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Biomedical subjects

H E Brondsted

Publications and source records attributed to H E Brondsted.

9 recordsLinked to original sources

Increased vesicular transfer of horseradish peroxidase across cerebral endothelium, evoked by acute hypertension.

Acute hypertension in rats was produced by intravenous infusion of metaraminol bitartrate (Aramine). The permeability to intravenously injected horseradish peroxidase (HRP) was increased across the cerebral arterioles, capillaries and venules. From the basement membranes of the vessel walls the protein tracer moved into the extracellular spaces of the adjacent neuropil. No endothelial cell damage was observed. The tight junctions between endothelial cells were intact and prevented intercellular movement of peroxidase. Many HRP-labeled vesicles within the endothelial cells or connected with the luminal or abluminal surface, occurred in segments of the microvasculature. Otherwise the endothelium was unchanged. Diffuse uptake of HRP into the cytoplasm of neurons and glial cells was not observed. The alphablocker phentolamine (Regitin) was given to a group of rats simultaneously to Aramine. The increase in blood pressure was thus prevented; furthermore, the permeability remained as under normal conditions. The Aramine, Regitin and HRP did not significantly influence the pH, PO2 and pCO2 of the arterial blood. It is concluded that acute hypertension increases the vesicular transport of HRP across the endothelium of cerebral arterioles, venules and capillaries that normally occurs to a small extent only after intravenous injection of the tracer.

Blood Vessels↗

Sodium-dependent transport of sugars and iodide from the cerebral venticles of the rabbit.

1. The objective was to discover whether the extraction of sugars and iodide from the perfused cerebral ventricles is Na(+)-dependent.2. In the ventriculo-aqueductal and ventriculo-cisternal perfusion systems in the rabbit the extraction of (14)C-labelled D-hexoses (glucose, 3-O-methyl-glucose, alpha-methyl-glucoside and galactose), (131)I(-) and (24)Na was inhibited when 82% of the Na(+) in the perfusion fluid was replaced by choline. The extraction returned to control levels when the Na(+) concentration in the perfusion fluid was returned to normal.3. Ouabain, 5 x 10(-5)M in the perfusion fluid inhibited the extraction of the above (14)C sugars and (131)I(-), but hardly affected that of [(3)H]2-deoxy-D-glucose. It enhanced the extraction of (24)Na. C.s.f. production was usually totally inhibited.4. The extraction of [(14)C]urea remained unchanged during perfusion with low Na(+) fluid or ouabain.5. Recovery from brain of [(14)C]3-O-methyl-glucose, [(3)H]2-deoxy-glucose and (131)I(-) was low while recovery of [(14)C]alpha-methyl-glucoside and (24)Na was high. On an equal weight basis recovery of [(14)C]3-O-methyl-glucose was about twelve times higher from the choroid plexus than from the brain.6. Part of the movement of (14)C sugars may be explained on basis of a Na(+)-gradient hypothesis with involvement of the Na(+) pump at the blood-c.s.f. or blood-brain barriers.7. The rate of c.s.f. production from the first three ventricles comprised about 40% of the rate from all four ventricles. The extraction of sugars, urea and cations was similar in both perfusion systems while the extraction of (131)I(-) was higher in the ventriculo-cisternal system than in the ventriculo-aqueductal system.

Animals↗

Ouabain-sensitive carrier-mediated transport of glucose from the cerebral ventricles to surrounding tissues in the cat.

1. Artificial cerebrospinal fluid containing isotopically labelled sugars was perfused from the lateral cerebral ventricles to an effluent catheter inserted into the cerebral aqueduct of anaesthetized cats. This system was used for a quantitative study of the absorption of the sugars during steady state.2. A saturable mechanism was involved in the absorption of [U-(14)C]D-glucose and [(14)C]D-galactose. Absorption of [U-(14)C]D-glucose in the dead animal was similar to that of [(3)H]D-mannitol.3. 5 x 10(-5)M ouabain in the inflow reduced cerebrospinal fluid formation and the unidirectional fluxes of glucose from the ventricles into brain tissue and plasma. Ouabain did not alter the absorption of [(3)H]D-mannitol.4. Three types of unidirectional fluxes of glucose from the cerebral ventricles were separated. One was ouabain-sensitive and followed Michaelis-Menten kinetics. The second was insensitive to ouabain and the third occurred by simple diffusion.5. At normal ventricular glucose concentrations (3.5 mM) the three fluxes comprised (roughly): 25% (ouabain-sensitive), 35% (ouabain-insensitive) and 40% (simple diffusion) of total, unidirectional transport.

Animals↗