Biomedical subjects
Publications and source records attributed to H Lund-Andersen.
A method for dynamic angiography and quantitative measurement of fluorescence in ocular vessels in an in vitro experiment and in corneo-conjunctival angiography is described.
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Light and electron microscope autoradiography indicated that 3H-labelled inulin was taken up by neurons and glia cells of rat brain cortex in vitro. The mechanism, by which inulin passed the cell membranes, was studied by comparing the transport of inulin (molecular weight 5000) with the transport of dextran (molecular weight 75000). The half-time for the cellular in- and efflux for the two molecules was the same although their diffusion coefficients differed by a factor of 4-5. The transport mechanism was therefore interpreted as bulk transport, and vesicular transport is suggested. Efflux of inulin from brain cortex exposed to inulin in vivo indicated that cellular uptake of inulin also occurred in vivo.
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The K+-permeability of the blood-brain barrier at the capillary level was estimated from determinations of brain extracellular K+-concentration in response to an isotonic bolus containing KCl injected into the carotid artery. A very low permeability appeared from the fact that the extracellular K+-concentration--measured by aid of K+-sensitive microelectrodes--remained unchanged during the passage of the bolus. An upper limit for the blood-brain barrier K+-permeability in the rat was estimated to be 2.8 X 10(-7) cm. with s-1.
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Differential ocular spectrofluorometry was used to assess the passive permeability of the blood-retina barrier in healthy subjects and in patients with retinitis pigmentosa by determination of the rate of inward leakage of fluorescein and fluorescein glucuronide after intravenous injection of fluorescein. In five healthy subjects we found permeabilities of 1.3 (0.6-2.8) nm/s [log-mean (range)] for fluorescein and 1.3 (0.6-3.1) nm/s for fluorescein glucuronide. Six patients with retinitis pigmentosa all had a markedly increased blood-retina barrier leakage, with inward permeabilities of 8.2 (3.4-25) nm/s for fluorescein and 8.2 (5.6-27) nm/s for fluorescein glucuronide. Since no detectable difference was found between the permeabilities of the two tracers the passive permeability of the blood-retina barrier appears to be independent of the 18-fold difference in lipid solubility between the two tracers, both in retinitis pigmentosa and in healthy subjects. Presumably, the structural substrate for leakage of small hydrophilic molecules through the blood-retina barrier is a water-filled pore, since diffusion through lipid cellular membranes would favor fluorescein over its more water soluble glucuronide.