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PubMed1988

[Changes in capillary permeability in experimental brain tumor].

It is still controversial whether edema fluid around a malignant brain tumor is derived from capillaries inside the tumor itself or not only from tumor vessels but also from peritumoral tissue. The purpose of this study is to clarify the region where the capillary permeability is increased using double autoradiographic method. A suspension of 1 X 10(4) rat glioma cells (RG-12) was stereotactically implanted into the right basal ganglia of C-D Fisher rats. In this model, all animals are dead 20 +/- 1 days after the implantation. Two kinds of tracers, 14C-alpha-aminoisobutyric acid (AIB) and 131I-human serum albumin (HSA), were administered 14 to 17 days after the tumor implantation. In all rats, 14C-AIB was intravenously injected 10 min before decapitation. 131I-HSA was given 10 min before decapitation in five animals (group 1), one hour before in four animals (group 2), and six hours before in three animals (group 3). Autoradiograms for 131I-HSA were exposed for initial one to two days after the decapitation, while the exposure for 14C-AIB was delayed until 4 months later. Autoradiograms of these two tracers were compared with the corresponding sections with H-E stain for neuropathological examination. In group 1, the distribution of HSA as well as AIB was quite similar to tumor itself. In group 2 and group 3, the distributions of AIB were similar to the tumor. However, the distributions of HSA were 1.4 fold larger (group 2) and 3.6 fold larger (group 3) than the tumor and expanded into the peritumoral region.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗
PubMed1980

Effect of calciotropic hormones and cyclic nucleotides on aminoaciduria and phosphaturia.

Parathyroid extract (PTE), dibutyrylcyclic AMP (dbcAMP), adenosine cyclic 3':5'-monophosphate (cAMP). calcitonin (CT), and calcium chloride were infused separately into anesthetized, sham-operated, or TPTX vitamin D-fed adult rats to examine the effect of these calciotropic agents on fractional excretion (FE) of alpha-aminoisobutyric acid (AIB), and phosphate anion (Pi). AIB is a nonmetabolizable amino acid. Inulin clearance, FEAIB, and FEPi were stable in the intact (n = 10) and TPTX rat (n = 10). TPTX decreased FEAIB, and FEPi significantly (P less than 0.001 for both). PTE and dbcAMP both increased FEAIB in the intact rat (P less than 0.001); failure to obtain this response in the TPTX animal was a key finding. PTE and dbcAMP increased FEPi (P less than 0.001) in both the intact and TPTX animal. CT was the only agent (versus PTE, dbcAMP, adenosine cyclic 3':5'-monophosphate, and CaCl2) to increase FEAIB (P less than 0.001) in the TPTX rat; furthermore, it was the only agent that did not increase FEPi in the TPTX rat although it had hypocalcemic and hypophosphatemic effects. Changes in inulin clearance or plasma concentration of AIB, following infusion of calciotropic agents, do not explain the unique responses in FEAIB in the TPTX rat. Our findings suggest that hyperaminoaciduria induced by parathyroid hormone and cyclic nucleotide in the intact animal may be mediated by CT. Hyperphosphaturia is not a necessary response to small-dose (25 milliunits/kg.hr) infusions of CT.

Aminoisobutyric Acids↗
PubMed1986

The lack of effects of alkylating agents on mammalian cell membranes.

The importance of cell membrane components as target sites for the action of 2,3,5-tris(ethyleneimino)-benzoquinone (Trenimon), mechlorethamine hydrochloride (HN2) and tris(2-chloroethyl) amine hydrochloride (HN3) was investigated. Uptake of 2-aminoisobutyric acid (AIBA) was studied under nonsaturating conditions where the transport system was rate-limiting for the uptake. Uptake of AIBA into L5178Y leukaemic cells was either inhibited or stimulated, depending on the type of the drug, the drug concentration and the length of incubation. Treatment of human erythrocytes with 10(-3) M HN3 produced new high-molecular-weight protein bands on SDS-polyacrylamide gel electrophoresis. Conversely, HN3 had no effect on L5178Y cell membrane proteins. Neither HN2 nor Trenimon produced any detectable changes in membrane proteins of L5178Y cells or human erythrocytes. None of the three drugs at concentrations and incubation conditions which inhibited cell replication changed the stoichiometry or dissociation constant of concanavalin A (Con A) binding sites on L5178Y cells. Trenimon at highly toxic concentrations had no effect on the fluidity of phospholipid membranes or of membranes of Ehrlich ascites tumour cells as analysed by ESR spin-label methods. The results presented here do not support the hypothesis that cell membranes are the primary target sites for alkylating drugs.

Alkylating Agents↗
PubMed1986

In vitro studies on the effect of yolk sac antisera on functions of the visceral yolk sac: I. Pinocytosis and transport of small molecules.

The production of congenital malformations by the administration of teratogenic antisera to pregnant animals has been reported from many laboratories. This work has focused our attention on the importance of the yolk sac placenta in supporting the rat embryo during early organogenesis and the significance of yolk sac dysfunction in rodent teratogenesis. The studies reported in this article deal with the effect of teratogenic antisera on the process of yolk sac transport; specifically pinocytosis (as measured by 14C-sucrose uptake) and small-molecule transport utilizing 14C-alpha-aminoisobutyric acid (AIB) and 3H-2-deoxyglucose (DOG). We sought to determine whether several different yolk sac localizing antibodies interfere with these transport processes, and, if so, which transport processes were most affected. The results of the experiments indicated that teratogenic antisera interfered with the process of pinocytosis in the yolk sac and that pinocytosis can be reduced as much as 40%. Nonteratogenic antisera, even when they localized in the yolk sac, did not interfere with the process of pinocytosis. Furthermore, the teratogenic antisera did not interfere with the transport of small molecules (either AIB or DOG) in the yolk sac. These results indicated that while fluorescent localization of an antiserum in the yolk sac did not invariably indicate the potential for teratogenicity, it is likely that the reduction in pinocytosis may directly correlate with the teratologic and embryopathic events. This work reaffirms the view that the yolk sac in important during rodent organogenesis and that yolk sac dysfunction can play an important role in the development of congenital malformations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗
PubMed1995

The effects of dexamethasone on experimental brain tumors: I. Transcapillary transport and blood flow in RG-2 rat gliomas.

Dexamethasone dramatically improves cerebral edema associated with malignant gliomas. Although the pathophysiology of this effect is not clearly understood, many investigators have postulated that tumor capillary permeability is reduced by dexamethasone. We studied blood-to-tissue transport and blood flow in 178 RG-2 transplanted gliomas in a control group and four groups given dexamethasone at doses of 3, 6, 9, and 12 mg/kg for four days. 14C-alpha aminoisobutyric acid (AIB) was used to study blood-to-tissue transport in 31 animals; in an additional 27 animals 14C-AIB and 131I-iodoantipyrine (IAP) were used in double label experiments to study blood-to-tissue transport and blood flow. Regional measurements of the transfer constant (K) of AIB and blood flow (F) were made with quantitative autoradiography. There were significant differences between the control and dexamethasone-treated groups with regard to weight loss and plasma glucose. However, there was no significant effect of dexamethasone on values of K or F, regardless of the tumor or brain region examined, and regardless of the dose of dexamethasone administered. Analysis of the profiles of the transfer constant of AIB in the brain around tumor showed that the K of AIB decreased within 0.5 mm of the tumor edge in direct relationship to the dexamethasone dose. These results do not support the hypothesis that dexamethasone reduces brain tumor capillary permeability, and suggest that dexamethasone may decrease tumor-associated cerebral edema by effects on bulk flow away from the tumor margin.

Aminoisobutyric Acids↗
PubMed2006

Effects of anti-VEGF antibody on blood-brain barrier disruption in focal cerebral ischemia.

Since cerebral ischemia increases expression of vascular endothelial growth factor (VEGF) and exogenous VEGF can aggravate BBB disruption in cerebral ischemia, we hypothesized that inhibition of endogenous VEGF would attenuate BBB disruption. To test this hypothesis, rats were mechanically ventilated with isoflurane and a craniotomy (5 mm in diameter) was performed to expose the cerebral cortex. Anti-VEGF antibody was applied topically (75 mug) 1 h before middle cerebral artery (MCA) occlusion and additional anti-VEGF antibody was applied (25 mug) immediately after MCA occlusion (anti-VEGF group). For the control animals, normal saline was applied instead of anti-VEGF antibody on the surface of the cortex (control group). One hour after MCA occlusion, the transfer coefficient (K(i)) of (14)C-alpha-aminoisobutyric acid and volume of (3)H-dextran (70,000 Da) distribution were determined to measure the degree of BBB disruption. There was no significant difference in vital signs, blood gases, and pericranial temperature between the control and the anti-VEGF group. In both of the groups, the K(i) of the ischemic cortex (IC) was higher than that of the corresponding contralateral cortex (CC) (p<0.05). The K(i) of the IC of the anti-VEGF group was significantly lower than that of the IC of the control group (-34%, p<0.05). The K(i) of the CC and pons were similar between these two groups. The data of volume of dextran distribution followed the same pattern as that of K(i) but without a statistical significance. Our data demonstrated that inhibition of endogenous VEGF by topical application of anti-VEGF antibody in the ischemic cortex decreased the K(i) of (14)C-AIB and suggest that endogenous VEGF is in part responsible for the BBB disruption during the early stage of focal cerebral ischemia.

Administration, Topical↗
PubMed1979

Heterogeneity of AtT-20 cell glucocorticoid binding sites: evidence for a membrane receptor.

In previous studies we have found that intact AtT-20 cells contained two glucocorticoid binding sites with distinctly different affinities and specificity. In this paper, the nature of these sites was investigated by studying glucocorticoid binding to cytosol and to plasma membranes isolated from AtT-20 mouse pituitary tumor cells. Plasma membrane vesicles were isolated from AtT-20 cells and found to take up alpha-aminoisobutyric acid, indicating that they were properly oriented and functionally intact. Corticosterone bound to these vesicle in a time- and temperature-dependent manner. The binding exhibited a glucocorticoid preference since non-glucocorticoids such as progesterone, testosterone or estradiol were unable to inhibit binding. In addition, binding specificity differed from that of the cytoplasmic receptor since the synthetic glucocorticoids were also ineffective competitors. The major inhibitors of binding were corticosterone greater than 11-dehydrocorticosterone greater than 11-ketoprogesterone greater than cortisol. In other complementary studies, AtT-20 cell cytosol was tested to determine whether heterogenous soluble sites exhibiting a preference for the natural vs the synthetic steroid could also be identified. We found that binding sites for both steroid classes were approximately similar in number, specificity and behavior on ion-exchange chromatography. We conclude that, in addition to a classical soluble cytoplasmic glucocorticoid receptor, AtT-20 cells contain plasma membrane glucocorticoid binding sites. The affinity and specificity of these sites for the natural ligand, corticosterone, suggest that they play an important role in the subcellular mechanism of glucocorticoid action.

Aminoisobutyric Acids↗
PubMed1992

Regulation of biological functions by an insulin receptor monoclonal antibody in insulin receptor beta-subunit mutants.

We investigated the effects of MA-5, a human-specific monoclonal antibody to the insulin receptor alpha-subunit, on transmembrane signaling in cell lines transfected with and expressing both normal human insulin receptors and receptors mutated in their beta-subunit tyrosine kinase domains. In cell lines expressing normal human insulin receptors, MA-5 stimulated three biological functions: aminoisobutyric acid (AIB) uptake, thymidine incorporation, and S6 kinase activation. Under conditions where these biological functions were stimulated, there was no detectable stimulation of receptor tyrosine kinase. We then combined the use of this monoclonal antibody with cells expressing insulin receptors with mutations in the beta-subunit tyrosine kinase domain; two of ATP binding site mutants V1008 (Gly----Val) and M1030 (Lys----Met) and one triple-tyrosine autophosphorylation site mutant F3 (Tyr----Phe at 1158, 1162, and 1163). In cells expressing V1008 receptors, none of the three biological functions of insulin was stimulated. In cells expressing M1030 receptors, AIB uptake was stimulated to a small, but significant, extent whereas the other two functions were not. In cells expressing F3 receptors, AIB uptake and S6 kinase activation, but not thymidine incorporation, were fully stimulated. The data suggest, therefore, that (1) activation of insulin receptor tyrosine kinase may not be a prerequisite for signaling of all the actions of insulin and (2) there may be multiple signal transduction pathways to account for the biological actions of insulin.

Aminoisobutyric Acids↗
PubMed1993

Changes in the permeability of the blood-brain barrier in acute hyperammonemia. Effect of dexamethasone.

This study was designed to determine the contribution of elevated plasma ammonia levels to blood-brain barrier (BBB) abnormalities in the presence of intact liver. The permeability changes of the BBB were investigated grossly with Evans blue (EB) and quantitatively by measuring the blood-to-brain transfer content for alpha-aminoisobutyric acid (AIB) in normal rats and rats subjected to sublethal doses of ammonium acetate (NH4OAc) (750 and 600 mg/kg ip; at 30-min intervals). Some rats were pretreated with dexamethasone (DXN). Injection of NH4OAc increased both plasma and brain ammonia concentrations about 16-and 5-fold, respectively, above the control level. In rats receiving NH4OAc injection, the blood-to-brain transfer constant (Ki) for AIB was increased 3- to 11-fold. The elevated Ki values were limited to certain gray matter areas and less pronounced permeability changes were detected in white matter. Extravasation sites of EB were more restricted and were especially observed in thalamus and cerebellum, whereas cortex and white matter were unaffected. Dexamethasone pretreatment for 3 d reduced both leakage of EB and the Ki for AIB in NH4OAc injected animals, whereas acute treatment appeared ineffective. Dexamethasone did not prevent the development of coma but slightly decreased the ammonia concentration in plasma and brain. The results obtained indicate that hyperammonemia may disrupt BBB integrity not only to AIB and EB but also enhance the transport of other solutes.

Acetates↗
PubMed2000

Effects of duration of positive-pressure ventilation on blood-brain barrier function in premature lambs.

We have been studying the ontogeny of the blood-brain barrier function in ovine fetuses and lambs. During these studies, we have found that the duration of ventilation also influences blood-brain barrier permeability in premature lambs. Chronically instrumented hysterotomy-delivered surfactant-treated premature lambs were studied at 90% or 137 days of gestation (n = 9). Blood-brain barrier function was quantified with the blood-to-brain transfer constant K(i) to alpha-aminoisobutyric acid. Linear regression analysis was used to compare the K(i) values in the brain regions, as the dependent variable, to the duration of ventilation, as the independent variable. There were direct correlations (P < 0.05) between the K(i) values and the duration of ventilation [306 min (mean), 162-474 min (range)] in the cerebral cortex, cerebellum, medulla, caudate nucleus, hippocampus, superior colliculus, inferior colliculus, thalamus, pons, cervical spinal cord, and choroid plexus, but not in the pituitary gland. Ventilatory pressures and rates were established before the onset of the permeability studies. Calculated mean airway pressures [14 cmH(2)O (mean), 7-20 cmH(2)O (range)] from similarly studied premature lambs did not correlate with the duration of positive-pressure ventilation. We conclude that increases in the duration of positive-pressure ventilation predispose premature lambs to increases in regional blood-brain barrier permeability. These alterations in barrier function occur over relatively short time intervals (minutes to hours). In our study, these changes in permeability are most likely not attributable to changes in mean airway pressure.

Aminoisobutyric Acids↗
PubMed2006

Gold nanoclusters protected by conformationally constrained peptides.

The preparation and properties of a series of gold nanoclusters protected by thiolated peptides based on the alpha-aminoisobutyric acid (Aib) unit are described. The peptides were devised to form 0-3 C=O...H-N intramolecular hydrogen bonds, as required by their 3(10)-helical structure. The monolayer-protected clusters (MPCs) were prepared, using a modified version of the two-phase Brust-Schiffrin preparation, and fully characterized with (1)H NMR spectrometry, IR and UV-vis absorption spectroscopies, transmission electron microscopy (TEM), thermogravimetric analysis (TGA), and X-ray photoelectron spectroscopy (XPS). The MPCs were obtained with core diameters in the range of 1.1-2.3 nm, depending on the reaction conditions. Structured peptides formed smaller clusters. The smallest MPC obtained is in agreement with the average formula Au(38)Pep(18). The results showed that the chemical integrity of the peptide is maintained upon monolayer formation and that the average number of peptide ligands per gold cluster is typically 75-85% the value calculated for alkanethiolate MPCs of similar sizes. The IR and NMR spectra indicated that in the monolayer the peptides are involved in both intra- and interligand C=O...H-N hydrogen bonds.

Aminoisobutyric Acids↗
PubMed1994

Intracarotid infusion of bradykinin selectively increases blood-tumor permeability in 9L and C6 brain tumors.

This study investigated the effects of bradykinin on blood-tumor barrier (BTB) permeability in transplanted 9L gliosarcomas (9L) and C6 gliomas (C6) in rats. Permeability, expressed as the unidirectional transfer constant, Ki (microliter/g/min), was measured by quantitative autoradiography. Tracers used to examined permeability included radiolabeled alpha-aminoisobutyric acid ([14C]AIB), sucrose ([14C]sucrose) and dextran ([14C]dextran). Intracarotid infusion of bradykinin (10 mg/kg/min) significantly increased the BTB permeability in both 9L and C6 tumors to [14C]AIB and [14C]sucrose, but did not increase permeability to [14C]dextran. Blood-brain barrier (BBB) permeability in normal (non-tumor) brain was not significantly increased to any of the tracers by intracarotid bradykinin infusion. Ki values for [14C]AIB, [14C]sucrose and [14C]dextran of 9L tumors in the bradykinin group versus control group were 41.6 +/- 12.6 vs. 24.8 +/- 6.30 (P < 0.02), 17.5 +/- 9.34 vs. 9.05 +/- 4.36 (P < 0.05), and 3.90 +/- 2.59 vs. 2.42 +/- 1.76, respectively (mean +/- S.D.). Ki values to [14C]AIB, [14C]sucrose and [14C]dextran of C6 tumors in the bradykinin group versus control group were 41.4 +/- 19.0 vs. 19.5 +/- 11.4 (P < 0.01), 18.0 +/- 8.88 vs. 7.06 +/- 3.05 (P < 0.01), and 4.07 +/- 1.45 vs. 2.27 +/- 1.26, respectively (mean +/- S.D.). Intracarotid infusion of bradykinin did not significantly increase the blood volume in tumor or brain tissue despite its known vasodilative effect. Intracarotid infusion of bradykinin may be a useful technique for selective delivery of compounds to brain tumors.

Aminoisobutyric Acids↗
PubMed1996

Factors regulating insulin-like growth factor-binding protein-3 binding, processing, and potentiation of insulin-like growth factor action.

In this study, we investigated the effects of various biochemical and pharmacological agents on insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) cell binding and action in cultured bovine fibroblasts. When cells were preincubated for 48 h with 50 nM recombinant human (rh) IGFBP-3, IGF-I-stimulated [3H]aminoisobutyric acid ([125H]AIB) uptake was enhanced 2- to 3-fold. The addition of cytoskeletal disrupting agents during the preincubation with rhIGFBP-3 did not affect IGFBP-3 potentiation of IGF-I action, nor did a variety of serine, aspartate, and metalloproteinase inhibitors. On the other hand, ammonium chloride and chloroquine, weak bases that neutralize the pH of acidic cell compartments, blocked IGFBP-3 potentiation of IGF-I-stimulated [3H]AIB uptake. Chloroquine and ammonium chloride had no effect alone and did not inhibit IGF-I receptor binding or action in the absence of rhIGFBP-3. Bafilomycin A, a specific inhibitor of ATP-dependent hydrogen ion pumps, also inhibited IGFBP-3 potentiation of IGF-I-stimulated [3H]AIB uptake. Competitive [125I]IGF-I binding and affinity cross-linking experiments suggested structure/function changes in cell-bound IGFBP-3 that were altered in the presence of chloroquine and bafilomycin. Heparin markedly decreased initial IGFBP-3 cell adherence, but could not promote dissociation of IGFBP-3 from cells after the 48-h preincubation. Moreover, heparin did not inhibit IGFBP-3 potentiation of IGF-I action. In summary, these data indicate that IGFBP-3 undergoes specific pH-dependent structural and/or environmental modifications that mediate the enhancing effect of IGFBP-3 on IGF-I action in bovine fibroblasts. They also suggest that IGFBP-3 binding to heparin-like molecules on the cell surface is not directly involved in this process.

Adenosine Triphosphate↗
PubMed1983

Regional blood-to-tissue transport in RT-9 brain tumors.

Regional blood-to-tissue transport, expressed as a unidirectional transfer rate constant (K), was measured in experimental RT-9 brain tumors using 14C-alpha-aminoisobutyric acid (AIB) and quantitative autoradiographic techniques. The magnitude of K depends on the permeability, surface area, and blood flow of the tissue capillaries. The transfer rate constant was variable within tumor tissue (range 0.001 to 0.178 ml/gm/min) and depended on tumor size, location (intraparenchymal, meningeal, or choroid plexus associated), and to a lesser extent on necrosis and cyst formation. Brain adjacent to tumor had higher K values, particularly around larger tumors (0.004 to 0.014 ml/gm/min), than corresponding brain regions in the contralateral hemisphere (0.001 to 0.002 ml/gm/min). Estimates of the fractional extraction of AIB by intraparenchymal tumors were between 0.008 and 0.4 ml/gm/min. Values of fractional extraction in this range indicate that tumor capillaries are not freely permeable to this solute. The values of K measured with AIB in this study, for the most part, approximate the permeability-surface area product of tumor and brain capillaries. The experimental data suggest that the permeability-surface area characteristics of the microvasculature in small RT-9 tumors are similar to those of the host tissue, whereas the microvasculature of larger RT-9 tumors is influenced more by intrinsic tumor factors.

Aminoisobutyric Acids↗
PubMed1984

Murine sarcoma virus-induced brain tumors. Concurrent measurements of blood flow and transcapillary transport.

Intracerebral inoculation of Murine Sarcoma Virus (MSV) into rats induces highly vascular brain tumors. Blood flow, F, and a unidirectional blood-to-tissue transfer constant, K, were measured concurrently in 16 separate brain tumors in 13 rats. Regional measurements of F and K were obtained using double-label quantitative autoradiography with 131I-iodoantipyrine, 14C-alpha aminoisobutyric acid, and computerized microdensitometry with image analysis. Regional tissue extraction fractions (E) were calculated for different brain and tumor regions. The following observations were made: intracerebral inoculation of MSV in rats of different ages produced a single histologic tumor type (angiosarcoma), although tumor yield decreased and latency increased when older rats were inoculated; whole tumor blood flow values averaged 63.9 +/- 20.9 (SD) ml hg-1 min-1, less than F of tumor-free gray matter; the mean value of the transfer constant was 1.19 +/- 0.84 ml hg-1 min-1, 5 times the value in contralateral tumor-free brain; moderate regional variation of F and K values were observed within each tumor, with increased K values extending into the regions of brain around tumor; mean extraction fractions (E) of AIB for whole tumor were low (range = 0.0021 to 0.08), with a distinct and decreasing gradient from tumor center to BAT; there was poor correlation between F, K and E values, and tumor histology, including regions that microscopically appeared highly vascular; in most regions of the MSV-induced brain tumors, capillary permeability and/or surface area seem to be determinant in blood-to-tissue transport processes.

Aminoisobutyric Acids↗
PubMed1987

The effect of 125I interstitial radiotherapy on blood-brain barrier function in normal canine brain.

Blood-brain barrier (BBB) function was studied in 14 normal dogs at time periods from 7 to 717 days after permanent insertion of 5- to 7-mCi seeds of iodine-125 (125I) for interstitial radiation. The BBB function was measured with carbon-14-labeled alpha aminoisobutyric acid (AIB) and quantitative autoradiography, and expressed as a unidirectional blood-to-brain transfer constant, K. The 125I radiation lesions consisted of three concentric histologically and functionally distinct zones: 1) a central zone of calcified necrosis; 2) a spongy fluid-filled zone; and 3) a narrow rim (2.6 +/- 0.6 mm wide) of viable brain tissue with increased permeability. Within this rim, the mean value of the K of AIB was 5.8 times that of normal cortex. Over the 7- to 392-day time period the value of K remained rather constant, and by 716 days K values had returned to normal. There was moderate regional variation in the value of K; it was highest in the white matter and lowest in the gray matter surrounding the radiation lesion. The radiation lesion progressively increased in size from 7 to 80 days, after which there was little change. This study illustrates that the geographically circumscribed radiation from 125I seeds is accompanied by similarly well-defined changes in BBB function, which may persist for over 1 year following insertion of the 125I seed. This altered BBB function is probably responsible for the cerebral edema associated with 125I interstitial radiotherapy.

Aminoisobutyric Acids↗
PubMed1996

A quantitative spatial analysis of the blood-spinal cord barrier. II. Permeability after intraspinal fetal transplantation.

In previous experiments we utilized quantitative autoradiography to temporally describe vascular permeability of a radiolabeled vascular tracer following spinal contusion injury in the rat. In the present report we compare these findings with permeability assessments following fetal grafting in the contused rat spinal cord. At 10 days postinjury, Embryonic Day 14 spinal tissue was grafted into the lesioned spinal cord of Sprague-Dawley rats. At 7, 14, and 28 days postgrafting the alpha-aminoisobutyric acid (AIB) technique was used to assess blood-to-tissue transfer rates in graft and host tissue over several segments of the injured spinal cord. Regional changes in permeability were assessed using four distinct image analysis techniques. Using these methods, we have previously shown that contusion injury alone results in a chronic relapse in vascular permeability. The present data indicate that fetal transplants at 7 days postgrafting have AIB transfer rates that are significantly above uninjured control levels and are similar in magnitude to neighboring host spinal tissue. In addition, permeability in 14- and 28-day intraspinal grafts decreased relative to that of the 7-day transplant group, but remained significantly elevated at and rostral to the injury epicenter. Alternately, graft and host tissue in regions caudal to the injury epicenter (e.g., T10--L2) acquired a functional barrier to AIB as early as 14 days posttransplantation. These experiments suggest that graft development occurs in a different manner or at a different rate in segments of the injured spinal cord rostral and caudal to the injury site. Additionally, it appears that vascular permeability of the injured spinal cord can be influenced by the process of intraspinal transplantation.

Aminoisobutyric Acids↗
PubMed2002

Effects of 17beta-estradiol on blood-brain barrier disruption during focal ischemia in rats.

This study was performed to test whether 17beta-estradiol could attenuate the blood-brain barrier disruption caused by middle cerebral artery occlusion in the ovariectomized rats. Rats aged twelve to fourteen weeks were used in this study. Their ovaries were removed one week prior to the implantation of the pellets. For the 17beta-estradiol group, a 500 microg 17beta-estradiol 21 day-release pellet was implanted and for the control group, a vehicle pellet was implanted 21 days before the experiments. One hour after middle cerebral artery occlusion under isoflurane anesthesia, the transfer coefficient of 14C-alpha-aminoisobutyric acid (104 Daltons) and the volume of 3H-dextran (70,000 Daltons) distribution were determined to represent the degree of blood-brain barrier disruption. Blood pressures and blood gases were similar between controls and 17beta-estradiol-treated rats. In both groups, the transfer coefficient of the ischemic cortex was higher than that of the corresponding contralateral cortex (control: Ischemic Cortex 12.5 +/- 5.9 microl/g/min, Contralateral Cortex 3.0 +/- 1.6, p < 0.001; 17beta-estradiol: Ischemic Cortex 6.7 +/- 3.3 micro l/g/min, Contralateral Cortex 2.2 +/- 0.9, p < 0.01). There was no significant difference in the transfer coefficient of the contralateral cortex between these two groups. However, the transfer coefficient of the Ischemic Cortex of the 17beta-estradiol-treated animals was 46 % lower than that of the control, vehicle-treated rats (p < 0.05). The increase of the volume of 3H-dextran distribution with middle cerebral artery occlusion was significant in the vehicle-treated rats (Ischemic Cortex: 6.4 +/- 2.7 ml/100 g, Contralateral Cortex: 3.8 +/- 0.8, p < 0.01) but not in the 17beta-estradiol-treated animals. Our data suggest that chronic 17beta-estradiol treatment was effective in reducing blood-brain barrier disruption during focal ischemia in the ovariectomized rats.

Aminoisobutyric Acids↗