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PubMedDate not supplied

Flow behavior of erythrocytes in microvessels and glass capillaries: effects of erythrocyte deformation and erythrocyte aggregation.

Flow behavior of erythrocytes in microvessels and glass capillaries with an inner diameter of 10-50 microns was compared in relation to erythrocyte deformation and erythrocyte aggregation. This study was focused on the formation of a marginal cell-free layer, and the thickness was determined using an image processor. Human erythrocytes were perfused through a part of microvascular networks isolated from rabbit mesentery and through glass capillaries. Erythrocyte deformability was modified by treating erythrocytes with diamide, diazene-dicarboxylic acid bis[N,N-dimethylamide], and erythrocyte aggregation was accelerated by adding dextran (with a molecular weight of 70,400) to the perfusion medium. The thickness of the cell-free layer increased with an increase of the inner diameter of flow channel, with lowering the hematocrit, and with increasing the flow velocity of erythrocytes, in both microvessels and glass capillaries. Furthermore, the thickness of cell-free layer decreased with decreasing erythrocyte deformability, while it increased with accelerating erythrocyte aggregation. However, the alteration of the cell-free layer in response to the changes of these hemorheological conditions was more sensitive in microvessels than in glass capillaries. The present study concludes that flow behavior of erythrocytes in microvessels is qualitatively similar to, but quantitatively different from those in glass capillaries, as far as evaluated by the change of the thickness of the marginal cell-free layer.

Animals↗

PubMed2003

Electron spin resonance detection of hydrogen peroxide as an endothelium-derived hyperpolarizing factor in porcine coronary microvessels.

OBJECTIVE: Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in modulating vascular tone, especially in microvessels, although its nature has yet to be elucidated. This study was designed to examine whether hydrogen peroxide (H2O2) is an EDHF in porcine coronary microvessels with use of an electron spin resonance (ESR) method to directly detect H2O2 production from the endothelium. METHODS AND RESULTS: Isometric tension and membrane-potential recordings demonstrated that bradykinin and substance P caused EDHF-mediated relaxations and hyperpolarizations of porcine coronary microvessels in the presence of indomethacin and Nomega-nitro-L-arginine. The contribution of H2O2 to the EDHF-mediated responses was demonstrated by the inhibitory effect of catalase and by the relaxing and hyperpolarizing effects of exogenous H2O2. Endothelial production of H2O2 was quantified in bradykinin- or substance P-stimulated intact blood vessels by ESR spectroscopy. Tiron, a superoxide scavenger that facilitates H2O2 formation, enhanced bradykinin-induced production of H2O2, as well as the EDHF-mediated relaxations and hyperpolarizations. By contrast, cytochrome P-450 inhibitors (sulfaphenazole or 17-octadecynoic acid) or a gap junction inhibitor (18alpha-glycyrrhetinic acid) failed to inhibit the EDHF-mediated relaxations. Involvement of endothelium-derived K+ was not evident in experiments with ouabain plus Ba2+ or exogenous K+. CONCLUSIONS: These results provide ESR evidence that H2O2 is an EDHF in porcine coronary microvessels.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗

PubMedDate not supplied

Long-term cholesterol feeding alters the reactivity of primate coronary microvessels to platelet products.

Hypercholesterolemia impairs endothelium-dependent relaxations to several platelet-derived substances in large vessels. The effect of hypercholesterolemia on the response of coronary microvessels to platelet products and thrombin is less well defined. Three groups of cynomolgus monkeys were studied: normal (n = 6), short-term hypercholesterolemic (8-11 weeks, n = 5), and long-term hypercholesterolemic (18-80 months, n = 6). Responses of coronary microvessels, 100-200 microns in diameter, to thrombin (0.1-10 units/ml) and the platelet products ADP (1 nM-100 microM), serotonin (1 nM-100 microM), and the thromboxane A2 analogue U46619 were studied using an in vitro microvessel imaging apparatus. Vessels were studied after preconstriction with thromboxane A2 analogue U46619 to evaluate both relaxations and constrictions to each agent. Concentrations of U46619 to attain preconstriction were much lower for the long-term group (16 +/- 19 nM) as compared with the control and short-term hypercholesterolemic groups (689 +/- 48 and 664 +/- 63 nM, respectively, p less than 0.01). Relaxations of long-term hypercholesterolemic vessels to ADP tended to be less than those of either control or short-term hypercholesterolemic vessels. Thrombin, when added to normal or short-term hypercholesterolemic vessels, caused identical relaxations but paradoxically caused constrictions in microvessels of long-term hypercholesterolemic monkeys (55 +/- 17% of KCl contraction, p less than 0.001 vs. other groups). Peak constrictions to serotonin were markedly enhanced in the long-term hypercholesterolemic group (59 +/- 7% of maximal KCl responses) compared with control and short-term hypercholesterolemic responses (28 +/- 8% and 32 +/- 5%, respectively, both p less than 0.05 vs. long-term hypercholesterolemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗

PubMed1998

Endothelium-dependent relaxation of collateral microvessels after intramuscular gene transfer of vascular endothelial growth factor in a rat model of hindlimb ischemia.

BACKGROUND: Recent investigations have demonstrated the ability of vascular endothelial growth factor (VEGF) to augment the development of collateral arteries in vivo. In vitro studies have suggested that the use of VEGF also improves the endothelium-dependent relaxation of collaterals at the microvascular level. The purpose of this study was to determine in vivo the extent to which vasomotor responses of collateral microvessels are altered after VEGF treatment. METHODS AND RESULTS: Ischemia was induced in the hindlimb of 35 rats by excision of the femoral artery. Immediately thereafter, 400 microg of a plasmid encoding VEGF or ss-galactosidase (control) was transfected into limb muscles. Four weeks later, synchrotron radiation microangiography, with a spatial resolution of 30 microm, was performed to document the reactivity of collateral microvessels. Administration of the endothelium-dependent vasodilator acetylcholine failed to induce dilation of collateral microvessels in control animals. By contrast, profound dilation of collaterals was observed after acetylcholine in VEGF-treated animals. This response was evident in vessels with a linear appearance but not in those with an undulating appearance. The resulting blood flow in the ischemic limb after administration of acetylcholine in the control animals was only 64.6+/-17.0% of that of the contralateral normal limb, whereas blood flow was augmented to 106.1+/-8.4% in VEGF-treated animals (P<0.05). CONCLUSIONS: These results demonstrate in vivo that the use of VEGF restores impaired vasomotor responses in some types of collateral microvessels, which may help to provide a basis for understanding the microcirculation after therapeutic angiogenesis with VEGF.

Acetylcholine↗

PubMed1999

Influence of female sex hormones on endothelium-derived vasoconstrictor prostanoid generation in microvessels of spontaneously hypertensive rats.

Although female sex hormones may attenuate endothelial dysfunction in spontaneously hypertensive rats (SHR) by increasing endothelium-derived relaxing factors (EDRFs), the influence of ovarian hormones on the generation of endothelium-derived contracting factors (EDCFs) remains unknown. The aim of this study was to evaluate the effect of estrogen and progesterone on the generation of vasoconstrictor prostanoids and superoxide anion (O2(-)) by microvessels from SHR. Vascular reactivity to norepinephrine (NE), acetylcholine (ACh), and sodium nitroprusside (SNP) were evaluated in the mesenteric arteriolar bed from estrous (OE) and ovariectomized (OVX) SHR. OVX-SHR were treated for 24 hours or 15 days with estradiol and for 15 days with estradiol+progesterone. The vascular reactivity was evaluated in the absence or presence of indomethacin (INDO, 10 micromol/L) and sodium diclofenac (DIC, 10 micromol/L), ridogrel (RID, 50 micromol/L), dazoxiben (DAZ, 10 micromol/L), or superoxide dismutase (SOD, 100 U/mL). Prostanoid levels in the arteriolar perfusate of mesenteries with or without endothelium were measured by enzyme immunoassay. An increased reactivity to NE and reduced sensitivity to ACh were observed in microvessels from OVX-SHR compared with OE-SHR. There were no differences in the responses to SNP. Treatments with estradiol and estradiol+progesterone similarly restored these altered responses. INDO, DIC, RID, and SOD also restored the NE and ACh responses in OVX-SHR. DAZ had no effect on the vascular reactivities. The release of PGF(2alpha), but not of TXB(2) and 6-keto-PGF(1alpha), was greater in OVX-SHR than in OE-SHR microvessels with endothelium when stimulated by NE. This response was normalized by hormonal treatments. Neither NE nor ACh stimulated prostanoid production by microvessels without endothelium. These results suggest that estrogen may protect female SHR against severe hypertension partly by decreasing the synthesis of EDCFs such as PGH(2)/PGF(2alpha) and O2(-).

Animals↗

PubMed2003

Enhanced smooth muscle cell coverage of microvessels exposed to increased hemodynamic stresses in vivo.

During vascular remodeling in adult organisms, new capillary growth is often coupled with the adaptation of arterioles and venules, a process that requires the recruitment and differentiation of precursor cells into smooth muscle. We studied the in vivo adaptation of microvessels in the presence of elevated pressure and circumferential wall stress using a ligation strategy for mesenteric microvascular networks. Acute pressure increases of 42.6+/-18% and 17.1+/-2.3% were respectively elicited in the 25- to 30-microm-diameter venules and arterioles supplying the networks. Wall shear rates were not significantly changed; however, diameters were increased in >10-microm-diameter venules and >20-microm-diameter arterioles. Smooth muscle cell contractile phenotype was determined in all microvessels by observing the expression of smooth muscle myosin heavy chain (SM-MHC; a marker of fully differentiated smooth muscle) and smooth muscle alpha-actin (a marker for all smooth muscle, including immature smooth muscle of fibroblast/pericyte lineage). The ratio of SM-MHC positive vessel length to smooth muscle alpha-actin-positive vessel length increased >2-fold after 5 and 10 days of the ligation treatment. Smooth muscle proliferation was studied by bromodeoxyuridine incorporation, and the increase in SM-MHC-labeled microvessel length density was accompanied by no measurable change in proliferation of SM-MHC-labeled cells 5 and 10 days after ligation. These results indicate that after a period of 5 or 10 days, mesenteric microvessels <40 microm in diameter exposed to elevated pressure and wall strain exhibit an enhanced coverage of mature, fully differentiated smooth muscle cells.

Actins↗

PubMed1986

Phasic blood flow velocity pattern in epimyocardial microvessels in the beating canine left ventricle.

We quantitated phasic epimyocardial microcirculatory coronary blood flow velocity patterns in the beating left ventricle. Using a newly developed floating objective and high-speed cinematography, red cell velocities in small arterioles, capillaries, and small venules and microvascular diameters in the superficial layer of the epimyocardium of beating left ventricle were determined throughout the entire cardiac cycle in open-chest anesthetized dogs. Heart rate was maintained at 140 beats/min by means of left atrial pacing. Peak red cell velocity was observed in midsystole in small arterioles and capillaries, and in late systole in small venules. Abrupt decline in red cell velocity and, in many cases, a momentary cessation or reverse of flow, was observed in these microvessels during the pre-ejection period. The internal diameter of small venule was increased in late systole, while that of small arteriole remained almost constant during the cardiac cycle. Furthermore, in these epimyocardial microvessels, a higher percentage of the total area under the velocity curve occurred during the ejection phase; 51% in small arterioles, 43% in capillaries, and 40% in small venules. These findings indicate that the phasic blood flow pattern is markedly different in the subepimyocardial microvessels from that in the large epicardial artery and the septal artery. During vasodilation following dilazep (50 micrograms/kg, i.v.), an adenosine potentiator, red cell velocity increased throughout the entire cardiac cycle in epimyocardial microvessels with significant increases in the total area under the velocity curves accompanied by significant dilation of the arterioles. The present data will provide information useful in predicting or simulating transmural differences in the phasic blood flow pattern.

Animals↗

PubMed1990

Diameter change and pressure-red blood cell velocity relations in coronary microvessels during long diastoles in the canine left ventricle.

The objective of this study was to determine whether coronary vascular resistance remains constant during long diastoles and whether critical closure of arterial microvessels occurs at zero-flow pressure. For this purpose, we directly measured internal diameters and red blood cell velocities in arterial and venous coronary microvessels during long diastoles under maximal vasodilation. The epicardial coronary microcirculation was viewed in anesthetized, open-chest mongrel dogs through an intravital microscope equipped with a newly developed floating objective. Coronary microvascular diameters and red blood cell velocities were measured with high-speed cinematography. During maximal vasodilation (150 micrograms/kg body wt i.v. dilazep), long diastoles were induced by vagal nerve stimulation. Internal diameters of all small arteries and arterioles (n = 12) gradually declined with decreasing aortic pressure during long diastoles, and the reduction of the diameter was greatest when aortic pressure was less than 35 mm Hg. The mean internal diameter (88.8 +/- 52.2 microns) at minimal aortic pressure (19.2 +/- 6.4 mm Hg) was significantly less than that at an aortic pressure of 100 mm Hg (116.2 +/- 68.5 microns, p less than 0.01). The internal diameters of small veins and venules remained nearly constant during long diastoles. When red blood cell progression in coronary microvessels stopped at the nadir of aortic pressure, all arterial coronary microvessels remained open; that is, there was no evidence of "critical closure."(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Resistance to blood flow in microvessels in vivo.

Resistance to blood flow through peripheral vascular beds strongly influences cardiovascular function and transport to tissue. For a given vascular architecture, flow resistance is determined by the rheological behavior of blood flowing through microvessels. A new approach for calculating the contribution of blood rheology to microvascular flow resistance is presented. Morphology (diameter and length), flow velocity, hematocrit, and topological position were determined for all vessel segments (up to 913) of terminal microcirculatory networks in the rat mesentery by intravital microscopy. Flow velocity and hematocrit were also predicted from mathematical flow simulations, in which the assumed dependence of flow resistance on diameter, hematocrit, and shear rate was optimized to minimize the deviation between measured and predicted values. For microvessels with diameters below approximately 40 microns, the resulting flow resistances are markedly higher and show a stronger dependence on hematocrit than previously estimated from measurements of blood flow in narrow glass tubes. For example, flow resistance in 10-microns microvessels at normal hematocrit is found to exceed that of a corresponding glass tube by a factor of approximately 4. In separate experiments, flow resistance of microvascular networks was estimated from direct measurements of total pressure drop and volume flow, at systemic hematocrits intentionally varied from 0.08 to 0.68. The results agree closely with predictions based on the above-optimized resistance but not with predictions based on glass-tube data. The unexpectedly high flow resistance in small microvessels may be related to interactions between blood components and the inner vessel surface that do not occur in smooth-walled tubes.

Animals↗

PubMedDate not supplied

Ischemic brain edema following occlusion of the middle cerebral artery in the rat. II: Alteration of the eicosanoid synthesis profile of brain microvessels.

Using the rat middle cerebral artery occlusion model, alterations in the eicosanoid synthetic capacity of brain microvessels following ischemia were studied by radiochromatography. Brain microvessels of normal rats predominantly produced hydroxyacids with relatively small amounts of PGD2 and PGE2 from exogenous arachidonic acid. Confirmation that hydroxyacids and prostaglandins were products respectively of lipoxygenase(s) and cyclooxygenase was obtained by experiments using indomethacin and eicosatetraynoic acid. The eicosanoid synthetic capacity of the brain microvessel, especially of hydroxyacids, was significantly enhanced 24 and 72 hours after the onset of ischemia. Because this is the phase of maximum edema in the present model, enhanced eicosanoid production in the brain microvessel may be involved in the mechanisms that underly ischemic brain edema.

Animals↗

PubMed2004

Aging is associated with increased collagen type IV accumulation in the basal lamina of human cerebral microvessels.

BACKGROUND: Microvascular alterations contribute to the development of stroke and vascular dementia. The goal of this study was to evaluate age and hypertension related changes of the basal lamina in cerebral microvessels of individuals, who died from non-cerebral causes. RESULTS: We examined 27 human brains: 11 young and 16 old patients. Old patients were divided into two subgroups, those with hypertension (n = 8) and those without hypertension (n = 8). Basal lamina changes of the cerebral microvessels were determined in the putamen using antibodies against collagen type IV and by quantitative analysis of vessel number, total stained area of collagen, thickness of the vessel wall and lumen, and relative staining intensity using immunofluorescence. The total number of collagen positive vessels per microscopic field was reduced in old compared to young subjects (12.0+/-0.6 vs. 15.1+/-1.2, p = 0.02). The relative collagen content per vessel (1.01+/-0.06 vs. 0.76+/-0.05, p = 0.01) and the relative collagen intensity (233.1+/-4.5 vs. 167.8+/-10.6, p < 0.0001) shown by immunofluorescence were higher in the older compared to the younger patients with a consecutive reduction of the lumen / wall ratio (1.29+/-0.05 vs. 3.29+/-0.15, p < 0.0001). No differences were observed for these parameters between old hypertensive and non-hypertensive patients. CONCLUSIONS: The present data show age-related changes of the cerebral microvessels in sections of human putamen for the first time. Due to the accumulation of collagen, microvessels thicken and show a reduction in their lumen. Besides this, the number of vessels decreases. These findings might represent a precondition for the development of vascular cognitive impairment. However, hypertension was not proven to modulate these changes.

Adult↗

PubMed1989

The effects of platelet-derived growth factor in cultured microvessel endothelial cells.

The effects of platelet-derived growth factor (PDGF) on thymidine incorporation into DNA and glucose and neutral amino acid uptake were studied in endothelial cells cultured from macrovessels (bovine aorta and pulmonary artery) and microvessels (bovine fat and mouse brain). Similar to previous studies, PDGF did not bind to macrovessel cells, nor did it influence their metabolic function. In contrast, PDGF bound specifically to the two types of microvessel cell culture and in these cells also stimulated the uptake of glucose and neutral amino acids as well as the incorporation of thymidine into DNA. Stimulatory effects of PDGF occurred at concentrations of 2 ng/ml, with maximal stimulation up to 5-fold of the control value for amino isobutyric acid and glucose uptake and up to 8- to 10-fold for thymidine incorporation. The maximal effects of PDGF were additive to those of insulin-like growth factor, I, a known stimulator of all three metabolic processes in microvessel endothelial cells. The binding of PDGF to the endothelial cells was, in general, equivalent to PDGF binding to human foreskin fibroblasts, both in the magnitude of tracer binding and in the affinity of binding. Similar effects were found with recombinant and platelet-derived PDGF. We conclude that these two cultured microvessel endothelial cells not only produce PDGF-like material, but are capable of binding and responding to PDGF.

Adipose Tissue↗

PubMed1982

Characterization of beta-adrenergic receptors on human cerebral microvessels.

Cerebral microvessels were separated and prepared from human brain cortex by albumin floatation and glass bead filtration. The binding of a specific beta-adrenergic antagonist, (125I) iodohydroxybenzylpindolol, to the microvessel preparation was characterized by high affinity, saturability, and stereospecificity. The presence of specific beta-adrenergic receptor sites in human cerebral microvessels supports the hypothesis of adrenergic regulation of the function of cerebral microvessels.

Brain↗

PubMed2006

Prognostic significance of intratumoral microvessel density in canine soft-tissue sarcomas.

The prognosis of canine soft-tissue sarcomas (STS) has traditionally been based on histologic grading. We have recently demonstrated the prognostic value of cellular proliferation markers in canine STS. Another method of predicting the behavior of neoplasms is intratumoral microvessel density (IMD), which is a measure of tumor angiogenesis. The prognostic significance of IMD has been documented in many human neoplasms and in a limited number of canine and feline neoplasms. To evaluate the prognostic value of IMD in canine STS, we studied 57 STS and compared IMD with histologic features, histologic grade, cellular proliferation, metastatic propensity, and survival. Using immunohistochemistry, the STS were labeled with anti-factor VIII-related antigen (FVIII-RA) and anti-CD31 antibodies to determine 3 IMD parameters: mean microvessel density, high microvessel density, and microvessel area. Using FVIII-RA and CD31, increasing IMD was statistically associated with increasing histologic grade, necrosis scores, and mitotic scores. Higher FVIII-RA IMD values were significantly associated with higher median argyrophilic nucleolar organizing region (AgNOR) values (as previously investigated) and increased metastatic propensity. Fibrosarcomas appear to be the least vascularized of STS. There is no correlation between IMD and survival. Our results indicate that IMD is of prognostic value for histologic grade, histologic features, cellular proliferation (based on AgNOR), and metastatic propensity of canine STS, specifically when using FVIII-RA as the endothelial marker. Assessing histologic grading, cellular proliferation, and IMD of canine STS at the time of diagnosis could therefore provide better prognostic information for the veterinary clinician.

Animals↗

PubMed2006

The relationship between microvessel density, proliferative activity and expression of vascular endothelial growth factor-A and its receptors in eutopic endometrium and endometriotic lesions.

Studies were performed to elucidate the possible relationship between microvessel density, proliferative activity and angiogenesis in eutopic endometrium from women with and without endometriosis and peritoneal endometriotic lesions. The question whether changes in these parameters in endometriotic lesions were reflected by the level of vascular endothelial growth factor-A (VEGF-A) in serum and peritoneal fluid was also studied. Biopsy specimens of both eutopic endometrium and peritoneal endometriotic lesions from women with endometriosis (n = 25) as well as eutopic endometrium from women without endometriosis (n = 14) were analysed immunohistochemically regarding microvessel density, proliferative activity, and expression of VEGF-A and its receptors vascular endothelial growth factor receptors 1 and 2 (VEGFR-1 and VEGFR-2) in stroma, glands and blood vessels. The VEGF-A concentration was measured in peritoneal fluid and serum. Secretory phase eutopic endometrium from women with endometriosis had significantly higher microvessel density, expression of VEGF-A in glandular epithelium and VEGFR-2 in endometrial blood vessels than those from women without endometriosis. Endometriotic lesions with high proliferative activity had a higher microvessel density and showed higher vascular expression of VEGFR-2 as well as being accompanied by higher levels of VEGF-A in peritoneal fluid and serum, compared with lesions with low proliferative activity. In conclusion, there seems to be a dysregulation of angiogenic activity in the eutopic endometrium of women with endometriosis and endometriotic lesions with high proliferative activity were accompanied by higher local angiogenic activity and higher levels of VEGF in serum and peritoneal fluid.

Adult↗

PubMed1986

Existence of lipoprotein lipase in rat brain microvessels.

To clarify the possibility that brain microvessels could utilize very low density lipoprotein (VLDL)-triglyceride, the hydrolysis of [14C] triolein in VLDL by rat brain microvessels was examined. The rat brain microvessels were prepared under microscopy. In the homogenate, triolein hydrolyzing activity was observed only in the presence of apolipoprotein C-II. That activity was diminished by the addition of 1 M NaCl. [14C] triolein incorporated in VLDL was hydrolyzed time- dependently. These results suggested that there exists lipoprotein lipase in brain microvessels and the brain can utilize VLDL triglyceride as a source of fatty acids.

Animals↗

PubMed1991

Endoneurial microvessels in human diabetic neuropathy. Endothelial cell dysjunction and lack of treatment effect by aldose reductase inhibitor.

Endoneurial microvascular abnormalities have been invoked in the pathogenesis of diabetic distal symmetric polyneuropathy. Detailed morphometric analysis of the endoneurial microvasculature was correlated with previously published data on nerve fiber morphometry and teased fiber analysis obtained from the same sural nerve biopsies. Biopsy specimens from neuropathic diabetic patients were obtained before and after 12 mo of aldose reductase inhibitor (ARI) treatment and compared to 15 carefully age-matched control subjects. Diabetic microvessels showed basement membrane thickening and loss of endothelial cell tight junctions. Microvascular density and the frequency of microvessels closed by endothelial cells increased with age in diabetic and control nerves and were unaffected by diabetes. The density of microvessels showing patent lumina did not differ between control and diabetic subjects and was not related to age or diabetes. Closed microvessels were composed of postcapillary venules that were otherwise devoid of ultrastructural abnormalities. We suggest that microvascular closure by endothelial cells may be a physiological condition and is unlikely to have any pathogenetic significance in diabetic neuropathy. Based on the current limited biopsy material, we conclude that 12 mo of ARI treatment that induced significant fiber repair and regeneration had no detectable effect on endoneurial microvascular abnormalities. These data suggest that endoneurial vascular pathology is not a rate-limiting factor in fiber damage or repair at this stage of diabetic neuropathy.

Adult↗

PubMed2004

Single-level dynamic spiral CT of hepatocellular carcinoma: correlation between imaging features and density of tumor microvessels.

AIM: To investigate the correlation of enhancement features of hepatocellular carcinoma (HCC) revealed by single-level dynamic spiral CT scanning (DSCT) with tumor microvessel density (MVD), and to determine the validity of DSCT in assessing in vivo tumor angiogenic activity of HCC. METHODS: Twenty six HCC patients were diagnosed histopathologically. DSCT was performed for all patients according to standard scanning protocol. Time-density curves were generated, relevant curve parameters were measured, and gross enhancement morphology was analyzed. Operation was performed to remove HCC lesions 1 to 2 weeks following CT scan. Histopathological slides were carefully prepared for the standard F(8)RA immunohistochemical staining and tumor microvessel counting. Enhancement imaging features of HCC lesions were correlatively studied with tumor MVD and its intra-tumor distribution characteristics. RESULTS: On DSCT images of HCC lesions, three patterns of time-density curve and three types of gross enhancement morphology were recognized. Histomorphologically, the distribution of positively stained tumor endothelial cells within tumor was categorized into 3 types. Curve parameters such as peak enhancement value and contrast enhancement ratio were significantly correlated with tumor tissue MVD (r=0.508 and r=0.423, P<0.01 and P<0.05 respectively). Both the pattern of time-density curve and the gross enhancement morphology of HCC lesions were also correlated with tumor MVD, and reflected the distributive features of tumor microvessels within HCC lesions. Correlation between the likelihood of intrahepatic metastasis of HCC lesions with densely enhanced pseudocapsules and rich pseudocapsular tumor MVD was found. CONCLUSION: Enhancement imaging features of HCC lesions on DSCT scanning are correlated with tumor MVD, and reflect the intra-tumor distribution characteristics of tumor microvessels. DSCT is valuable in assessing the angiogenic activity and tumor neovascularity of HCC patients in vivo.

Adult↗