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PubMedDate not supplied

Analysis of vessel absorption profiles in retinal oximetry.

The optical densities of vessel absorption features in small bandwidth fundus photographs have been used by many people for finding the oxygenation of the blood in retinal vessels. The purpose of this article is to show that the information found in this way can be made more accurate, and more information can be found by considering the details of the absorption profile (intensity as a function of distance across the vessel). The "wings" of the profile are primarily determined by the line-spread function of the video camera or film. A four-parameter curve fitting procedure using the line-spread function and an "ideal" vessel profile can be used to eliminate the effects both of the line-spread function and of any central reflection (vessel reflex) that may be present, yielding estimates of the vessel diameter and central absorption. The conclusions concerning the reflection are supported by studies of reflections from capillary tubes and wires in a model eye.

Biophysical Phenomena↗
PubMed2004

Cerebral venous thrombosis is associated with major vessel disease in Behçet's syndrome.

OBJECTIVE: To examine the association between the type of central nervous system (CNS) involvement (parenchymal disease and cerebral venous thrombosis (CVT)) and extra-cranial large vessel events, mainly venous thrombosis, in Behcet's syndrome (BS). METHODS: Conventional venous angiograms, Doppler ultrasonography, computed tomography, and MR angiography were used to study 88 patients with BS, with (n = 88) and without (n = 80) CNS disease for the presence of major vessel disease. RESULTS: Major vessel involvement among the male patients with and without CNS disease (21/73 (29%) v 18/80 (23%), respectively) showed no significant differences (p = 0.374). When patients with CNS disease were stratified according to the type of CNS involvement, 7/11 (64%) patients with CVT had major vessel disease compared with 15/77 (19%) patients with parenchymal disease (p = 0.004). The mean (SD) age of onset of CVT (23.1 (8.8) years) among the male patients was significantly earlier than among the men with parenchymal disease (32.0 (7.5); p = 0.002). CONCLUSIONS: CVT in BS was strongly associated with peripheral major vessel disease and occurred earlier in the disease course than the parenchymal type of CNS disease. As superficial thrombophlebitis also occurs more frequently in patients with major vessel disease in BS, this may suggest a common pathogenic mechanism.

Adult↗
PubMed1991

Does bipolar electrocoagulation time affect vessel weld strength?

The value of the bipolar electrocoagulator in the haemostasis of bleeding ulcers is controversial. We have therefore investigated the effect of different coagulation times on vessel weld strength achieved by the bipolar device. Welds were then made in vessels of known diameter using a standard 10F endoscopic haemostatic probe at coagulation times of two and 20 seconds. The intravascular temperature achieved at each time was measured. Vessel weld strength achieved by bipolar electrocoagulation was much greater at 20 seconds (approximately twice that at two seconds) and was highly significantly greater at all vessel diameters. There was a gradual reduction in weld strength with increasing vessel diameter, an effect that was seen for both two and 20 seconds of electrocoagulation. Intravascular temperature was significantly higher at 20 seconds than at two seconds. We conclude that vessel weld strength is related to coagulation time and that any future studies comparing the bipolar electrocoagulator with other haemostatic devices should use longer periods of bipolar electrocoagulation and record the coagulation time in order to optimise the clinical value of the device.

Animals↗
PubMed1992

Use of an autoperfusion catheter in the treatment of acute refractory vessel closure after coronary balloon angioplasty: immediate and six month follow up results.

OBJECTIVE: To determine the usefulness of the Stack autopersion dilatation catheter in patients with acute recurrent vessel closure during coronary angioplasty. DESIGN: Prospective data collection. SETTING: University hospital. PATIENTS: In 37 of 1003 consecutive patients undergoing angioplasty between November 1989 and December 1990 acute vessel closure developed that could not be redilated by a conventional balloon catheter. 13 (35%) of these 37 patients were sent immediately for emergency bypass surgery. INTERVENTION: In the remaining 24 patients an attempt was made to reopen the vessel with a Stack catheter. MAIN OUTCOME MEASURE: Successful reopening of the vessel. All successfully treated patients were followed for at least six months to detect recurrent ischaemia. RESULTS: In 16 patients (67%) the Stack procedure was successful. Of the eight patients in whom reopening of the occluded vessel was not achieved, seven were sent for bypass surgery and one was successfully treated by emergency stent implantation. The 16 patients successfully treated with the Stack autoperfusion system were followed up for a mean (SD) of 6.7 (2.6) (range 2 to 11) months. Ten patients remained symptom free but early clinical restenosis developed in four (25%). Overall, only three (19%) of 16 patients experienced recurrence of severe (class III-IV) symptoms and required further mechanical revascularisation. CONCLUSION: These data support the use of the Stack autoperfusion catheter system in selected patients with acute vessel closure not responsive to attempted redilatation with conventional balloon catheters. The short-term outcome seen in this series of patients who were successfully treated with this coronary autoperfusion system is encouraging.

Acute Disease↗
PubMed2004

Prognostic impact of VEGF, CD31, CD34, and CD105 expression and tumour vessel invasion after radical surgery for IB-IIA non-small cell lung cancer.

AIMS: To evaluate the prognostic impact of tumour angiogenesis assessed by vascular endothelial growth factor (VEGF), microvessel density (MVD), and tumour vessel invasion in patients who had undergone radical resection for stage IB-IIA non-small cell lung cancer (NSCLC). METHODS: Fifty one patients (42 men, nine women; mean age, 62.3 years; SD, 6.9) undergoing complete surgical resection (35 lobectomy, 16 pneumonectomy) of pathological stage IB (n = 43) and IIA (n = 8) NSCLC were evaluated retrospectively. No patient underwent postoperative chemotherapy or neoadjuvant treatment. Tumour specimens were stained for VEGF and specific MVD markers: CD31, CD34, and CD105. RESULTS: VEGF expression significantly correlated with high CD105 expression (p < 0.0001) and tumour vessel invasion (p = 0.04). Univariate analysis showed that those patients with VEGF overexpression (p = 0.0029), high MVD by CD34 (p = 0.0081), high MVD by CD105 (p = 0.0261), and tumour vessel invasion (p = 0.0245) have a shorter overall survival. Furthermore, multivariate Cox regression analysis showed that MVD by CD34 (p = 0.007), tumour vessel invasion (p = 0.024), and VEGF expression (p = 0.042) were significant predictive factors for overall survival. Finally, the presence of both risk factors, tumour vessel invasion and MVD by CD34, was highly predictive of poor outcome (odds ratio, 3.4; 95% confidence interval, 1.7 to 6.5; p = 0.0002). CONCLUSIONS: High MVD by CD34 and tumour vessel invasion are more closely related to poor survival than the other neoangiogenetic factors in stage IB-IIA NSCLC. This may be because these factors are more closely related to the metastatic process.

Adult↗
PubMed1978

Structural basis for the changing physical properties of human pulmonary vessels with age.

Circumferential strips of pulmonary vessel wall were obtained at necropsy from the major arterial and venous branches at the lung hilum in patients aged 7-87 years. The extensibility of these strips was measured using the tension balance method of Harris et al. (British Heart Journal, 1965, 27, 651-659). The vessels were then bisected, and half of each strip was submitted for structural analysis using morphometric methods on paraffin sections stained to show the collagen, elastin, and muscle content. The other halves of the formalin-fixed vessel strips were examined chemically to determine their collagen content by estimation of the total hydroxyproline content. The thickness of the vessel media was measured microscopically on all of the sections examined. Quantitative measurements were made on 42 arteries and 37 veins. Contrary to expectation, there was a steady fall in medial collagen content with increasing age in arteries and veins. The decrease in collagen content was similar in the morphometric and chemical studies and was statistically significant. The thickness of the vessel media did not change significantly with age. The pulmonary artery and vein strips were less extensible in the older age groups, the main change occurring in the elastic phase of the vascular stress/strain curves. It is suggested that changes in the elastic tissue at a molecular and lamellar level are responsible for the increasing stiffness of pulmonary vessels rather than changes in the medial collagen content.

Adolescent↗
PubMed1982

Failure to show decrease in small pulmonary blood vessels in rats with experimental pulmonary hypertension.

We induced chronic pulmonary hypertension in one group of rats by exposing them to chronic hypobaric hypoxia (380 mm Hg for three weeks) and in another group by administering a single subcutaneous dose of monocrotaline (60 mg/kg body weight). Both groups of rats showed increase of the right ventricular mean systolic blood pressure and right ventricular hypertrophy. We measured the surface area of histological sections of the left or right lungs and counted all small blood vessels with an external diameter of less than 50 microns and with a definite elastic coat lying distal to respiratory bronchioles. In the 10 rats with chronic hypoxic pulmonary hypertension the mean total number of small pulmonary blood vessels was 428.8 +/- 96.9 (SD) compared with 337.8 +/- 91.9 in 10 untreated control rats. The number of small pulmonary blood vessels per mm2 of lung tissue was 4.0 +/- 1.3 in the chronically hypoxic rats compared with 3.8 +/- 1.2 in the controls. The mean total number of small pulmonary blood vessels in nine rats with monocrotaline-induced pulmonary hypertension was 396.8 +/- 61.7 compared with 384 +/- 55.4 in three control rats. The number of small pulmonary blood vessels per mm2 lung tissue was 3.3 +/- 0.6 in the rats treated with monocrotaline compared with 3.6 +/- 0.6 in the control group. We conclude that the number of small pulmonary blood vessels is not reduced in rats with pulmonary hypertension induced by chronic hypoxia or monocrotaline.

Animals↗
PubMed2006

Arterial wall imaging: evaluation with 16-section multidetector CT in blood vessel phantoms and ex vivo coronary arteries.

PURPOSE: To evaluate the diagnostic performance of 16-section multidetector computed tomography (CT) for assessment of plaques in phantoms and ex vivo coronary arteries, with intravascular ultrasonography (US) and optical coherence tomography (OCT) as reference standards. MATERIALS AND METHODS: Research protocol was HIPAA compliant and approved by institutional review board, without informed consent required. Blood vessel and lesion composition phantoms and ex vivo coronary arteries were imaged with 16-section CT. Wall areas of phantoms and ex vivo coronary arteries were measured with multidetector CT and intravascular US. Sensitivity and specificity for lipid detection were determined in lesion composition phantoms. CT numbers of blood vessel wall were determined in ex vivo coronary arteries and compared with lesion classification results from OCT. Agreement in dimensional measurements was compared (paired t tests). CT numbers within blood vessel wall of CT cross sections classified as lipid rich, fibrous, and calcified at OCT were compared (Kruskal-Wallis tests). RESULTS: Mean blood vessel wall areas measured with CT and US in phantoms were 9.2 mm(2) +/- 1.8 (standard deviation) and 10.4 mm(2) +/- 3.4 (bias, -1.3 mm(2) +/- 3.1; P < .05), respectively. Mean blood vessel wall areas measured in ex vivo coronary arteries with CT and US were 10.9 mm(2) +/- 4.1 and 9.1 mm(2) +/- 3.1 (bias, 1.8 mm(2) +/- 3.0; P < .001), respectively. Sensitivity and specificity of 93% and 92%, respectively, for identification of lipid-rich lesions were observed in lesion composition phantoms. Mean CT numbers in blood vessel wall of ex vivo coronary arteries identified at OCT as predominantly lipid rich, fibrous, and calcified were 29 HU +/- 43, 101 HU +/- 21, and 135 HU +/- 199, respectively (P < .001). CONCLUSION: Determination of composition of individual plaques from attenuation values can be more challenging because of overlapping values for different tissue types.

Coronary Angiography↗
PubMed1999

Crossing vessels at the ureteropelvic junction: detection with contrast-enhanced color Doppler imaging.

PURPOSE: To investigate the feasibility of imaging crossing vessels at the ureteropelvic junction (UPJ) preoperatively by means of contrast agent-enhanced color Doppler imaging (CDI). MATERIALS AND METHODS: Twenty-nine patients (13 female patients, 16 male patients; age range, 17-76 years; mean age, 45 years) with symptomatic UPJ obstruction were examined with CDI before and after intravenous infusion of the contrast agent. The type (i.e., arterial or venous) and position of the vessel relative to the UPJ (i.e., anterior or posterior) were assessed. The CDI findings were correlated with the surgical findings at laparoscopic pyeloplasty. RESULTS: Among the 29 patients, crossing vessels were detected with nonenhanced CDI in 15 patients, with enhanced CDI in 22 patients, and with laparoscopy in 23 patients. Enhanced CDI depicted crossing vessels in 22 (96%) of the 23 laparoscopically confirmed cases compared with nonenhanced CDI, which depicted 15 (65%) of the 23 cases. The rate of detecting crossing vessels increased significantly with use of the contrast agent (P < .016, McNemar test). CONCLUSION: Compared with nonenhanced CDI, contrast-enhanced CDI significantly improves the detection of crossing vessels at the UPJ and is useful in the presurgical evaluation of UPJ obstruction.

Adolescent↗
PubMed2006

Transport in rat vessel walls. I. Hydraulic conductivities of the aorta, pulmonary artery, and inferior vena cava with intact and denuded endothelia.

In this study, filtration flows through the walls of the rat aorta, pulmonary artery (PA), and inferior vena cava (IVC), vessels with very different susceptibilities to atherosclerosis, were measured as a function of transmural pressure (DeltaP), with intact and denuded endothelium on the same vessel. Aortic hydraulic conductivity (L(p)) is high at 60 mmHg, drops approximately 40% by 100 mmHg, and is pressure independent to 140 mmHg. The trends are similar in the PA and IVC, dropping 42% from 10 to 40 mmHg and flat to 100 mmHg (PA) and dropping 33% from 10 to 20 mmHg and essentially flat to 60 mmHg (IVC). Removal of the endothelium renders L(p)(DeltaP) flat: it increases L(p) of the aorta by approximately 75%, doubles L(p) of the PA, and quadruples L(p) of the IVC. Specific resistance (1/L(p)) of the aortic endothelium is approximately 47% of total resistance; i.e., the endothelium accounts for approximately 47% of the DeltaP drop at 100 mmHg. The PA value is 55% at >40 mmHg, and the IVC value is 23% at 10 mmHg. L(p) of the intact aorta, PA, and IVC are order 10(-8), 10(-7), and 5 x 10(-7) cm.s(-1).mmHg(-1), and wall thicknesses are 145.8 microm (SD 9.3), 78.9 microm (SD 3.3), and 66.1 microm (SD 4.1), respectively. These data are consistent with the different wall structures of the three vessels. The rat aortic L(p) data are quantitatively consistent with rabbit L(p)(DeltaP) (Tedgui A and Lever MJ. Am J Physiol Heart Circ Physiol 247: H784-H791, 1984; Baldwin AL and Wilson LM. Am J Physiol Heart Circ Physiol 264: H26-H32, 1993), suggesting that intimal compression under pressure loading may also play a role in L(p)(DeltaP) in these other vessels. Despite very different driving DeltaP, nominal transmural water fluxes of these three vessels are very similar and, therefore, cannot alone account for their differences in disease susceptibility. The different fates of macromolecular tracers convected by these water fluxes into the walls of these vessels may account for this difference.

Animals↗
PubMed2003

Rho-Rho kinase pathway is involved in the regulation of myogenic tone and pump activity in isolated lymph vessels.

To evaluate whether or not Rho-Rho kinase pathway is involved in the regulation of mechanical activity of lymph vessels, effects of Y-27632 and okadaic acid on lymph pump activity and myogenic, pressure- and agonist-induced tone were examined in isolated rat lymph vessels. Y-27632 caused a significant dilation with a cessation of the lymph pump activity. Y-27632 also produced a dose-related dilation of the lymph vessels precontracted by norepinephrine (NE)-, U-46619- or 80 mM KCl. Okadaic acid significantly constricted the lymph vessels and reduced the frequency of the lymph pump activity. Okadaic acid also produced a dose-related constriction of the lymph vessels precontracted by NE or U-46619. The Y-27632-induced decrease of the frequency of lymph pump activity was significantly reversed by the pretreatment with okadaic acid. In the presence of Y-27632, the pressure-mediated tone of the lymph vessel was significantly decreased. On the other hand, okadaic acid significantly increased the pressure-mediated tone. These findings suggest that Rho kinase and myosin phosphatase activity in lymphatic smooth muscles may contribute to the regulation of lymph pump activity and may be also involved in the control of myogenic pressure- and agonist-induced tone.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

Vessel tone affects transmural distribution of coronary flow during hypoperfusion.

Subendocardial flow is selectively impaired during coronary hypoperfusion. Systolic compression of intramyocardial vessels not only stops capillary flow but empties vessels as well, leading to reversed flow in the arteries that penetrate the myocardium. The tone of these vessels influences the magnitude of flow oscillation during the cardiac cycle, but whether vessel tone is an independent determinant of subendocardial perfusion during coronary hypoperfusion has not been determined. The discovery of endothelin (ET-1) has made it possible to counteract metabolic vasodilation and increase vessel tone during hypoperfusion. A shunt from a carotid artery to the left anterior descending coronary artery was installed in open-chest pigs anesthetized with halothane. Arterial pressure and heart rate were held constant, and coronary pressure was reduced in stages by restricting shunt flow during intracoronary infusion of ET-1 (n = 7) or adenosine (n = 5). Microspheres were injected at each stage to determine layer flow. Coronary resistance was two- to three-fold higher and subendocardial flow was lower at similar coronary pressures in the animals receiving ET-1 than in those receiving adenosine. In contrast, flow distribution across the left ventricular wall was more homogeneous with ET-1 than with adenosine, even at coronary pressures low enough to cause lactate production and regional hypokinesis. These results demonstrate that vessel tone has an independent effect on absolute subendocardial flow as well as transmural flow distribution during coronary hypoperfusion.

Adenosine↗
PubMed2004

Interleukin-6 impairs endothelium-dependent NO-cGMP-mediated relaxation and enhances contraction in systemic vessels of pregnant rats.

IL-6 is elevated in plasma of preeclamptic women, and twofold elevation of plasma IL-6 increases vascular resistance and arterial pressure in pregnant rats, suggesting a role of the cytokine in hypertension of pregnancy. However, whether the hemodynamic effects of IL-6 reflect direct effects of the cytokine on the mechanisms of vascular contraction/relaxation is unclear. The purpose of this study was to test the hypothesis that IL-6 directly impairs endothelium-dependent relaxation and enhances vascular contraction in systemic vessels of pregnant rats. Active stress was measured in aortic strips isolated from virgin and late pregnant Sprague-Dawley rats and then nontreated or treated for 1 h with IL-6 (10 pg/ml to 10 ng/ml). In endothelium-intact vascular strips, phenylephrine (Phe, 10(-5) M) caused an increase in active stress that was smaller in pregnant (4.2 +/- 0.3) than virgin rats (5.1 +/- 0.3 x 10(4) N/m(2)). IL-6 (1,000 pg/ml) caused enhancement of Phe contraction that was greater in pregnant (10.6 +/- 0.7) than virgin rats (7.5 +/- 0.4 x 10(4) N/m(2)). ACh and bradykinin caused relaxation of Phe contraction and increases in vascular nitrite production that were greater in pregnant than virgin rats. IL-6 caused reductions in ACh- and bradykinin-induced vascular relaxation and nitrite production that were more prominent in pregnant than virgin rats. Incubation of endothelium-intact strips in the presence of N(omega)-nitro-L-arginine methyl ester (10(-4) M) to inhibit nitric oxide (NO) synthase, or 1H-[1,2,4]oxadiazolo[4,3]-quinoxalin-1-one (ODQ, 10(-5) M) to inhibit cGMP production in smooth muscle, inhibited ACh-induced relaxation and enhanced Phe-induced stress in nontreated but to a lesser extent in IL-6-treated vessels, particularly those of pregnant rats. Removal of the endothelium enhanced Phe-induced stress in nontreated but not IL-6-treated vessels, particularly those of pregnant rats. In endothelium-denuded strips, relaxation of Phe contraction with sodium nitroprusside, an exogenous NO donor, was not different between nontreated and IL-6-treated vessels of virgin or pregnant rats. Thus IL-6 inhibits endothelium-dependent NO-cGMP-mediated relaxation and enhances contraction in systemic vessels of virgin and pregnant rats. The greater IL-6-induced inhibition of vascular relaxation and enhancement of contraction in systemic vessels of pregnant rats supports a direct role for IL-6 as one possible mediator of the increased vascular resistance associated with hypertension of pregnancy.

Acetylcholine↗
PubMed1979

Effect of parenchyma and length changes on vessel pressure-diameter behavior in pig lungs.

At several transpulmonary pressures (Ptp), the pressure-diameter (PD) behavior of the largest intraparenchymal arterial segment in the isolated pig lung was compared with the behavior of the segment after its excision from the parenchyma and its extension to lengths equivalent to those in the intact state. For physiological changes in length, as may occur with lung inflation during Ptp changes from 4 to 25 cmH2O, excised-vessel diameters did not change significantly at a constant transmural pressure. The excised-vessel PD behavior was not significantly different from the intact-vessel PD behavior at a Ptp of 4 cmH2O. At any constant arterial pressure, intact-vessel diameters became larger as Ptp increased. Estimates of the perivascular pressure (Px) obtained by directly comparing intact-vessel and excised-vessel PD curves were as follows: 1) Px was equal to pleural pressure at a Ptp approximating the functional residual capacity; 2) Px decreased almost linearly as Ptp increased; and 3) Px decreased with a fall in arterial pressure. These results are consistent with direct measurements of the perivascular interstitial fluid pressure.

Animals↗
PubMed1985

Extra-alveolar vessel fluid filtration coefficients in excised and in situ canine lobes.

We continuously weighed fully distended excised or in situ canine lobes to estimate the fluid filtration coefficient (Kf) of the arterial and venous extra-alveolar vessels compared with that of the entire pulmonary circulation. Alveolar pressure was held constant at 25 cmH2O after full inflation. In the in situ lobes, the bronchial circulation was interrupted by embolization. Kf was estimated by two methods (Drake and Goldberg). Extra-alveolar vessels were isolated from alveolar vessels by embolizing enough 37- to 74-micron polystyrene beads into the lobar artery or vein to completely stop flow. In excised lobes, Kf's of the entire pulmonary circulation by the Drake and Goldberg methods were 0.122 +/- 0.041 (mean +/- SD) and 0.210 +/- 0.080 ml X min-1 X mmHg-1 X 100 g lung-1, respectively. Embolization was not found to increase the Kf's. The mean Kf's of the arterial extra-alveolar vessels were 0.068 +/- 0.014 (Drake) and 0.069 +/- 0.014 (Goldberg) (24 and 33% of the Kf's for the total pulmonary circulation). The mean Kf's of the venous extra-alveolar vessels were similar [0.046 +/- 0.020 (Drake) and 0.065 +/- 0.036 (Goldberg) or 33 and 35% of the Kf's for the total circulation]. No significant difference was found between the extra-alveolar vessel Kf's of in situ vs. excised lobes. These results suggest that when alveolar pressure, lung volume, and pulmonary vascular pressures are high, approximately one-third of the total fluid filtration comes from each of the three compartments.

Animals↗
PubMed1994

Loss of endothelium-dependent vasodilation in the pulmonary vessels of sheep after prolonged endotoxin.

We examined the hemodynamic response of awake sheep to prolonged endotoxin infusion (10 ng.kg-1 x min-1 for 12 h) and the in vitro endothelium-dependent relaxation of pulmonary arterial vessels excised 12 h after the end of endotoxin infusion to determine whether the development of pulmonary hypertension after endotoxin is associated with loss of endothelium-dependent relaxation. In seven of nine sheep, there was a maintained increase (4-68% of baseline) in pulmonary arterial pressure 24 h after the beginning of endotoxin infusion. The greater the increase in pulmonary arterial pressure in vivo, the greater was the in vitro deficit in endothelium-dependent relaxation of the pulmonary vessels. The maximum in vitro vessel dilation was 59% for pulmonary artery rings isolated from sheep without a sustained increase in pulmonary arterial pressure 24 h after endotoxin. Prolonged endotoxin infusion did not alter the in vitro response of pulmonary arterial vessels to KCl or 10(-5) M norepinephrine. Force development, response to 10(-5) M norepinephrine, and vasodilation in response to acetylcholine were also not altered in pulmonary vessels taken from control sheep and exposed in vitro to tumor necrosis factor-alpha (400 U/ml). Our results suggest that loss of endothelium-dependent relaxation in pulmonary vessels supports the sustained pulmonary hypertension that develops after prolonged exposure to endotoxin.

Acetylcholine↗
PubMed2004

Comparison of resistance and conduit vessel nitric oxide-mediated vascular function in vivo: effects of exercise training.

Exercise training improves vascular function in subjects with cardiovascular disease and risk factors, but there is mounting evidence these vascular adaptations may be vessel bed specific. We have therefore examined the hypothesis that exercise-induced improvements in conduit vessel function are related to changes in resistance vessel function. Endothelium-dependent and -independent conduit vessel function were assessed by using wall-tracking of high-resolution brachial artery ultrasound images of the response to flow-mediated dilation (FMD) and nitroglycerine [glyceryl trinitrate (GTN)] administration. Resistance vessel endothelium-dependent and -independent function were assessed using intrabrachial administration of acetylcholine (ACh) and nitroprusside (SNP). Randomized crossover studies of 8-wk exercise training were undertaken in untreated hypercholesterolemic (n = 10), treated hypercholesterolemic (n = 10), coronary artery disease (n = 8), and Type 2 diabetic subjects (n = 15). Exercise training significantly enhanced responses to ACh (P < 0.05) and FMD (P < 0.0001). There were no significant changes in either SNP or GTN responses. The correlation between ACh and FMD responses at entry was not significant (r = 0.186; P = 0.231), and training-induced changes in the ACh did not correlate with those in FMD (r = -0.022; P = 0.890). Similarly, no correlation was evident between the SNP and GTN responses at entry (r = -0.010; P = 0.951) or between changes in these variables with training (r = -0.211; P = 0.191). We conclude that, although short-term exercise training improves endothelium-dependent nitric oxide-mediated vascular function in both conduit and resistance vessels, the magnitude of these improvements are unrelated.

Acetylcholine↗
PubMed2005

Hair follicle-derived blood vessels vascularize tumors in skin and are inhibited by Doxorubicin.

We have recently shown that the neural-stem cell marker nestin is expressed in hair follicle stem cells and the blood vessel network interconnecting hair follicles in the skin of transgenic mice with nestin regulatory element-driven green fluorescent protein (ND-GFP). The hair follicles were shown to give rise to the nestin-expressing blood vessels in the skin. In the present study, we visualized tumor angiogenesis by dual-color fluorescence imaging in ND-GFP transgenic mice after transplantation of the murine melanoma cell line B16F10 expressing red fluorescent protein. ND-GFP was highly expressed in proliferating endothelial cells and nascent blood vessels in the growing tumor. Results of immunohistochemical staining showed that the blood vessel-specific antigen CD31 was expressed in ND-GFP-expressing nascent blood vessels. ND-GFP expression was diminished in the vessels with increased blood flow. Progressive angiogenesis during tumor growth was readily visualized during tumor growth by GFP expression. Doxorubicin inhibited the nascent tumor angiogenesis as well as tumor growth in the ND-GFP mice transplanted with B16F10-RFP. This model is useful for direct visualization of tumor angiogenesis and evaluation of angiogenic inhibitors.

Animals↗