Transport Mechanisms in Certain Blood‐brain Barrier Phenomena‐a Hypothesis

Steinwall, O.

doi:10.1111/j.1600-0447.1961.tb08409.x

Cited by 43 publications

(4 citation statements)

References 8 publications

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“…The results of the present investigation show that a concomitant blood-brain barrier alteration could be demonstrated by means of one or both of the applied barrier function tests in all but one ofthe animals (no.6) where a macroscopic cerebral lesion was achieved. This result is in conformity with those obtained by previous investigators (Broman et al 1949, Bakay et al 1956, Klatzo et al 1958, 1961, h t r o m et al 1961. A complete correlation of the dye tests and the penicillin test was obtained both in the 5 animals where no macroscopic lesion was present (no.…”

Section: Discussionsupporting

confidence: 94%

“…A similar tendency to restitution of a concomitant blood-brain barrier alteration in physically induced structure-deranging cerebral lesions has been demonstrated in previous investigations by means of different acidic dye indicators (Broman et al 1949, Bakay et al 1956, Klatzo rt al. 1958, 1961, Astrom et al 1961 or by means of normally-barred EEG-activating drugs (Gonsette 1956).…”

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Blood‐Brain Barrier Alteration after Experimental Cold Injury of the Rabbit Brain, Indicated by Penicillin G in EEG and by Dye Tests

Flodmark

1965

Acta Physiologica Scandinavica

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I.'lodmark, S. Blood-brain barrier alteiatiori after experimental cold injuv of the rabbit brain, indicated by penicillin G in EGG and by dye tests. Acta physiol. scand. 1965.63.225-235. -Two previous known methods to indicate blood-brain barrier alterationsintravital dye tests and EEG test after drug activationwere applied in parallel in 25 short-or long-term experiments on cold-induced cerebral lesions in the rabbit. The method of cold application was a modification of that of Hass and Taylor, supplemented by a recording of the extradural temperature. A new type of permanent electrode for EEG recording is described. In 19 of 20 animals in which a structure-deranging lesion was induced, a concomitant blood-brain barrier alteration could be demonstrated. In 11 of these 19 expts. a complete correlation of the two methods of barrier indication was obtained (8 animals inconsistent results). In 6 animals in which no blood-brain barrier alteration was induced a concordance of negative results with the two methods was also seen. Three to four days was the maximum duration of blood-brain barrier damage noted among the 13 animals in which the tendency to restitution of barrier function was studied. The results are in conformity with those of previous investigators and seem to justify the use of normally-barred EEG activating drugs such as penicillin, as detectors of blood-brain barrier alteration. These drugs seem particularly suitable for iterative studies in living animals. By means of a method for study of the interrelation between EEG and blood-brain barrier phenomena (Flodmark and Steinwall 1962) the reversibility of some chemically induced blood-brain barrier alteration as primarily shown by Broman and Olsson (1948) has recently been confirmed (Flodmark and Steinwall 1963 b). A similar tendency to restitution of a concomitant blood-brain barrier alteration in physically induced structure-deranging cerebral lesions has been demonstrated in previous investigations by means of different acidic dye indicators (Broman et al. 1949, Bakay et al. 1956, Klatzo rt al. 1958, 1961, Astrom et al. 1961 or by means of normally-barred EEG-activating drugs (Gonsette 1956). 225

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Section: Discussionsupporting

confidence: 94%

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confidence: 99%

Blood‐Brain Barrier Alteration after Experimental Cold Injury of the Rabbit Brain, Indicated by Penicillin G in EEG and by Dye Tests

Flodmark

1965

Acta Physiologica Scandinavica

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“…The brains of dye-pretreated rats (dye-ECS) did not stain in contrast to nondye-pretreated rats (saline-ECS) following posttest injection oftrypan blue, thus indicating that permeability of the BBB of dye-EC~ animals might not have been appreciably altered by ECS. Trypan blue is unable to pass from blood to brain under normal barrier conditions but can pass with any impairment of the BBB (Steinwall, 1961;Flodmark, 1965). The present data suggest that permeability changes in the BBB are probably not significant determinants in the mechanism of ECS-induced impairment in the learning of taste aversions.…”

Section: Inspection Ofmentioning

confidence: 54%

Electroconvulsive shock impedes the learning of taste aversions: Absence of blood-brain-barrier involvement

Omer

Kral

1971

Psychon Sci

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“…Sperber ( 1947, 1949) has pointed out that detoxication mechanisms frequently collaborate with excretory mechanisms in such a manner that detoxication products are actively secreted by the kidney tubules and/or the liver. The transport systems found by Becker and by Pappenheimer add another dimension: substances excreted by the kidney are kept out of the eye and, as foreseen by Steinwall (1961), the brain by what is in effect an extrarenal kidney. But is there an extrahepatic liver too?…”

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Inhibition by Hippurate and Probenecid of in vitro Uptake of Iodipamide and o‐Iodohippurate. A Composite Uptake System for Iodipamide in Choroid Plexus, Kidney Cortex and Anterior Uvea of Several Species

Bárány

1972

Acta Physiologica Scandinavica

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Slices of kidney cortex and liver, pieces of lateral choroid plexus and of ciliary body with or without iris were incubated in a potassium‐rich medium containing labelled iodipamide often together with labelled o‐iodohippurate. Tissues were from rabbits, guinea‐pigs, monkeys (3 species), dogs, cats and chicken. Iodipamide at 0.5—2 μM depresses uptake of labelled iodipamide by rabbit kidney cortex wthout affecting uptake of o‐iodohippurate. Hippurate at 30 mM suppresses uptake of o‐iodohippurate in all tissues tested but leaves a fraction of iodipamide uptake in all tissues and species tested. The findings with o‐iodohippurate uptake are compatible with a single uptake system, the findings with iodipamide and the kinetics derived for this substance are incompatible with a single uptake system. Iodipamide seems to be accumulated by one hippurate‐sensitive system shared with o‐iodohippurate and at least one other, hippurate‐insensitive system. This latter system usually is a minority system in kidney cortex and anterior uvea but dominates in liver and choroid plexus and in cat kidney cortex. The hippurate‐insensitive system can be suppressed by probenecid but needs a higher concentration than the hippurate‐sensitive one.

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Transport Mechanisms in Certain Blood‐brain Barrier Phenomena‐a Hypothesis

Cited by 43 publications

References 8 publications

Blood‐Brain Barrier Alteration after Experimental Cold Injury of the Rabbit Brain, Indicated by Penicillin G in EEG and by Dye Tests

Blood‐Brain Barrier Alteration after Experimental Cold Injury of the Rabbit Brain, Indicated by Penicillin G in EEG and by Dye Tests

Electroconvulsive shock impedes the learning of taste aversions: Absence of blood-brain-barrier involvement

Inhibition by Hippurate and Probenecid of in vitro Uptake of Iodipamide and o‐Iodohippurate. A Composite Uptake System for Iodipamide in Choroid Plexus, Kidney Cortex and Anterior Uvea of Several Species

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