PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 3395069

Structural and functional variations in capillary systems within the brain.

J Fenstermacher·P Gross·N Sposito·V Acuff·S Pettersen·K Gruber
View original source ↗Export metadata ↓

Abstract

The major hypothesis of this study is that there are differences among brain areas in capillary bed structure and function. Three general differences between circumventricular organ and non-CVO capillary beds were found. First, the PS products for AIB were about 300 times greater in CVO capillaries than in non-CVO (blood-brain barrier) capillaries. Second, the frequency of endothelial cell fenestrations was much greater in CVO capillaries than in non-CVO capillaries and the fenestrae may be structural modifications of endothelial cells that permit ready passage of solutes such as AIB. Third, the frequency of mitochondria was greater in BBB capillaries than in CVO capillaries; this high metabolic potential of BBB capillaries may be associated, in part, with "carrier-mediated" transport of various solutes between plasma and cerebral interstitial fluid. Capillary bed differences among all (i.e., both CVO and non-CVO) brain structures were also observed. Among these differences are: rate of blood flow, mean transit time of albumin, capillary volume and surface area, perfused microvessel blood volume, apparent percentage of perfused capillaries, PS products for AIB, and frequency within the endothelium of vesicular profiles.

Explore related subjects

Aminoisobutyric AcidsAnimalsBlood VolumeBlood-Brain BarrierCapillariesCerebrovascular CirculationModels, CardiovascularModels, NeurologicalSerum AlbuminJournal ArticleResearch Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Fenstermacher, P Gross, N Sposito, V Acuff, S Pettersen, K Gruber. 1988. Structural and functional variations in capillary systems within the brain.. https://doi.org/10.1111/j.1749-6632.1988.tb51416.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1997

Buthionine sulfoximine (BSO) and N-(3,5-dichlorophenyl)succinimide nephrotoxicity: temporal aspects of BSO administration and BSO effects on renal transport systems.

The agricultural fungicide, N-(3,5-dichlorophenyl)succinimide (NDPS) induces acute polyuric renal failure which is attenuated by pretreatment with the glutathione depletors, diethyl maleate or buthionine sulfoximine (BSO). In the present study, the temporal aspects of BSO attenuation of NDPS nephrotoxicity were investigated. In addition, the ability of BSO to alter the renal accumulation of selected organic ions was examined as a possible mechanism for BSO's ability to attenuate NDPS nephrotoxicity. In the first set of experiments, NDPS (0.2 or 0.4 mmol/kg) or vehicle (sesame oil, 2.5 ml/kg) was administered intraperitoneally (i.p.) to groups of male Fischer 344 rats (4-8 rats/group) 0.25 or 2 h prior to BSO (890 mg/kg, i.p.) and renal function was monitored at 24 and 48 h. NDPS (0.4 mmol/kg) nephrotoxicity was markedly attenuated by administration of BSO at 0.25 h post-NDPS, but was not substantially altered by injection of BSO at 2 h post-NDPS. NDPS (0.2 mmol/kg)-induced renal effects were not potentiated by BSO injected at 0.25 h post-NDPS, and only 1 of 8 rats exhibited marked nephrotoxicity when BSO was administered at 2 h post-NDPS. In the second set of experiments, rats (4/group) were administered BSO (890 mg/kg, i.p.) or vehicle (0.9% saline, 10 ml/kg) and kidneys harvested at 2 or 5 h post-treatment. The ability of renal cortical slices to accumulate organic ions (p-aminohippurate [PAH], alpha-aminoisobutryic acid [AIB] or tetraethylammonium [TEA]) during a 90 min incubation was studied. Only TEA accumulation by renal cortical slices prepared from the 2 h post-treatment group was reduced. Studies were also conducted to examine the in vitro effects of BSO (10(-7)-10(-4) M) on the accumulation of PAH, AIB and TEA by renal cortical slices following 5, 15 or 90 min co-incubations of BSO and an organic ion BSO had no significant effects on the accumulation of any organic ion studied at any time point. These results indicate that BSO can still attenuate NDPS nephrotoxicity when administered at 0.25 h post-NDPS, but BSO loses effectiveness when given 2 h post-NDPS. These results also suggest that BSO is attenuating NDPS nephrotoxicity via glutathione depletion rather than altering renal accumulation of NDPS metabolites via renal PAH, TEA or AIB transporters.

Aminoisobutyric Acids↗
PubMed1997

Cryopreservation of isolated rat hepatocytes: effects of iron-mediated oxidative stress of metabolic activity.

In an attempt to quantitatively evaluate the destructive effects of free radicals on metabolism, freshly prepared and cryopreserved isolated rat hepatocytes were exposed to and incubated with Fe2+ compounds, reputedly inducing oxygen-derived free radicals (OFR) capable of attacking the lipid structures of cellular membranes. Malondialdehyde (MDA) formation was interpreted as an expression of free radical interaction with polyunsaturated lipids, and in vitro incubations were carried out during the period of constant MDA formation. Protein synthesizing activity was evaluated by incubating control hepatocytes and cells previously exposed to 100 microM of Fe2+, to 100 microM of Fe2+, and 100 microM of desferrioxamine and to 100 microM of desferrioxamine alone with 0.1 microCi of L-[U-14C]isoleucine and in the presence of these compounds. Membrane transport activity was similarly evaluated by following the cellular uptake of alpha-amino-[1-14C]isobutyric acid. Protein-synthesizing activity of freshly prepared and cryopreserved hepatocytes was not affected by Fe2+ treatment, nor by the additions of the iron chelator desferrioxamine. Amino acid transport, however, was inhibited by 100 microM of Fe2+, but was effectively neutralized by the simultaneous addition of 100 microM of desferrioxamine. Cryopreserved hepatocytes equally presented a significantly inhibited amino acid transport activity over the incubation period. The results suggest that the metabolic depression measured in thawed hepatocytes does not result to any large extent from iron-catalysed OFR effects. When OFR production was deliberately induced, the most significant early change was seen in transmembrane amino acid uptake in both fresh and cryopreserved cells.

Aminoisobutyric Acids↗
PubMed1997

Effects of hyperosmolar mannitol on regional oxygen supply and consumption in the newborn pig.

Previous work indicated that opening the blood-brain barrier with hyperosmotic mannitol decreased local venous O2 saturation and increased cerebral O2 consumption. This study was performed to assess the vascular effect of hypertonic mannitol on oxygen supply/consumption balance in the newborn pig and to determine the role of nitric oxide in mediating the effects of mannitol. Animals were anesthetized with alpha-chloralose and mechanically ventilated to maintain their blood gases within normal range. Retrograde catheterization of the right carotid artery was performed to inject 12 ml to 25% mannitol over a 30 sec interval. In one group of animals (n = 5), the blood-brain barrier transfer coefficient (Ki) to 14C-alpha aminoisobutyric acid or 14C-urea (n = 4) was measured 12 min after mannitol. In another group of animals (n = 9), regional cerebral blood flow and small vein O2 saturation was measured using 14C-iodoantripyrine and microspectrophotometry. Similar measurements were made in other groups of animals (n = 9) after pretreatment with 10 mg kg-1 i.v. of N-omega-nitro-L-arginine methyl ester (L-NAME), 20 min before mannitol injection. The mannitol injection did not increase Ki or local cerebral O2 consumption. It resulted in a decreased small vein O2 saturation in the ipsilateral cortex (46 +/- 3%) in comparison to the contralateral cortex (55 +/- 2%). The O2 supply/consumption ratio decreased in the ipsilateral cortex in the mannitol injected animals (2.14 +/- 0.23) in comparison to the contralateral cortex (2.76 +/- 0.28). Pretreatment with L-NAME abolished this effect of mannitol (small vein O2 saturation 59 +/- 2% in ipsilateral cortex and 58 +/- 2% in the contralateral cortex; O2 supply/consumption 2.68 +/- 0.17 in the ipsilateral cortex and 2.65 +/- 0.16 in the contralateral cortex). We conclude that hypertonic mannitol adversely affects O2 supply/consumption balance, without increasing blood-brain barrier transport, and this effect is blocked by L-NAME, a nitric oxide synthase antagonist.

Aminoisobutyric Acids↗