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Biomedical subjects

H Davson

Publications and source records attributed to H Davson.

At least 37 records · Page 2Linked to original sources
PubMed1982

Cerebrospinal fluid drainage as influenced by ventricular pressure in the rabbit.

Artificial cerebrospinal fluid (CSF) containing radioisotope iodinated (125I) serum albumin (RISA) and either blue dextran or indigo carmine was given to white New Zealand rabbits over 4 hours. In one group it was given by ventriculocisternal perfusion, in one by ventricular infusion, and in one by cisterna magna infusion. Blood was sampled continuously from the superior sagittal sinus (SSS) or intermittently from the systemic arterial circulation. Removal of CSF from the cisterna magna during the ventriculocisternal perfusion kept the intracranial pressure (ICP) at 0 to 5 torr, whereas ventricular or cisterna magna infusion raised the ICP to 20 to 30 torr and 15 to 20 torr, respectively. In the two groups with raised ICP, an increased concentration of RISA was present in the optic nerves, olfactory bulbs, episcleral tissue, and deep cervical lymph nodes; but this was not found in the group with normal ICP. In all three groups, the concentration of RISA in the SSS blood was the same as in the systemic arterial blood. The concentration gradient of RISA across the cerebral cortex was similar in both the ventriculocisternal perfusion and the ventricular infusion groups. With cisterna magna infusion, the concentration of RISA was the same on the cortical surface and less in the ventricles compared with the ventricular infusion. It is concluded that, with elevated ICP, CSF drained via pathways that are less evident under normal pressure. Drainage of CSF was similar irrespective of whether the infusion site was the ventricles or cisterna magna. It did not appear that acute dilatation of the ventricles during ventricular infusion compromised the subarachnoid space over the surface of the hemisphere, as the concentration of RISA on the convexities and in the SSS blood did not significantly differ between the groups. Transcortical bulk transfer of CSF was not evident with raised ICP.

Animals↗
PubMed1981

The effect of severe hypoglycemia upon cerebrospinal fluid formation, ventricular iodide clearance, and brain electrolytes in rabbits.

Severe insulin-induced hypoglycemia in rabbits reduces cerebrospinal fluid (CSF) formation, but not ventricular iodide clearance as measured by ventriculocisternal perfusion. This indicates that CSF production is ultimately glucose-dependent but that ventricular iodide clearance is not. The data suggest that severe hypoglycemia results in intracellular potassium loss within the brain and show that extracellular sodium replaces lost intracellular potassium. Hypoglycemia probably results in cellular adenosine triphosphate (ATP) reduction which affects membrane Na/K ATPase and the ability of the brain cell to maintain a potassium gradient. Potassium levels in the CSF also rise consequent to hypoglycemia. Homeostatic mechanisms that maintain a constant CSF potassium, therefore, are also affected by hypoglycemia.

Adenosine Triphosphate↗
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

Facilitated transport of prostaglandins across the blood-cerebrospinal fluid and blood-brain barriers.

1. Ventriculo-cisternal perfusions were performed on rabbits with artificial cerebrospinal fluid containing blue dextran and tritium-labelled prostaglandin F(2alpha) ([(3)H]PGF(2alpha)). In order to study the nature of prostaglandin (PG) transfer across the blood-brain barrier, high concentrations of PGF(2alpha) or potential PG transport inhibitors were added to the perfusion fluid after the normal rate of [(3)H]PGF(2alpha) clearance was established.2. The [(3)H]PGF(2alpha) clearance was inhibited by 10(-6) to 10(-3)M PGF(2alpha), PGF(2beta), probenecid, iodipamide or bromcresol green but not by perchlorate.3. The (3)H content of the brain, relative to the (3)H-activity in the ventricular system, was also increased by high concentrations of PGF(2alpha), iodipamide or bromcresol green.4. It is concluded that the removal of PGs from the extracellular fluids of the brain is mediated by saturable, facilitated transport processes across both the choroidal and extrachoroidal regions of the blood-brain barrier system. In the case of the mammalian brain, such facilitated PG transport appears to be the primary mechanism for the termination of the action of these potent, endogenously produced autacoids.

Journal Article↗
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↗
PubMed1973

Active transport of 131-I across the blood-brain barrier.

The ventricular space of rabbits was perfused with a low-viscosity silicone oil for the purpose of (1) collecting freshly secreted cerebrospinal fluid (c.s.f.) uninfluenced by diffusional exchanges with the brain and (2) studying passage of solutes from the blood into the brain, uncomplicated by exchanges with c.s.f. The freshly secreted c.s.f. appeared as fine droplets suspended in the less dense silicone, and accumulated at the bottom of the collected silicone. Studies on the penetration of (24)Na from blood into this fluid indicated that considerable exchanges with the brain had occurred between its secretion and collection, in spite of this method of collection. The second objective was attained, in that the exchanges between the freshly secreted fluid and the brain were quantitatively insufficient to affect the measure of kinetics of uptake by brain from the blood. In consequence, it was possible to demonstrate unequivocally that the increased uptake by brain of (131)I, when treated with perchlorate, was due to inhibition of an active process occurring across the blood-brain barrier. Other studies, involving ventriculo-cisternal perfusion with artificial c.s.f., lent further support to this concept. (131)I distribution is some 32% of the brain weight, a figure close to the ;chloride-space'.

Animals↗