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PubMed1993

Activity of dihydrothienopyridine S312 enantiomers on L-type Ca2+ channels in isolated rat aorta and cerebral microvessels.

The activity of the two enantiomers of the dihydrothienopyridine S312 was characterized in isolated rat aorta and cerebral microvessels. The interaction of S312 with 1,4-dihydropyridine and phenylalkylamine binding sites was also investigated in depolarized rat cerebral microvessels and in membranes from rat ileum. Both S-(+)-S312 and R-(-)-S312 dose dependently inhibited KCl-evoked contraction of the rat aorta, with IC50 values of 0.14 (0.13-0.16) and 2.98 (2.67-3.33) nM, respectively. When the aorta was preincubated with S-(+)-S312 in a depolarizing medium, the inhibitory effect was significantly increased, but this increased inhibition was not reversed by incubation in physiological medium. The effect of R-(-)-S312 was not affected by preincubation in a depolarizing medium. In rat cerebral microvessels, S-(+)-S312 inhibited the KCl-induced contraction and KCl-stimulated Ca2+ influx with similar potency. [3H](+)-PN 200-110 specific binding was competitively displaced by the two enantiomers in depolarized cerebral microvessels. The calculated Ki values were 0.12 nM for S-(+)-S312 and 2.4 nM for R-(-)-S312. Only 20% of [3H]D888 specific binding in rat ileum membranes was displaced by S-(+)-S312. The dissociation rate of [3H]D888 was markedly decreased by S-(+)-S312, and this allosteric interaction was significantly more marked than with nitrendipine. It is concluded that the dihydrothienopyridine S312 could interact with Ca2+ channels in a manner different to that of genuine dihydropyridines.

Animals↗

PubMed1982

Fatty acid oxidation of rat brain microvessels in hypertension, aging and experimental diabetes.

Microvessels were prepared from rat brain and their fatty acid oxidation was investigated. This activity was much higher in brain microvessels than in other vessels or organs, suggesting that brain microvessels have a high capacity for energy production. The activity was decreased in some pathological conditions, such as hypertension, aging and diabetes mellitus. The relationship between changes in fatty acid oxidation activities and injuries of brain microvessels is discussed.

Aging↗

PubMed1994

Flow dynamics of erythrocytes in microvessels of isolated rabbit mesentery: cell-free layer and flow resistance.

A part of microvascular bed isolated from rabbit mesentery (composed of a few branches of superior mesenteric artery) was used for the study of the flow dynamics of erythrocytes in microvessels. The flow resistance in the microvascular bed was analyzed with respect to the thickness of a cell-free layer formed along the inner wall of vessels and the suspension viscosity of erythrocytes (in terms of hematocrit and erythrocyte deformability). The thickness of the cell-free layer increased with the increase in the inner diameter of microvessels. By lowering the hematocrit, the thickness increased and the flow resistance decreased. Meanwhile, by decreasing the erythrocyte deformability with diamide, the thickness decreased and the flow resistance increased. However, the thickness was not altered in microvessels less than 10 microns by the diamide treatment. The maximum inner diameter of microvessel required to induce parachute- and/or slipper-like deformation (at flow velocity of erythrocytes less than 2 mm s-1) was 13 microns for control cells and 6 microns for diamide-treated cells. The thickness of the cell-free layer could not be closely related to the flow resistance, while a good relationship applicable to both control and diamide-treated cells was obtained between the flow resistance and the suspension viscosity. The present results conclude that the flow resistance in the isolated microvascular bed is mainly provided by both hematocrit and erythrocyte deformability.

Animals↗

PubMed1983

Pseudo-on-line fast response microvessel dimensions video graphic recorder with electrical signal output.

The present article describes a new method of microvessel dimensions measurement in which a writing oscilloscope is used to continuously and graphically record the microvessel video signal from television microscopy at a fast rate of 50 records per second. Dimensions of interest, such as the microvessel red blood cell flux diameter, are then easily marked out manually from the graphic records and a dynamic electrical signal proportional to the dimensions is generated. The signal is then recorded on one channel of a multichannel voltage recorder and is synchronised with other experimental signals which have previously been recorded on-line during the experiment. The result is that the dimension signal appears to have been recorded on-line during the experiment as well. This is desirable for electronic signal correlation and processing. This method is useful when poor experimental conditions, commonly encountered, make automatic recording of microvessel dimension unsatisfactory and manual inspection and processing become necessary.

Animals↗

PubMed1988

Lead activates protein kinase C in immature rat brain microvessels.

We investigated the effects of inorganic lead upon calcium-, phospholipid-dependent protein kinase (protein kinase C) in brain microvessels isolated from 6-day-old rat pups. We found that (a) in broken cell preparations, lead at micromolar concentrations activates this enzyme to an extent equivalent to that of micromolar calcium (10.3 +/- 1.3 and 9.2 +/- 1.6 pmol/mg/min, respectively) and (b) preincubation of intact microvessels with lead results in a translocation of protein kinase C from the soluble to the particulate fraction. The cytosolic kinase activity stimulated by lead has the same requirements for diacylglycerol and phospholipid as the calcium-stimulated enzyme, suggesting that lead activates the kinase by mimicking calcium. The hypothesis that lead affects protein kinase C activity through a mechanism similar to that of calcium is supported by the similar time courses of substrate phosphorylation and dephosphorylation mediated by lead and calcium. When intact microvessels are preincubated with micromolar concentrations of lead, the translocation of protein kinase C occurs in a dose- and time-dependent manner. The relocalization is virtually complete at 0.1 microM lead and by 30 min of exposure. We propose that the sensitivity of protein kinase C to lead, described here in immature brain microvessels, makes this regulatory enzyme a potential mediator of lead toxicity.

Animals↗

PubMed1992

Developmental changes in enzymatic systems involved in protection against peroxidation in isolated rat brain microvessels.

Activities of 3 enzymes involved in the major detoxification pathway for peroxides were assessed in rat brain microvessels. Between the 7th and 60th day after birth, glutathione peroxidase specific activity remained constant in microvessels, while glutathione reductase specific activity increased from day 14 to day 60. On the other hand, the specific activity of these two enzymes evolved similarly in total brain homogenate: they increased between day 7 and day 30, and then reached a plateau. In contrast, catalase specific activity in microvessels was markedly decreased from day 7 to day 60. A significant decrease in this enzyme specific activity was also observed in brain homogenate during development. However, in microvessels, catalase specific activity remained higher than that of brain homogenate throughout the time period studied. Our results support the idea that enzymatic mechanisms against peroxidative damage are required in early age, and could be potent at the level of the blood-brain barrier.

Aging↗

PubMed1995

Mechanism of valproic acid uptake by isolated rat brain microvessels.

In an effort to characterize putative transport systems of valproic acid (VPA) at the blood-brain barrier, the effects of various substrates and inhibitors of known anion transporters on the equilibrium vessel-to-medium concentration (vessel/medium) ratio of VPA were investigated using isolated rat brain microvessels. The equilibrium vessel/medium ratio of VPA was decreased by the presence of high millimolar concentration of unlabeled VPA, indicating that a saturable transport system was involved in VPA transport from medium to microvessels. Short-chain monocarboxylates such as propionic acid, pyruvic acid, and L-lactic acid did not alter the vessel/medium ratio, whereas medium-chain fatty acids and unsaturated metabolites of VPA significantly inhibited the net transport of VPA. Dicarboxylates, tricarboxylate, and p-aminohippuric acid did not affect VPA accumulation in the brain microvessels. Several anionic drugs including salicylic acid, penicillin G, cefazolin, and probenecid significantly reduced the vessel/medium ratio of VPA. In addition, disulfonate inhibitors of inorganic anion exchangers, SH-group modifying reagent, and metabolic inhibitor showed remarkable inhibitory effects on the net transport of VPA between brain microvessels and medium. These results suggest that VPA may be actively transported through the antiluminal membrane via a carrier-mediated system shared by other anionic drugs.

Animals↗

PubMed1994

Changes in brain microvessel endothelial cell monolayer permeability induced by adrenergic drugs.

Brain microvessel endothelial cell monolayers have been shown to be a suitable blood-brain barrier in vitro system to study adrenergic regulation of permeability. We tested adrenergic drugs on bovine brain microvessel endothelial cell monolayer permeability to a biomembrane impermeant molecule, sodium fluorescein. Endogenous catecholamines noradrenaline and adrenaline were tested as well as the alpha-adrenoceptor agonist phenylephrine, the beta-adrenoceptor agonist clenbuterol and the alpha-adrenoceptor antagonist prazosin. Results showed an alpha-adrenoceptor mediated increase and a beta-adrenoceptor mediated decrease in monolayer permeability. Both alpha- and beta-adrenoceptor mediated changes in permeability were abolished by inhibiting fluid-phase pinocytosis, either by vincristine or by avoiding bovine brain microvessel endothelial cell's energy utilization. The reverse transport (i.e., from brain to blood side) was also influenced by adrenergic drugs; alpha- or beta-adrenoceptor stimulation induced a permeability-reducing effect. We conclude that alpha-adrenoceptor stimulation increases bovine brain microvessel endothelial cell monolayer permeability and that beta-adrenoceptor stimulation has the opposite effect. Reverse transport results obtained with beta-adrenoceptor stimulation seem controversial and deserve further study. These results also support in vivo findings that demonstrated adrenergic influences on blood brain barrier permeability.

Adrenergic Agents↗

PubMed2004

VEGF and bFGF expression and microvessel density of maxillary sinus squamous cell carcinoma in relation to p53 status, spontaneous apoptosis and prognosis.

We have previously reported that p53 mutations, loss of bax expression or decreased spontaneous tumor apoptosis were associated with poorer prognoses in maxillary sinus squamous cell carcinoma (SCC)(Cancer 94: 1968-1980, 2002). In the present study, we analyzed tumor angiogenesis monitored by expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and tumor microvessel density, in correlation with p53 status, spontaneous apoptosis or disease prognosis in the same group of 70 maxillary sinus SCC patients. Tumor biopsy specimens obtained prior to initiation of treatment were examined for expression of VEGF and bFGF and tumor microvessel density using immunohistological methods. Average vessel density (AVD) (range: 3-75; median: 25) and maximum vessel density (MVD) (range: 4-125; median: 53) were assessed by the number of microvessels stained with anti-CD31 mAb in tumor lesions. VEGF was expressed in 35 (50%) of 70 patients and bFGF was in 43 (61%). Patients with VEGF expression showed significantly higher levels of MVD than those without VEGF expression (57 vs. 38; P=0.019). The VEGF expression was observed more frequently in patients with p53 overexpression and/or mutation than in those with normal p53 status (P=0.048). The MVD inversely correlated with the apoptotic index (AI) defined as the number of single stranded (ss)-DNA-positive cells per 1000 tumor cells (r= -0.23; P=0.022). Patients with neck lymph node and/or distant metastases after surgery showed significantly higher levels of MVD than patients without any metastasis (64 vs. 42; P=0.048). Low histological effectiveness of radiochemotherapy correlated with bFGF expression (P=0.0059). To clarify actual prognostic factors for maxillary sinus SCC, we selected 57 patients treated uniformly with preoperative radiochemotherapy followed by maxillectomy. Kaplan-Meier analysis showed that survival was significantly worse in patients with high MVD (> or =80) than in those with low MVD (<80) (P=0.042). These data suggest that the VEGF expression in association with the p53 overexpression and/or mutations may cause increased microvascularity, decreased spontaneous apoptosis or metastases, while the bFGF expression may be associated with resistance to radiochemotherapy, thereby resulting in poorer prognoses in maxillary sinus SCC. VEGF and bFGF expression and tumor microvessel density in tumor lesions were analyzed in 70 patients with maxillary sinus squamous cell carcinoma. The VEGF expression dependent of p53 overexpression and/or mutations was associated with angiogenesis, decreased spontaneous tumor apoptosis and metastases, while the bFGF expression was associated with resistance to radiochemotherapy, resulting in poor prognosis.

Adult↗

PubMed2006

Prognostic significance of microvessel density and vascular endothelial growth factor expression in sinonasal carcinomas.

The prognostic significance of microvessel density and proliferative activity of the neoplastic cells, evaluated respectively by CD31 and Ki-67 positivity, and immunohistochemical expression of vascular endothelial growth factor (VEGF) was retrospectively investigated in 105 cases of sinonasal carcinoma (80 surgical specimens and 25 biopsies). The most represented histologic types were intestinal-type adenocarcinoma found in 36 patients (34.3%), squamous cell carcinoma (SCC) in 34 (32.4%), mucinous adenocarcinoma (mainly made up of signet-ring cell patterns) in 15 (14.3%), and adenoid cystic carcinoma in 7 (6.7%). Microvessel density values (in vessels per square millimeter), VEGF, and Ki-67 were not dependent on histologic type but were rather correlated to the histologic grading in SCC. Clinical data were available for 92 (87.6%) of 105 patients, with minimum follow-up of 48 months. Most of the patients (81.5%) were at an advanced stage (T3-T4) at diagnosis. The values of all markers were correlated to tumor stage (P = .03). Multivariate analysis showed that both microvessel density and proliferative activity of the neoplastic cells were independent prognostic parameters (mortality hazard ratio, 1.33 and 1.60, respectively). Although VEGF expression was not correlated to prognosis on the whole series (P = .06), it was a powerful prognostic marker when the analysis was restricted to the group of SCCs (hazard ratio, 3.02; 90% confidence interval, 1.58-5.80). These results show that tumor neoangiogenesis, expressed by microvessel density, together with proliferative activity, is a pathologic marker with a strong prognostic impact in sinonasal carcinomas. Therefore, it may be a useful tool in this field so as to carry out therapeutic protocol planning, which may be further enhanced by the adoption of the more recent antiangiogenic molecules.

Adenocarcinoma↗

PubMed2005

Evaluation of tumor angiogenesis measured with microvessel density (MVD) as a prognostic indicator in nasopharyngeal carcinoma: results of RTOG 9505.

PURPOSE: The objective of this study was to evaluate tumor angiogenesis as measured by microvessel density (MVD) as an independent prognostic factor in patients with nasopharyngeal carcinoma (NPC) treated with radiotherapy alone. METHODS AND MATERIALS: Eligible patients included those with NPC treated with radiotherapy. Paraffin blocks of the primary tumor had a hematoxylin and eosin-stained section prepared at the block face. One representative section for tumor was stained for factor VIII-related antigen using a standard immunoperoxidase staining technique. MVD was determined by light microscopy in areas of invasive tumor containing the highest numbers of capillaries and microvessels per area. Individual microvessel counts were made on a 200x field within the area of most intense tumor neovascularization. Results were expressed as the highest number of microvessels identified within any single 200x field. Using a breakpoint of MVD <60 vs. > or =60, the distributions between the two MVD groups were compared by the method of Gray. Overall survival rates were estimated by the Kaplan-Meier method and compared by the log-rank test. A multivariate Cox proportional hazard model was employed to examine the relationship between MVD and disease outcomes while adjusting for other concomitant variables. RESULTS: One hundred sixty-six were eligible, of whom 123 had values determined for MVD. The MVD values ranged from 9 to 243 with a median of 70. In the multivariate analysis of overall survival, distant metastases, and local-regional failure, MVD did not significantly improve the model containing T stage, N stage, age, radiation dose, and World Health Organization class. CONCLUSIONS: We found no significant differences in overall survival, time to distant metastasis, or time to local-regional failure using a breakpoint of MVD <60 vs. MVD > or =60. The study was perhaps limited by the small size of the NPC samples.

Adolescent↗

PubMed2006

Adventitial microvessel formation after coronary stenting and the effects of SU11218, a tyrosine kinase inhibitor.

OBJECTIVES: The aim of this study was to delineate the temporal profile of adventitial microvessel (Ad-MV) formation after stenting, its relationship to arterial wall hypoxia, and the effects of a tyrosine kinase inhibitor (TKI), SU11218, on Ad-MV and in-stent intimal hyperplasia (IH). BACKGROUND: Adventitial microvessels have been reported after arterial injury; however, the underlying stimulus for this response and its relationship to IH is unknown. METHODS: Coronary stenting was performed in 40 pigs randomized to SU11218 (n = 20) or placebo (n = 20). Vessel wall hypoxia was assessed by pimonidazole adducts and hypoxia-inducible factor (HIF)-1 alpha expression. Adventitial microvessels were quantified by three-dimensional microscopic computed tomography (3D micro CT). Intimal hyperplasia was measured by intravascular ultrasound (IVUS), 3D micro CT, and morphometry. The effects of SU11218 were assessed in vitro on smooth muscle cell (SMC) and endothelial cell (EC) functions and in vivo on Ad-MV and IH. RESULTS: Hypoxia was evident in the vessel wall at 48 h and persisted for four weeks. Adventitial microvessels increased significantly at one week (24 +/- 7 microvessels/segment) and four weeks (23 +/- 7 microvessels/segment) compared with uninjured arteries (16 +/- 2 microvessels/segment; p < 0.001) and correlated with IH (r = 0.77, p < 0.001). The TKI SU11218 inhibited platelet-derived growth factor receptor-beta phosphorylation, EC and SMC DNA synthesis, and migration in a dose-dependent manner in vitro and significantly inhibited Ad-MV (16 +/- 5 vs. 23 +/- 7 microvessels/segment in placebo, p < 0.001) and produced approximately 80% reduction in IH (0.52 +/- 0.51 mm2 vs. 2.47 +/- 1.66 mm2 in placebo, p < 0.001) at four weeks in vivo. CONCLUSIONS: Arterial stenting causes arterial wall hypoxia followed by Ad-MV formation. The TKI SU11218 inhibits both Ad-MV formation and IH and represents a promising therapeutic agent to prevent in-stent restenosis.

Animals↗

PubMed2006

Calponin and caldesmon cellular domains in reacting microvessels following traumatic brain injury.

Calponin (Cp) and caldesmon (Cd) are actin-binding proteins involved in the regulation of smooth muscle (SM) tone during blood vessel contraction. While in vitro studies have reported modifications of these proteins during vessel contractility, their role in vivo remains unclear. Traumatic brain injury (TBI) causes disruption of cerebral microvascular tone, leading to sustained contractility in reacting microvessels and cerebral hypoperfusion. This study aimed to determine the spatial and temporal expressions of Cp and Cd in rat cerebral cortical and hippocampal microvessels post-TBI. Reacting microvessels were analyzed in control, 4, 24, and 48 h post-injury. Single and double immunocytochemical techniques together with semiquantitative analyses revealed a Cp upregulation in SM at all time frames post-TBI; with the protein migrating from SM cytosol to the vicinity of the cell membrane. Similarly, Cd immunoreactivity significantly increased in both SM and endothelial cells (En). However, while Cp and Cd in SM remained elevated, their levels in En returned to normal at 48 h post-TBI. The results suggest that Cp and Cd levels increase while compartmentalizing to specific subcellular domains. These changes are temporally associated with modifications in the cytoskeleton and contractile apparatus of SM and En during blood vessel contractility. Furthermore, these changes may underlie the state of sustained contractility and hypoperfusion observed in reacting microvessels after TBI.

Animals↗

PubMed1997

Angiotensin-converting enzyme inhibitors promote nitric oxide production in coronary microvessels from failing explanted human hearts.

We have previously shown that nitric oxide (NO) release by the coronary circulation in the failing and nonfailing human heart is, in part, regulated by local kinin production in coronary microvessels. Angiotensin-converting enzyme (ACE) also known as kininase II, inactivates kinins. ACE inhibitors prevent kinin breakdown by ACE, thereby increasing the concentration of bradykinin (BK) and related kinins. The goal of this study was to determine if kinins contribute to the therapeutic action of ACE inhibitors. Six hearts from end-stage heart failure patients were harvested at the time of orthotopic cardiac transplantation. Microvessels were prepared as previously described, and nitrite production, a metabolic product of NO in vitro, was determined by the Griess reaction. Microvessels were incubated in the presence of kininogen and bradykinin, and with the ACE inhibitors ramiprilat, enalaprilat, or captopril. All caused dose-dependent increases in nitrite. For instance, ramiprilat increased nitrite from 76 +/- 5.6 to 155 +/- 15 pmol/min per mg wet weight. Nitrite production in response to ACE inhibition was blocked by N-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, and icatibant (HOE 140), a B2-kinin receptor-specific antagonist. Furthermore, NO production was prevented by 3 different serine protease inhibitors, which block kallikrein, the enzyme responsible for conversion of kininogen to kinins. Our results indicate that ACE/kininase inhibitors increase NO production by the coronary microvasculature in the failing human heart, through increased available active kinins. The therapeutic action of ACE inhibition in the failing human heart may result in part from increased NO production by coronary microvessels.

Adolescent↗

PubMed1985

Membrane-bound lipoxygenase of rat cerebral microvessels.

The microvessels isolated from rat cerebral cortex has arachidonate lipoxygenase activity, which was not due to possible contamination of the platelets. The major product was identified to be 12-hydroxyeicosatetraenoic acid. After homogenization and sonication of the microvessel preparations, the lipoxygenase activity was recovered both in the membrane- and the cytosol-fractions, whereas that in the platelets was recovered in the cytosol fraction. Membrane-bound lipoxygenase of the microvessels has apparent Km value of 3.8 microM for arachidonic acid, which was corresponded to 1/5 of that in the platelet enzyme. Microvessel lipoxygenase was inhibited by nordihydroguaiaretic acid but not by indomethacin.

Animals↗

PubMed1997

Regulation of cerebral microvessels by glutamatergic mechanisms.

This study examined the role of glutamate receptor activation in the regulation of microvascular tone in the hippocampus and neocortex of the rat. Microvascular and neuronal responses were simultaneously recorded in brain slices using videomicroscopic analysis in conjunction with electrophysiological recording. Glutamate and other glutamate receptor agonists, including NMDA, kainic acid, and ACPD elicited dose-dependent dilation in preconstricted hippocampal microvessels. The lower concentrations of NMDA elicited dilation with an increase in neuronal excitability while dilatory responses to other agonists were associated with substantial depolarization. NMDA-mediated dilation was inhibited completely with a sodium channel blocker (TTX), an NOS inhibitor (L-NNA), or a specific inhibitor of neuronal NOS (7-NI). Inhibition of the GABA(A) or the A2 adenosine receptor did not attenuate the NMDA-induced dilation. The role of spontaneous glutamate receptor activation by endogenous glutamate in the regulation of resting dilatory tone was also examined. Blocking AMPA or metabotropic glutamate receptors did not induce significant responses in resting hippocampal vessels. However, the NMDA receptor antagonist, APV, elicited a dose-dependent constriction. In surface vessels of the neocortex, NMDA elicited a comparable dose-dependent dilation, and APV elicited a significantly smaller dose-dependent constriction. A 60 min period of hypoxia elicited a significant dilation of preconstricted hippocampal microvessels. APV did not significantly influence this dilatory response indicating that hypoxia-induced dilation is not mediated by NMDA receptor activation. Taken together, these results indicate that glutamate contributes to the dilatory tone of cerebral microvessels under physiologic conditions and that this effect is mediated by NMDA receptors. Glutamatergic vasodilation is dependent on neuronal discharge activity and the neuronal production of NO. The tonic influence is more pronounced in hippocampal microvessels than in neocortical vessels suggesting that the contribution of NMDA receptor activation to resting dilatory tone is dependent on the location of vessels within the brain.

2-Amino-5-phosphonovalerate↗

PubMed1999

Receptor tyrosine kinase tie 1 mRNA is upregulated on cerebral microvessels after embolic middle cerebral artery occlusion in rat.

Tie 1 is an endothelial specific transmembrane receptor tyrosine kinase and may be required during angiogenesis. Using in situ hybridization, we measured tie 1 mRNA in ischemic brain (n=15). Rats were subjected to middle cerebral artery (MCA) occlusion by a single fibrin rich clot. Expression of tie 1 was not detected in non ischemic brain. Cerebral microvessels expressed tie 1 in the ischemic lesion as early as 2 h after MCA occlusion. The number of microvessels containing tie 1 mRNA decreased in the ischemic lesion at 8 h after MCA occlusion. However, expression of tie 1 increased on microvessels at 24 h and 14 days after ischemia and tie 1 was primarily localized to the microvessels bordering pan necrotic tissue. Ninety-seven percent of cerebral vessels which expressed tie 1 mRNA had diameters of 3.7+/-0.17 microm. Our findings suggest a role for tie 1 in cerebral microvascular remodeling after embolic stroke.

Animals↗

PubMed1995

GLUT-1 glucose transporter is localized heterogeneously within the microvessels of the mouse hippocampus.

We investigated the distribution of the glucose transporter protein within the microvessels in the mouse hippocampus by immunohistochemical methods with an anti-rat brain glucose transporter 1 (GLUT-1) and confocal laser scanning microscopy. All intraparenchymal microvessels in the hippocampus showed intensive immunoreactivity and a heterogeneous distribution of GLUT-1 was seen in the microvessels. These data may suggest that glucose could be heterogeneously incorporated into the endothelial cells of the cerebral microvessels, and therefore morphological and physiological differences may be present among the endothelial cells.

Animals↗