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H Davson

Publications and source records attributed to H Davson.

8 recordsLinked to original sources
PubMed1990

A saturable mechanism for transport of immunoglobulin G across the blood-brain barrier of the guinea pig.

The existence of an immunological blood-brain barrier to homologous blood-borne immunoglobulin G (IgG) was investigated in the guinea pig using a vascular brain perfusion technique in situ. Cerebrovascular unidirectional transfer constants (Kin) for 125I-labeled IgG (2.5 micrograms/ml) estimated from the multiple-time brain uptake data, ranged from 0.53 to 0.58 ml min-1 g-1 X 10(3) in the parietal cortex, hippocampus, and caudate nucleus, the transfer rate being some 10 times higher than that for [3H]dextran (MW 70,000). In the presence of 4 mg/ml unlabeled IgG, unidirectional blood to brain transfer of 125I-IgG was markedly inhibited. Immunohistochemical analysis of the brain tissue after vascular perfusion with unlabeled IgG revealed a distribution of the blood-borne immunoglobulin in the endothelial cells of microvessels and in the surrounding perivascular tissue. It is concluded that there is a specific transfer mechanism for IgG at the blood-brain barrier in the guinea pig, which is saturated at physiological plasma levels of IgG.

Animals↗
PubMed1976

Inhibition of in vitro concentrative prostaglandin accumulation by prostaglandins, prostaglandin analogues and by some inhibitors of organic anion transport.

1. Incubation of rabbit choroid plexus, anterior uvea (iris-ciliary body complex) or slices of kidney cortex in a medium containing tritium-labelled prostaglandin F(2alpha) ([3H]PGF(2alpha) or E1 ([3H]PGE1) results in a four- to thirteenfold concentrative accumulation of 3H activity. 2. Addition of PGF(2alpha, PGF(1) or PGA(1), any one of five PG analogues or a PG precursor, arachidonic acid, at a concentration of 10(-4) M reduced the active accumulation of [3H]PGs by 47-97%. Octanoic acid, at the same concentration, had only a moderate effect on the choroid plexus and no significant inhibitory effect on [3H]PFG(2alpha) accumulation by anterior uvea or kidney cortex. 3. Inhibition was also obtained with 2 mM iodoacetate (under anaerobic conditions) and with 10(-4) M diploretin phosphate, probenecid, iodipamide, indomethacin or dinitrophenol. Perchlorate (10(-4) M) and iodide (10(-4) or 10(-3) M) had no inhibitory effect while 10(-4) M p-aminohippuric acid had a significant inhibitory effect on the kidney cortex at a concentration of 10(-4) M and on the anterior uvea at 10(-3) M. 4. It is concluded that the apparent carrier mediated PG transport systems of the choroid plexus, anterior uvea and kidney cortex are not related to the iodide transport system, but may represent a subcomponent of the iodipamide transport system of these tissues. 5. These results suggest that the systemic distribution and the rate of renal excretion of PGs could be altered by high concentrations of PGs, pharmacologically less active PG analogues, some inhibitors of organic acid transport, and by some inhibitors of PG synthesis and PG action.

Animals↗
PubMed1976

The effect of cerebrospinal fluid pressure on the size of drainage pathways.

The cerebrospinal fluid drainage pathways were studied using labeled molecules of different sizes. Following determination of the limiting size, the cerebrospinal fluid pressure was raised above the normal range and changes in transfer were measured. These data show that molecules smaller than the limiting size will transfer at an increased rate in response to elevated pressures. Larger molecules did not demonstrate an increased transfer with raised cerebrospinal fluid pressures, suggesting that the pathways did not enlarge.

Animals↗
PubMed1975

Further studies on the difference between ventricular and subarachnoid perfusion.

In order to study the exchanges between the subarachnoid fluid and the adjacent cortical tissue independently of the choroid plexus, artificial cerebrospinal fluid (CSF) was perfused from the supracallosal cistern to the cisterna magna in the rabbit. Test substances were introduced into the blood and held at a constant level. The degree of penetration by the blood-borne test substances into the artificial CSF perfused into the cortical subarachnoid space was noted. The degree of penetration of these test substances into the artificial CSF does not solely reflect rates of exchange between this fluid and the exposed cortex for it was shown histologically as well as physiologically that the artificial CSF does not remain in the subarachnoid space but also enters the subdural space to exchange with the blood via the dural capillaries. Thus this experimental model routinely produces an artefactual situation which restricts its use in the study of CSF-brain relations.

Animals↗