovascular permeability (PS-product) to the diffusion-limited solute mannitol was unchanged in six regions of the cerebral hemisphere, the cerebellum and the brainstem, suggesting that barrier integrity was not affected by the low dose lead treatment. Regional cerebrovascular permeability to nutrient tracers representing seven BBB transport classes was not impaired by lead treatment. However, the PS estimates for the amino acids lysine and histidine and for thiamine were greater than control in some regions of the cerebral hemisphere. These alterations in nutrient supply to the brain may reflect altered substrate utilization associated with repair processes or delayed maturation of the CNS.
Assuntos
Barreira Hematoencefálica , Encéfalo/crescimento & desenvolvimento , Intoxicação por Chumbo/fisiopatologia , Animais , Animais Recém-Nascidos , Encéfalo/efeitos dos fármacos , Permeabilidade Capilar/efeitos dos fármacos , Circulação Cerebrovascular/efeitos dos fármacos , Difusão , Histidina/farmacocinética , Lisina/farmacocinética , Manitol/farmacocinética , Compostos Organometálicos/administração & dosagem , Ratos , Ratos Endogâmicos , Tiamina/farmacocinéticaRESUMO
Methylmercuric chloride was given to rats in a neurotoxic dose regimen (six daily doses of 8 mg kg-1 p.o.). During the silent (asymptomatic) phase of intoxication, the rates of cerebral glucose influx and cerebral glucose phosphorylation were measured simultaneously using 2-deoxyglucose. Regional cerebral blood flow was also measured using iodoantipyrine. The unidirectional flux of glucose into brain was not affected by methylmercury, and differences in the rates of glucose phosphorylation from region to region remained coupled to the regional cerebral blood flow. However, the blood flow was reduced throughout the brain, an observation suggesting that the operational level of metabolically regulated blood flow had been reset. Thus, in spite of a generalised reduction in blood flow, there was no indication of impaired cerebral glucose supply or utilization during the silent phase of methylmercury intoxication.