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PubMed1996

Tonic protein kinase C-mediated vasoconstriction is unmasked when nitric oxide synthase is inhibited in cerebral microvessels.

Recent evidence indicates that nitric oxide participates in the modulation of vascular tone in a variety of vascular beds, including the parenchymal microvasculature of the brain. The present study examined the role of protein kinase activity in the induction and maintenance of the contractile response when endogenous nitric oxide production is inhibited in parenchymal microvessels of the rat hippocampus. Microvessels in in vitro slices of the hippocampus were monitored using computer-assisted video microscopy. The effects of inhibitors of two kinases, protein kinase C and calcium/calmodulin-dependent protein kinase, on the vasoconstrictor response to NG-nitro-L-arginine (L-NNA) were investigated. The resting luminal diameter of the microvessels examined in this study ranged from 9 to 29 microns. Addition of 100 microM L-NNA to the medium superfusing the slice constricted microvessels by 38.8 +/- 0.6%. The addition of protein kinase inhibitors reversed this constriction in a dose-dependent manner. H-7 (50 microM), a relatively non-selective protein kinase C inhibitor, elicited an 81.4 +/- 10.0% reversal of the L-NNA-induced constriction. Bisindolylmaleimide (5 microM), a selective protein kinase C inhibitor, reversed the constriction by 69.1 +/- 13.7%. KN-62, an inhibitor of calcium/calmodulin-dependent protein kinase II, elicited a smaller yet statistically significant reversal of 17.1 +/- 5.1%. Pretreatment with H-7 or bisindolyl-maleimide blocked the LNNA-induced constriction entirely, while KN-62 did not significantly inhibit the response. These findings indicate that the contractile response observed upon removal of endogenous nitric oxidergic vasodilation is mediated by protein kinase activity, and the contribution of protein kinase C to this effect is greater than that of calcium/calmodulin-dependent protein kinase II. The results suggest that a tonic nitric oxidergic influence serves to mask the potential for protein kinase C-mediated vasoconstriction in cerebral microvessels.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1994

Similarities of the in vivo and in vitro effects of mercuric chloride on [3H]ouabain binding and potassium activation of Na+/K(+)-ATPase in isolated rat cerebral microvessels.

A previous study revealed that a single i.p. administration of 6 mg/kg body wt. of mercuric chloride (MC) durably inhibits the rat cerebral microvascular Na+/K(+)-ATPase activity [1]. In this study, cerebral microvessels isolated 18 h after MC treatment were compared to those obtained from control rats and subsequently treated or not treated with MC in vitro, with regard to: (a) [3H]ouabain binding to, and (b) K(+)-activation kinetics of, the Na+/K(+)-ATPase. Microvessels from MC-treated rats showed a decrease of [3H]ouabain binding down to 62% of the control binding, and the same degree of inhibition was attained in microvessels treated in vitro with 5 microM MC. Analysis of the K(+)-activation kinetics of Na+/K(+)-ATPase revealed a decrease of Vmax from the control value of 13.1 to 7.67 mumol/mg/h in microvessels from MC-treated rats and 6.07 mumol/mg/h in microvessels treated in vitro with 5 microM MC, with no change in Km in either case. The similarity of the effects of in vivo and in vitro treatments suggests that the inhibition of the cerebromicrovascular Na+/K(+)-ATPase following in vivo administration of MC results from a direct interaction of Hg2+ with the enzyme.

Animals↗

PubMed1993

Anoxia/reoxygenation induces hydroxyl free radical formation in brain microvessels.

Isolated rat brain microvessels have been utilized to examine whether they produce hydroxyl free radicals if they are subjected to a 10- to 20-min anoxia period followed by a 40-min reoxygenation period. Hydroxyl free radical flux was assessed utilizing salicylate as a trap. The 2,3- and 2,5-dihydroxybenzoic acids (DHBA) products as well as salicylate in the microvessels were quantitated utilizing high-pressure liquid chromatography (HPLC) with electrochemical and fluorescence detection. The results show that a period of anoxia followed by reoxygenation resulted in an enhanced formation of DHBA compared to the normoxic control microvessels. Addition of superoxide dismutase (SOD) and catalase to the microvessels undergoing anoxia decreased the amount of hydroxyl free radicals trapped, suggesting that superoxide and hydrogen peroxide were produced and excreted from the endothelial cell surfaces and then unless quenched reentered the cells to form hydroxyl free radicals within. The amount of 2,5-DHBA formed closely correlated with the amount of 2,3-DHBA formed, indicating that either product can be used to assess hydroxyl free radical flux in brain microvessels.

Animals↗

PubMed2006

Comparative evaluation of microvessel density determined by CD34 or CD105 in benign and malignant gastric lesions.

Microvessel density (MVD) is regarded as a surrogate marker for angiogenesis and has been used for tumor prognosis. In this study, MVD was identified immunohistochemically by monoclonal antibodies against CD105 and CD34 in the tissues representing gastric carcinoma, chronic gastritis, and hyperplastic polyps, and the results were correlated with clinicopathologic features. The expression of CD105 in the microvessels within benign lesions was barely visible, and MVD was markedly lower than that determined by CD34. CD34 was strongly expressed in the microvessels within hyperplastic polyps and tissues with gastritis. In gastric carcinoma, CD105 expression in microvessels was as high as the MVD, compared with benign lesions. CD105 stained well-formed mature and newly formed immature vessels within the cancer mass. Correlation analysis showed that MVD determined by CD105 correlated with blood vessel invasion, distant metastasis, and formation of ascites. Survival analysis demonstrated an inverse correlation between MVD count and overall survival: patients with MVD counts of 32 or higher survived for a much shorter time than those with counts lower than 32. Multivariate analysis confirmed that MVD determined by CD105 was an independent prognostic factor for survival. Microvessel density determined by CD34 inversely correlated with overall survival, but it did not correlate with other clinicopathologic parameters except formation of ascites. In conclusion, CD34 was universally expressed in blood vessels within benign and malignant tissues, whereas CD105 expression was minimal in benign tissues but stronger in gastric carcinoma. These data suggest that both CD105 and CD34 could be used for quantification of angiogenesis, but preference should be given to CD105 in the evaluation of prognosis in gastric carcinoma.

Adult↗

PubMed2007

Carotid plaque instability and ischemic symptoms are linked to immaturity of microvessels within plaques.

BACKGROUND: Instability and rupture of carotid atherosclerotic plaques leads to thromboemboli and ischemic symptoms. Angiogenesis occurs within atherosclerotic plaques, and plaque vulnerability and symptomatic carotid disease have been associated with increased numbers of microvessels. In addition to microvessel number, it is possible that the phenotypes of intraplaque vessels could influence plaque stability. To test this, the morphology and maturity of vessels within plaques from symptomatic and asymptomatic patients was determined. METHODS: Carotid plaques were collected after endarterectomy from a cohort of 13 asymptomatic patients and 30 symptomatic patients. Plaques were sectioned and immunostained for the presence of endothelial cells, vascular smooth muscle cells, macrophages, and vascular endothelial growth factor. Sections were assessed for microvessel morphology, maturity as judged by smooth muscle cell cover, and the presence of vascular endothelial growth factor and macrophages. RESULTS: Two types of vascular structure were observed within plaques, microvessels and dilated, highly irregular multilobular vessels. These irregular dysmorphic vessels were found almost exclusively in plaques from symptomatic patients. The dysmorphic vessels lacked smooth muscle cells and were highly immature. Plaques also contained vascular endothelial growth factor, and this was observed adjacent to the dysmorphic vessels. This growth factor was found colocalized with macrophages. CONCLUSIONS: Symptomatic carotid plaques contain abnormal, immature microvessels similar to those found in tumors and healing wounds. Such vessels could contribute to plaque instability by acting as sites of vascular leakage by inflammatory cell recruitment. The immature vessels within plaques may be therapeutic targets for promoting plaque stabilization.

Aged↗

PubMed2004

Acute VEGF effect on solute permeability of mammalian microvessels in vivo.

To investigate the effect of vascular endothelial growth factor (VEGF) on solute permeability of mammalian microvessels, we measured the apparent permeability (P) of various-sized solutes on the postcapillary venules of rat mesentery in vivo. Exposure to 1 nM VEGF transiently increased P from a mean of 1.4 (+/-0.11 SE, n = 17) to a peak of 2.8 (+/-0.28 SE) x 10(-5) cm/s, a 2.4-fold increase for small solute sodium fluorescein (Stokes radius 0.45 nm), from a mean of 0.44 (+/-0.05 SE, n = 16) to a peak of 1.5 (+/-0.19 SE) x 10(-)5 cm/s, a 3.6-fold increase for intermediate-sized solute alpha-lactalbumin (Stokes radius 2.01 nm), from a mean of 0.049 (+/-0.0032 SE, n = 16) to a peak of 0.36 (+/-0.032 SE) x 10(-5) cm/s, a 7.9-fold increase for large solute bovine serum albumin (Stokes radius 3.55 nm), within 30 s. In approximately 2 min, all increased P returned to the baseline values. The response pattern of P to VEGF and the ratios of the peak to control values for rat mesenteric microvessels are similar to those of frog mesenteric microvessels [Am. J. Physiol.: Heart Circ. Physiol. 284 (2003) H2124]. Instead of considerable heterogeneity in the frog mesenteric microvessels, the acute response to 1 nM VEGF is homogeneous in the rat mesenteric microvessels.

Animals↗

PubMed2006

Effect of hypoxia/reoxygenation on CD73 (ecto-5'-nucleotidase) in mouse microvessel endothelial cell lines.

Cerebral ischemia and post-ischemic reperfusion commonly result in significant brain damage. Brain microvessel endothelial cells, the key target cells and regulating sites, can secrete adenosine which plays an important neuroprotective role in the ischemic brain. A primary determinant of localized production of adenosine at tissue interfaces is ecto-5'-nucleotidase (CD73). In our experiments, we used bEnd.3 cells, immortalized mouse brain microvessel endothelial cell lines, as the target cells to study the effect of hypoxia and posthypoxic reoxygenation on CD73 in brain microvessel endothelial cells. CD73 activity in bEnd.3 cells exposed to hypoxia significantly increased in time-dependent way. The upregulation of CD73 mRNA and protein expression induced by hypoxia in bEnd.3 cells were detected by RT-PCR and Western blot. However, for reoxygenation studies, CD73 activity, mRNA and protein expression decreased at the initial stages, but increased at prolonged reoxygenation. Our results suggest that hypoxia can induce upregulation of CD73 expression in brain microvessel endothelial cells, which can be reversed by reoxygenation of short duration. But CD73 expression increased gradually with the duration of reoxygenation. Then, we infer that CD73 in brain microvessel endothelial cells plays a very important role through forming adenosine during brain ischemia and reperfusion.

5'-Nucleotidase↗

PubMed1999

Microvessels from Alzheimer's disease brains kill neurons in vitro.

Understanding the pathogenesis of Alzheimer's disease is of widespread interest because it is an increasingly prevalent disorder that is progressive, fatal, and currently untreatable. The dementia of Alzheimer's disease is caused by neuronal cell death. We demonstrate for the first time that blood vessels isolated from the brains of Alzheimer's disease patients can directly kill neurons in vitro. Either direct co-culture of Alzheimer's disease microvessels with neurons or incubation of cultured neurons with conditioned medium from microvessels results in neuronal cell death. In contrast, vessels from elderly nondemented donors are significantly (P<0.001) less lethal and brain vessels from younger donors are not neurotoxic. Neuronal killing by either direct co-culture with Alzheimer's disease microvessels or conditioned medium is dose- and time-dependent. Neuronal death can occur by either apoptotic or necrotic mechanisms. The microvessel factor is neurospecific, killing primary cortical neurons, cerebellar granule neurons, and differentiated PC-12 cells, but not non-neuronal cell types or undifferentiated PC-12 cells. Appearance of the neurotoxic factor is decreased by blocking microvessel protein synthesis with cycloheximide. The neurotoxic factor is soluble and likely a protein, because its activity is heat labile and trypsin sensitive. These findings implicate a novel mechanism of vascular-mediated neuronal cell death in Alzheimer's disease.

Alzheimer Disease↗

PubMed2000

alpha(1)-Adrenergic receptor subtypes in rat cerebral microvessels.

To identify alpha(1)-adrenergic receptor subtypes involved in the regulation of cerebral microcirculation, we studied alpha(1)-adrenergic receptor subtypes expressed in the rat cerebral microvessels. The microvessels were prepared from rat cerebral cortex by albumin flotation and glass bead filtration techniques. [(125)I]HEAT binding to the cerebral microvessels was displaced by low concentrations of 5-methylurapidil, a selective antagonist for alpha(1A)-receptors, and modified Scatchard analysis of the data revealed that half of alpha(1)-receptors is alpha(1A)-subtype, and that alpha(1B)- and/or alpha(1D)-receptors are also present. The K(i) value of the high-affinity component for 5-methylurapidil was 3.90+/-1.08 nM, which is comparable with the value obtained in the rat cerebral cortex (2.17+/-0.88 nM). Reverse transcription and polymerase chain reaction experiments showed that mRNAs of alpha(1A)- and alpha(1B)-receptors, but not alpha(1D)-receptors, were expressed in the cerebral microvessels. These results suggest that alpha(1)-receptors involved in the regulation of cerebral microvessel function are alpha(1A)- and alpha(1B)-receptor subtypes.

Adrenergic alpha-Antagonists↗

PubMed2001

Increased microvessel density in adenomyosis uteri.

OBJECTIVE: To investigate microvessel density in adenomyosis compared to the endometrium in patients with adenomyosis and in normal controls. DESIGN: Uterine paraffin-embedded histologic specimens were immunostained for CD34. The area with the highest microvessel density in adenomyosis and in the endometrium was evaluated. All microvessels in a specific field of view (x200 magnification) were counted. SETTING: The Department of Gynecological Endocrinology and the Institute of Clinical Pathology, Department of Gynecopathology, in an university hospital. PATIENT(S): Specimens of 53 patients with adenomyosis, who had undergone hysterectomy. Endometrial specimens of 17 women without uterine pathology were investigated as normal controls. MAIN OUTCOME MEASURE(S): Microvessel density in adenomyosis and in the endometrium. RESULT(S): The mean microvessel density was significantly higher in adenomyosis than in the endometrium of the same patients (33.5 +/- 14.6 vs. 19.5 +/- 12.5 microvessels/field; P<.001 sign test). No significant difference between the endometrium of patients and of normal controls was observed (P=.805). CONCLUSION(S): Adenomyosis exhibits angiogenic properties. However, the endometrium of patients with adenomyosis is not more prone to express angiogenic activity compared to the endometrium of normal controls.

Adult↗

PubMed1999

Increased peripheral nerve microvessels in early experimental diabetic neuropathy: quantitative studies of nerve and dorsal root ganglia.

Microangiopathy is an important complication of diabetes mellitus and neovascularity is a feature of human diabetic retinopathy. The objective of this work was to evaluate numbers, areas and size distributions of whole nerve, endoneurial and dorsal root ganglia perfused microvessels in a detailed fashion using unfixed tissues from rats with experimental diabetes. Experimental neuropathy was studied in male Sprague-Dawley rats 12 weeks after streptozotocin or citrate buffer injection. Electrophysiological recordings of sciatic-tibial motor and caudal sensory fibers identified conduction slowing in diabetes indicating neuropathy. Diabetics had a rise in the numbers of whole nerve microvessels and endoneurial microvessels with associated rises in vessel densities and total vessel luminal areas. Increased vessel numbers in 15-30 microm diameter size ranges were particularly prominent. There was a rise in summed vascular areas in diabetics but the mean luminal area of vessels was not increased. Similar, but not significant trends were observed in a selective analysis of endoneurial vessels alone. In contrast, dorsal root ganglia microvessels were not increased in number. Early experimental diabetic neuropathy is associated with increased numbers of microvessels supplying the peripheral nerve trunk, likely representing neovascularity.

Animals↗

PubMed2001

Regional differences in peptide degradation by rat cerebral microvessels: a potential novel regulatory mechanism for communication between blood and brain.

The blood-brain barrier (BBB), composed of the microvessels of cerebral capillary endothelial cells, regulates the passage of peptides into the brain in several ways, mainly by saturable transport or passive diffusion. Here we describe an additional mechanism by which this regulatory function can occur. Cerebral microvessels were isolated from different regions of the brain and incubated with the mu-opiate selective endomorphin-1 (Tyr-Pro-Trp-Phe-NH2) or the opiate-modulating Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2), both tetrapeptides selectively tritiated at the Pro. Degradation was determined by HPLC. For both peptides, the metabolism by microvessels from the cerebral cortex was much greater than that by microvessels from the hypothalamus or pons. For endomorphin-1, the least degradation was in the pons; for Tyr-MIF-1 there was no difference in metabolism by microvessels from the pons or hypothalamus. The results show a novel mechanism at the BBB by which the BBB can selectively regulate the activity of different peptides in different regions of the brain.

Animals↗

PubMed1999

Increased permeability of primary cultured brain microvessel endothelial cell monolayers following TNF-alpha exposure.

TNF-alpha is a cytokine that produces increased permeability in the peripheral vasculature; however, little is known about the effects of TNF-alpha on the blood-brain barrier (BBB). Using primary cultured bovine brain microvessel endothelial cells (BBMEC) as an in vitro model of the BBB, this study shows that TNF-alpha produces a reversible increase in the permeability of the brain microvessel endothelial cells. The BBMEC monolayers were pre-treated with 100 ng/ml of TNF-alpha for periods ranging from 2 to 12 hours. Permeability was assessed using three molecular weight markers, fluorescein (376 MW), fluorescein-dextran (FDX-4400; 4400 MW), and FDX-70000 (MW 70000). The permeability of BBMEC monolayers to all three fluorescent markers was increased two-fold or greater in the TNF-alpha treatment group compared to control monolayers receiving no TNF-alpha. Significant changes in permeability were also observed with TNF-alpha concentrations as low as 1 ng/ml. These results suggest that TNF-alpha acts directly on the brain microvessel endothelial cells in a dynamic manner to produce a reversible increase in permeability. Exposure of either the lumenal or ablumenal side of BBMEC monolayers to TNF-alpha resulted in similar increases in permeability to small macromolecules, e.g. fluorescein. However, when a higher molecular weight marker was used (e.g. FDX-3000), there was a greater response following lumenal exposure to TNF-alpha. Together, these studies demonstrate a reversible and time dependent increase in brain microvessel endothelial cell permeability following exposure to TNF-alpha. Such results appear to be due to TNF's direct interaction with the brain microvessel endothelial cell.

Animals↗

PubMed1996

Neurons and microvessels of the nodose (vagal sensory) ganglion in young adult and aged rats: morphometric and enzyme histochemical studies.

The neuron cell bodies and microvessels in sections of the nodose (vagal sensory) ganglion (NG) of Wistar rats of 4- and 24-months of age have been examined morphometrically and by quantitative enzyme histochemistry. The range of neuronal somata areas was similar at the two ages and distributed unimodally, ranging approximately from 200-1500 microns 2 with the largest somata occurring in the older age group. The range of microvessel diameters was also comparable but the largest microvessels were seen in the older animals. The histological arrangement of the ganglion permitted analyses to be made of 'neuronal' and 'axonal' areas independently. The number of microvessels per unit area was less in regions of the ganglion occupied by axons at both ages. Random transects indicated that the percentage area occupied by neuron somata decreases and that of axons increases with age. Overall, however, the results suggest that the histological organization, the size of vagal sensory neurons, the ganglionic microvessels, and the relationship between them, does not change greatly in Wistar rats of up to 2 years of age. Ultrastructural features of the aged sensory neurons included the presence of secondary lysosomes, disrupted rough endoplasmic reticulum, swollen Golgi cisternae, and the presence of much filamentous material in the perikaryon similar to that seen in chromatolytic neurons. However, analysis of electron micrographs did not reveal significant changes in the numbers of mitochondria or Golgi bodies. There was an overall increased thickness in the microvascular wall in the older animals with the endothelium and pericyte covering being significantly increased, but the thickness of the basal lamina was unchanged. The activities of neuronal NADH tetrazolium reductase, succinate dehydrogenase and cytochrome oxidase were all increased with age. The results suggest that vagal sensory neurons are not greatly affected by age in the rat.

Aging↗

PubMed1994

Microvessel count and cerebrospinal fluid basic fibroblast growth factor in children with brain tumours.

Tumour growth is angiogenesis-dependent; brain tumours have more intense neovascularisation than other tumours and produce basic fibroblast growth factor, a potent angiogenic mediator. Because little is known about the release of basic fibroblast growth factor from brain tumours into extracellular fluids, we tested cerebrospinal fluid (CSF) from 26 children and young adults with brain tumours and 18 controls for basic fibroblast growth factor and for proliferative activity on cultured capillary endothelial cells. We also measured the density of microvessels in tumours by immunohistochemical staining. Basic fibroblast growth factor was detected in the CSF of 62% (16 of 26) patients with brain tumours but in none of the controls. Specimens with basic fibroblast growth factor stimulated DNA synthesis of capillary endothelial cells in vitro. Endothelial proliferative activity was blocked by neutralising antibodies to basic fibroblast growth factor. Basic fibroblast growth factor correlated with mitogenic activity in CSF in vitro (p < or = 0.0001), and with density of microvessels in histological sections (p < or = 0.005). A microvessel count of > or = 68 per 200 x field was associated with tumour recurrence (p = 0.005) and with mortality (p = 0.02). Basic fibroblast growth factor in brain tumours may mediate angiogenesis as measured by microvessel density in histological sections, so has potential as both a marker for neoplasia and a target for tumour treatments. Furthermore, evaluation of cerebrospinal fluid basic fibroblast growth factor, along with microvessel quantitation in biopsied tumours, may provide improved prognostic information for the management of patients with brain tumours.

Adolescent↗

PubMed2000

Interferon beta-1a prevents the effects of lipopolysaccharide on embryonic brain microvessels.

By means of light and electron microscopy we have studied the effect of interferon beta-1a (IFNbeta-1a) in the optic tecta of 20-day-old chick embryos under normal conditions and after exposure to lipopolysaccharide (LPS) which mimics the blood-brain barrier (BBB) disruption in meningoencephalitis. Optic tecta were examined for: (i) ultrastructure by means of transmission electron microscopy; (ii) the immunohistochemical localization of HT7 antigen, a specific marker of differentiation of the brain microvessels; (iii) the brain microvessel permeability, by means of horseradish peroxidase (HRP) tracer; (iv) the expression of microvessel glycoconjugates, by means of lectin histochemistry, using Ricinus communis agglutinin-I (RCA-I), specific for beta-D-galactosyl moieties and Wheat Germ agglutinin (WGA) specific for sialyl and N-acetylglucosaminyl moieties. A morphometric evaluation of brain microvessel permeability and of glycoconjugate expression was also performed. In control- and in IFNbeta-1a-treated embryos, HRP was confined to the vessel lumina which were sealed by the interendothelial tight junctions. RCA-I binding sites were recognizable both in the basal membranes and in the tight junctions, while WGA sites were present on the luminal side of the endothelial cells. HRP was blocked in the vessels lumina by the interendothelial tight junctions. After LPS treatment, HRP showed an extravascular localization and the labeling of microvessels by anti-HT7 antibodies disappeared. RCA-I binding was only found ultrastructurally and appeared as irregularly clustered gold particles, in the cleft of damaged tight junctions, but were no longer detectable in the endothelial basement membranes. After pretreatment of LPS-treated embryos with IFNbeta-1a, the vessel permeability to HRP strongly decreased and the vessels showed the normal pattern of HT7 protein and of the RCA-I binding sites. These results indicate that the changes induced by LPS in the endothelial cells are prevented by IFNbeta-1a.

Animals↗

PubMed2000

Prognostic significance of platelet and microvessel counts in operable non-small cell lung cancer.

BACKGROUND: Microvessel density, an indirect measure of angiogenesis, has been shown to be an independent prognostic marker in many solid tumours including non-small cell lung cancer (NSCLC). Platelets transport and release angiogenic growth factors. Platelets are increasingly likely to adhere to tumour microvessels due to raised expression of platelet-binding proteins and stasis in blood-flow. Increased vascular permeability in tumour microvessels facilitates platelet extravasation into the extracellular matrix. Adherence and extravasation both lead to platelet activation and release of growth factors capable of instigating the angiogenic process. METHODS: A total of 181 patients were identified who underwent resection of stage I-IIIa NSCLC with a post-operative survival >60 days. Patients were followed-up for a minimum of 24 months. Sections from the tumour periphery were stained for the endothelial marker CD34 (Novocastra NCL-END) using standard ABC immunohistochemistry. Chalkley counting was used to assess microvessel density. RESULTS: A pre-operative platelet count greater than the median and above the normal range (>400) was associated with a poor outcome (P=0.01 and P=0.04, respectively). Tumours with an above median and high Chalkley count (upper tertile) had a worse prognosis (P=0.007 and P=0.0006, respectively). There was no association between platelet count and Chalkley count. CONCLUSIONS: Platelet and microvessel counts are both potential prognostic markers for NSCLC. The role of platelets in the angiogenic process needs to be further investigated.

Adult↗

PubMed2003

Noninvasive augmentation of microvessel number in patients with peripheral vascular disease.

OBJECTIVE: Therapeutic angiogenesis has great potential for the treatment of ischemic diseases. One possible route for noninvasive induction of microvessels has recently been suggested by the finding that subcontractile electrical stimulation induces increased vascularization in animals. The present study tests the ability of such stimulation to augment microvessel number in patients with peripheral vascular disease. DESIGN OF STUDY: Overall, 36 patients were randomly assigned to control (n = 12) and treatment (n = 24) groups. Patients in the treatment group received localized subcontractile electrical stimulation on the feet of their ischemic limbs for three 60-minute periods each day over a 6-week period. Microvessel density was determined by capillary microscopy before treatment, at 3 and 6 weeks during treatment, and 4 weeks after completion. Transcutaneous oxygen tension was also determined at this site. RESULTS: Microvessel density determined by capillary microscopy was significantly increased (1.25-fold, P <.005) during and after treatment in patients receiving electrical stimulation. Transcutaneous oxygen tension was similarly increased in the treated patients (1.24-fold, P <.05). No changes were observed in these parameters in untreated patients examined in parallel. CONCLUSION: Localized subcontractile electrical stimulation can increase microvessel density and tissue perfusion in patients with peripheral vascular disease.

Aged↗