Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VESSELS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources
PubMed1995

Endothelium-independent vasoconstricting and vasodilating actions of halothane on rat mesenteric resistance blood vessels.

BACKGROUND: Whether volatile anesthetics produce changes in vascular resistance and blood flow because of direct effects on vascular tissue is unclear. Direct vasoconstricting and vasodilating actions have been demonstrated in isolated conductance arteries in vitro, but there is little information regarding direct effects on the small vessels that mediate resistance and flow changes in vivo. METHODS: We investigated the actions of halothane on 50-200 microM branches of the rat mesenteric artery that were cannulated and studied in vitro. The vessels were pressurized to 60 mmHg, and vascular dimensions were continuously monitored using a computer-based real-time image analysis system. The vessel bath was perfused with HCO3(-)-buffered saline (37 degrees C) equilibrated with 95% O2/5% CO2 (+/- halothane). The vascular endothelium was mechanically removed before cannulation in some vessels. RESULTS: In unstimulated vessels, halothane had a concentration-dependent vasoconstricting action (EC50 = 0.45 mM approximately 1.5 vol% at 37 degrees C) that was largely transient and was similar to that produced by caffeine. Both halothane and caffeine constrictions were unaffected by bath [Ca2+], nifedipine (1 microM) or Cd2+ (100 microM) and were abolished by ryanodine (10 microM). In addition, caffeine responses were attenuated by halothane in a concentration-dependent manner (EC50 = 1.6 mM). In vessels preconstricted with KCl (40 mM) or phenylephrine (10(-6) M), halothane produced transient constriction followed by concentration-dependent vasodilation. Ryanodine, which abolished halothane constrictions, had little effect on the amplitude of KCl- or phenylephrine-induced constrictions or the vasodilating action of halothane. Removal of the endothelium likewise had little effect on the vasoconstricting or the vasodilating actions of halothane in unstimulated, KCl- or phenylephrine-constricted vessels. Halothane completely relaxed KCl and phenylephrine constrictions with EC50 values of 0.36 mM (1.2% at 37 degrees C) and 0.75 mM (2.5%), respectively, in intact vessels before ryanodine; 0.25 mM (0.8%) and 0.59 mM (1.9%) in intact vessels after ryanodine; and 0.52 mM (1.7%) and 0.67 mM (2.2%) in endothelium-denuded vessels. CONCLUSIONS: Halothane has endothelium-independent vasoconstricting and vasodilating actions in isolated mesenteric resistance blood vessels. The vasoconstricting action appears to involve halothane-induced Ca2+ release from caffeine/ryanodine-sensitive intracellular store(s). The vasodilating action in phenylephrine- or KC1-constricted vessels is independent of the Ca(2+)-releasing action and most likely involves an effect(s) on sarcolemmal-dependent Ca2+ signaling (e.g., extracellular Ca2+ influx) and/or Ca2+ activation of contractile proteins. The magnitude of both the vasoconstricting and the vasodilating actions of halothane in these vessels at clinically relevant concentrations suggests these direct actions contribute to the overall cardiovascular effects of halothane in vivo.

Animals↗
PubMed2001

Role of angiography in the detection of aortic branch vessel injury after blunt thoracic trauma.

PURPOSE: The occurrence of aortic arch branch vessel injury as an isolated occurrence or in association with aortic injury after blunt chest trauma has not been emphasized in the literature. The imaging evaluation is also controversial. METHODS: We reviewed thoracic aortograms of 166 patients examined at our institution from May 1995 to May 1999 performed after blunt thoracic trauma. We evaluated the aortograms for aortic and arch branch vessel injuries. Twenty-four injuries were detected and all patients had either a wide mediastinum demonstrated on plain radiographs (22 patients) or mechanism of injury conducive to aortic injury. RESULTS: Of the 166 patients, 24 (14%; 16 men, 8 women; mean age, 50 years) had aortic or arch branch vessel injuries. Isolated aortic injury occurred in 15 (9%) of 166 patients. Branch vessel injury occurred in 9 (5%) of 166 patients; seven patients (10 branch vessels) had isolated branch vessel injury and two patients (three branch vessels) had branch vessel injury associated with aortic injury. The injured branch vessels were brachiocephalic artery (four), left common carotid artery (four), left subclavian artery (three), right internal mammary artery (one), and left vertebral artery (one). The types of branch vessel injuries included intimal tears (nine vessels; 69%), and transection causing a pseudoaneurysm (four vessels; 31%). Revised Trauma Scores in patients with branch vessel injuries were 12 in seven patients and 11 and 4 in one each. CONCLUSION: We emphasize the angiographic findings in these patients that can at times be quite subtle. Awareness of the incidence of such injuries either in isolation or associated with aortic injury has implications regarding evaluation of this patient population with less invasive techniques such as CT or transesophageal echocardiography.

Adolescent↗
PubMed2006

Quantification of total and perfused blood vessels in murine skin autografts using a fluorescent double-labeling technique.

BACKGROUND: Two theories exist regarding the revascularization of skin autografts: direct anastomosis between graft vessels and bed vessels, and ingrowth of bed vessels (angiogenesis) into the graft. This study characterizes revascularization, spatially and chronologically, in a murine skin autograft model using a double-labeling technique. METHODS: Full-thickness (1 cm2) skin grafts were performed on adult male C57/Bl6 mice. After 48 hours, 60 hours, 3 days, 5 days, and 14 days (n = 3 mice per time point) terminal intracardiac perfusion with a fluorescein/dextran dye demonstrated vascular filling of graft blood vessels. Fluorescence immunohistochemistry of CD31+ endothelial cells allowed counting of total vessels and fluorescein perfusion quantification of patent vessels in the lateral graft area, central graft area, graft bed, and wound margins. RESULTS: Initial filling of graft vessels was seen after 48 hours. This included vessels in the papillary dermis of the graft, and there was no significant difference in the percentage of filled vessels in the deep dermis of the graft compared with the papillary dermis of the graft. A rapid increase in vessel filling was seen between 48 and 60 hours in all areas of the graft. Vessel filling occurred mainly in the central area of the graft rather than in the lateral areas. CONCLUSIONS: The short time course of vessel filling indicates that the initial onset of revascularization is attributable to early anastomoses between graft and bed vessels, mainly in the central area of the graft. These findings have implications for both autograft revascularization in a clinical setting and in the development of tissue-engineered skin substitutes.

Anastomosis, Surgical↗
PubMedDate not supplied

The microcirculation in acute murine cutaneous incisional wounds shows a spatial and temporal variation in the functionality of vessels.

A mouse perfusion model using fluorescently labeled dextran has been developed to investigate the functionality of blood vessels during cutaneous wound healing. By immunostaining cryostat sections of perfused wounds with antibodies that identify vessels, we were able to assess their functionality. There was an increase in the proportion of CD31(+)-perfused vessels in all wound regions with time, although the vessels of the wound margins and superficial granulation tissue (GT) took the longest to become perfused. More than 50% of the latter vessels were not perfused at 10 days postwounding. This is consistent with the growth of functional vessels from the wound base proceeding to the more superficial GT. The CD34 marker was expressed by a subpopulation of CD31(+) vessels. However, in contrast to CD31(+) vessels, the functionality of CD34(+) vessels did not change significantly with time and 50-75% of CD34(+) vessels in the GT and wound margins were nonfunctional. This might be explained either by apoptosis of the CD34(+) vessels or the loss of the marker with time. This study has important implications for assays of wound-healing angiogenesis based on histology and immunohistochemical markers for vessels, because vessel functionality differs both spatially and temporally during wound healing.

Animals↗
PubMed2004

Abnormal vessel tortuosity as a marker of treatment response of malignant gliomas: preliminary report.

Despite multiple advances in medical imaging, noninvasive monitoring of therapeutic efficacy for malignant gliomas remains problematic. An underutilized observation is that malignancy induces characteristic abnormalities of vessel shape. These characteristic shape abnormalities affect both capillaries and much larger vessels in the tumor vicinity, involve larger vessels prior to sprout formation, and are generally not present in hypervascular benign tumors. Vessel shape abnormalities associated with malignancy thus may appear independently of increase in vessel density. We hypothesize that an automated, computerized analysis of vessel shape as defined from high-resolution MRA can provide valuable information about tumor activity during the treatment of malignant gliomas. This report describes vessel shape properties in 10 malignant gliomas prior to treatment, in 2 patients in remission during treatment, and in 2 patients with recurrent disease. One subject was scanned multiple times. The method involves an automated, statistical analysis of vessel shape within a region of interest for each tumor, normalized by the values obtained from the vessels within the same region of interest of 34 healthy subjects. Results indicate that untreated tumors display statistically significant vessel tortuosity abnormalities. These abnormalities involve vessels not only within the tumor margins as defined from MR but also vessels in the surrounding tissue. The abnormalities resolve during effective treatment and recur with tumor recurrence. We conclude that vessel shape analysis could provide an important means of assessing tumor activity.

Cerebrovascular Circulation↗
PubMed2002

Effect of vessel size on creation of hepatic radiofrequency lesions in pigs: assessment of the "heat sink" effect.

OBJECTIVE: The effect of vessels and their size on radiofrequency lesion creation in the liver was evaluated with respect to potential for vascular injury and perfusion-mediated "heat sink" effect. SUBJECTS AND METHODS: Radiofrequency lesions targeted to tissue adjacent to a variety of vessels were created in vivo in the liver of 10 Yorkshire pigs. Postablation contrast-enhanced CT and then histopathologic analysis of the vessels and lesions were performed after sacrifice of the pigs. Degree of vascular injury and viability of perivascular hepatocytes were recorded and tabulated according to vessel size for both CT and histologic data sets. RESULTS: At CT, 42 (95%) of 44 veins greater than 3 mm remained patent, and four (20%) of 20 veins less than 3 mm were occluded. Heat sink effect, indicated by invagination of enhancing tissue between vessel and radiofrequency lesion, was observed in 32 (73%) of 44 veins greater than 3 mm and in zero of 20 veins less than 3 mm. On histopathology, 111 (100%) of 111 vessels less than 3 mm showed at least partial vessel wall injury, characterized by endothelial cell necrosis and luminal thrombus. In 24 vessels greater than 3 mm, the extent of vessel wall injury decreased with increasing vessel diameter. Viable perivascular tissue indicative of heat sink effect was identified in 12 of 24 veins greater than 3 mm, increasing to seven of seven veins greater than 5 mm. None of 96 vessels less than 2 mm and three of 111 vessels less than 3 mm showed any heat sink effect. CONCLUSION: There appears to be a narrow transition zone for hepatic vessels at 2-4 mm, beyond which the heat sink effect was seen consistently and substantial vascular injury was rare.

Animals↗
PubMed2003

Workload of the steering work on a high-speed vessel.

The higher incidence of accidents occurring on board among the high-speed vessels has motivated this study focusing on the actual operating conditions contributing to the incidence. The working activities and workload of the officers and quartermasters were compared between the conventional and high-speed vessels of regular service ferry, by recording video-pictures and heart rate of the crews during actual navigations. An autopilot equipment was installed in the conventional vessel of over 6000 tons, but not in the high-speed vessel of about 1500 tons. Either on the conventional or high-speed vessel, dominant activities of the officers were lookout and watching radar, which were conducted in standing on the conventional vessel and in sitting on the high-speed vessel. Major works of the quartermasters were lookout and radar watch in standing on the conventional vessel and steering operations with a joystick in sitting on the high-speed vessel. Despite these differences in postural conditions, the mean % heart rate increase in both crews was significantly higher on the high-speed than on the conventional vessel. In the quartermaster, the events requiring steering maneuvers on the high-speed vessel were associated with increase in heart rate. The findings as a whole suggest occurrence of substantial mental strains in the crew on the high-speed vessel. These strains, certainly derived from caring for the safety in the absence of autopilot equipment, must have intensified the workload in the crew. In connection with the workload, the necessity for some fail-safe systems, including the autopilot facilities, and educational systems for techniques of steering high-speed vessels was discussed.

Accident Prevention↗
PubMed1996

Temporal expression of extracellular matrix metalloproteinases and tissue plasminogen activator in the development of collateral vessels in the canine model of coronary occlusion.

Although heart attack is caused by occlusion of a major coronary artery, some patients have occlusion without heart attack because these patients have sufficient collateral circulation to provide an alternate pathway for blood supply to the myocardium at ischemic risk. The growth of new capillary vessels (angiogenesis) and enlargement of preexisting vessels play an important role in the collateral development. We evaluated the hypothesis that extracellular matrix metalloproteinase (MMP) expression is altered in coronary collateral arteries (0.5-1 mm o.d.) isolated from canine hearts 2-4 months after surgical placement of an ameroid occluder around the proximal left circumflex artery (n = 4), during the development of collateral vessels and restructuring new vessels. Histologic studies (hematoxylin and eosin, trichrome, and van Gieson stains) indicated cellular proliferation and increased collagen and elastin content in collateral vessels compared with comparable-sized unoccluded arterial segments of the left anterior descending (LAD) artery. In situ MMP activity of collateral vessels, measured using denatured collagen in the gel matrix, indicated an increase in total MMP activity in the intima of collateral vessels compared with normal LAD vessels. To further identify the type of MMP, tissue homogenates were prepared from collateral and LAD vessels and analyzed by SDS-PAGE zymography. The results suggest induction of gelatinase A and gelatinase B expression in collateral vessels compared with normal LAD tissue, when identical amounts of total protein were loaded onto each lane in the gel. Based on plasminogen-casein zymography, we observed the tissue plasminogen activator level to be increased in collateral vessels. On the basis of immunoblot and mRNA (Northern blot) analyses, we determined that the MMP-1 level was induced in collateral vessels 2 and 4 months after ameroid occlusion. In contrast with MMP-1, the level of TIMP-1 (tissue inhibitor of metelloproteinases) was decreased significantly (p < 0.001) in collateral compared with LAD vessels, suggesting a role for arterial TIMP in anti-angiogenic activity. Collectively, these results suggest that chronic occlusion of a major coronary artery induces upregulation of vascular remodeling mechanisms subserving collateral development. Increased MMP-2 activity in collaterals may be associated with decreased levels of tissue inhibitor of metalloproteinases and fibrous tissue remodeling following angiogenic and (or) adaptive responses of the myocardium to chronic ischemia.

Animals↗
PubMed1997

Three-vessel view of the fetal upper mediastinum: an easy means of detecting abnormalities of the ventricular outflow tracts and great arteries during obstetric screening.

The three-vessel view is a transverse view of the fetal upper mediastinum is as simple to obtain as the four-chamber view. It demonstrates the main pulmonary artery, ascending aorta and superior vena cava in cross- or oblique sections. The purposes of this study were to describe the normal anatomy of the three-vessel view and to analyze what anatomical changes would occur in this view when there are lesions of the ventricular outflow tracts and/or great arteries. Sonograms of 29 fetuses with lesions involving the ventricular outflow tracts and/or great arteries were reviewed. Three-vessel views were evaluated in terms of vessel size, number, arrangement and alignment. Twenty-eight of 29 fetuses showed an abnormal three-vessel view that included abnormal vessel size (n = 12), abnormal alignment (n = 8), abnormal arrangement (n = 7) and abnormal vessel number (n = 3). The vessel size was abnormal in obstructive lesions of the right (n = 4) or the left (n = 8) side of the heart. An abnormal alignment was seen in tetralogy of Fallot (n = 6) and double-outlet right ventricle (n = 2) that showed anterior displacement of the aorta. An abnormal arrangement was seen in complete (n = 4) and corrected (n = 1) transposition, double-outlet right ventricle (n = 1) and pulmonary atresia with ventricular septal defect (n = 1). Only two vessels were seen in truncus arteriosus (n = 1). Four vessels were seen in persistent left superior vena cava (n = 2). A fetus with pulmonary atresia and intact ventricular septum showed a normal three-vessel view. In conclusion, most of the lesions involving the ventricular outflow tracts and/or great arteries showed an abnormal three-vessel view.

Aortic Valve Stenosis↗
PubMed2001

Assembly of trunk and limb blood vessels involves extensive migration and vasculogenesis of somite-derived angioblasts.

Vascular development requires the assembly of precursor cells into blood vessels, but how embryonic vessels are assembled is not well understood. To determine how vascular cells migrate and assemble into vessels of the trunk and limb, marked somite-derived angioblasts were followed in developing embryos. Injection of avian somites with the cell-tracker DiI showed that somite-derived angioblasts in unperturbed embryos migrated extensively and contributed to trunk and limb vessels. Mouse-avian chimeras with mouse presomitic mesoderm grafts had graft-derived endothelial cells in blood vessels at significant distances from the graft, indicating that mouse angioblasts migrated extensively in avian hosts. Mouse graft-derived endothelial cells were consistently found in trunk vessels, such as the perineural vascular plexus, the cardinal vein, and presumptive intersomitic vessels, as well as in vessels of the limb and kidney rudiment. This reproducible pattern of graft colonization suggests that avian vascular patterning cues for trunk and limb vessels are recognized by mammalian somitic angioblasts. Mouse-quail chimeras stained with both the quail vascular marker QH1 and the mouse vascular marker PECAM-1 had finely chimeric vessels, with graft-derived mouse cells interdigitated with quail vascular cells in most vascular beds colonized by graft cells. Thus, diverse trunk and limb blood vessels have endothelial cells that developed from migratory somitic angioblasts, and assembly of these vessels is likely to have a large vasculogenic component.

Animals↗
PubMed2005

Effect of vessel diameter on the creation of ovine lung radiofrequency lesions in vivo: preliminary results.

OBJECTIVE: We sought to evaluate the effect of radiofrequency ablation (RFA) on pulmonary vessels with respect to potential of injury of these structures, to assess perfusion-mediated "heat sink" effect, and to consider acute and chronic complications. MATERIAL AND METHODS: RFAs targeted to perihilar, middle third, and peripheral lung regions were created in vivo in the lung of 10 crossbred sheep. The RITA generator and the Starburst XLi electrode with deployable hooks were used. The approach was open, performed under general anesthesia. Lesions 4 cm in diameter at a target temperature of 80 degrees C were created. Acute (immediate postinterventional euthanasia), subacute (96 h), and chronic (28 days) lesions were evaluated macroscopically, and histologic analysis of the vessels was performed. Patency of the vessels, both arteries and veins, was macroscopically assessed by presence or absence of thrombus and the degree of vascular injury and the viability of perivascular pneumocytes as well as endobronchial injury were histologically assessed. RESULTS: In the acute, subacute, and chronic setting, heat sink effect, indicated by invagination of the tissue between vessel and ablated region, was only observed in vessels greater than 3 mm in diameter. Thrombus was seen in 20% of the vessels smaller than 3 mm. On histopathology, vessels smaller than 3 mm showed at least partial vessel wall injury, characterized by endothelial cell necrosis and luminal thrombus. In the vessels greater than 3 mm the extent of vessel wall injury decreased with increasing vessel diameter. No acute complications were noted. For the chronic complications a bronchopleural fistula and a lung abscess were found. CONCLUSION: There seems to be a narrow transition zone for pulmonary vessels around 3 mm, beyond which the heat sink effect was seen consistently and substantial vascular injury was rare.

Animals↗
PubMed2003

Tumor vessel development and maturation impose limits on the effectiveness of anti-vascular therapy.

The effect of anti-vascular agents on the growth of experimental tumors is well studied. Their impact on tumor vasculature, the primary therapeutic target of these agents, is not as well characterized, even though this primarily determines treatment outcome. Hypothesizing that the response of vessels to therapy is influenced by their stage of maturation, we studied vascular development and the vascular effects of therapy in several transplanted murine tumor models. Based on size, perfusion, endothelial cell (EC) proliferation, and the presence of pericytes, tumor vessels segregated into three categories. Least mature were highly proliferative, nonperfused EC sprouts emanating from functional vessels. Intermediate were small, perfused vessels which, like the angiogenic sprouts, were not covered by pericytes. Most mature were larger vessels, which were predominantly pericyte-covered with quiescent ECs and few associated sprouts. Thus, a developmental order, similar to that described during physiological neovascularization, was evident among vessels in growing tumors. This order markedly influenced tumor vessel response to anti-vascular therapy with recombinant interleukin-12. Therapy reduced tumor vessel density, which was attributable to a decrease in angiogenic sprouts and induction of EC apoptosis in pericyte-negative vessels. Although the great majority of vessels in growing tumors lacked pericyte coverage, selective loss of less mature vessels with therapy significantly increased the fraction of pericyte-positive vessels after therapy. These data indicate that the therapeutic susceptibility of tumor vasculature to recombinant murine IL-12 and, potentially, other anti-vascular agents is limited by its level of maturation. An implication is that tumor susceptibility is similarly limited, making pericyte coverage of tumor vasculature a potential indicator of tumor responsiveness.

Angiogenesis Inhibitors↗
PubMed2001

Central retinal vessel trunk exit and location of glaucomatous parapapillary atrophy in glaucoma.

OBJECTIVE: To evaluate whether the position of the central retinal vessel trunk exit on the lamina cribrosa spatially correlates with the location of parapapillary atrophy in glaucoma. DESIGN: Clinic-based, observational, cross-sectional study. PATIENTS: Color stereo optic disc photographs of 95 patients with primary or secondary open-angle glaucoma and 65 healthy persons were morphometrically evaluated. The intrapapillary and parapapillary region was divided into four quadrants. We determined the position of the central retinal vessel trunk exit on the lamina cribrosa surface and measured the area of parapapillary atrophy and neuroretinal rim in the four quadrants. MAIN OUTCOME MEASURES: The area of neuroretinal rim and parapapillary atrophy and the position of the central retinal vessel trunk exit. RESULTS: Comparing measurements between opposite disc quadrants showed that beta zone of parapapillary atrophy was significantly (P < 0.05) larger and that the neuroretinal rim was significantly smaller when beta zone and neuroretinal rim were measured in the disc quadrant most distant to the central retinal vessel trunk exit, than if the beta zone and neuroretinal rim were measured in the quadrant containing the vessel trunk exit. Comparing measurements in the disc quadrants between eyes with different positions of the central retinal vessel trunk exit revealed that, in the respective disc quadrant, the beta zone was significantly larger and the neuroretinal rim was smaller in eyes with the vessel trunk exiting in the opposite disc quadrant than in eyes with the vessel trunk exit located in the respective disc quadrant where the measurements were obtained. CONCLUSIONS: Position of the central retinal vessel trunk exit on the lamina cribrosa influences the location of parapapillary atrophy in glaucoma. The longer the distance to the central retinal vessel trunk exit, the more enlarged is parapapillary atrophy and the smaller is the neuroretinal rim. This relationship agrees with the spatial relationship between glaucomatous neuroretinal rim loss and enlarged parapapillary atrophy in glaucoma. Diagnostically, it may indicate that, in eyes with an abnormal configuration of parapapillary atrophy or with an abnormal position of the central retinal vessel trunk exit, early glaucomatous rim changes should be looked for in the disc sector that is most distant to the central retinal vessel trunk exit and where parapapillary atrophy may be relatively large.

Adult↗
PubMed1996

Endothelium-dependent vasodilation in well-developed coronary collateral vessels.

We examined endothelium-dependent vasodilator responses in well-developed coronary collateral vessels. Collateral vessels and size-matched normal epicardial coronary arteries were isolated from canine hearts 6 months after a hollow plug had been introduced into the left anterior descending coronary artery (LAD) to stimulate collateral vessel growth. Vessel segments were isolated and studied in organ chambers. After preconstriction with prostaglandin F2 alpha, (PGF2 alpha) responses to the endothelium-dependent vasodilators, acetylcholine (ACh), substance P, and bradykinin (BK), as well as the endothelium-independent vasodilator nitroglycerin (NTG), were measured. The maximum relaxation to ACh was greater in collateral vessels (129 +/- 3.6% of the preconstricted tension) than in normal vessels (110 +/- 6.2%, p < 0.001), although the EC50 value for ACh was not significantly different between collateral and normal vessels. Collateral vessels demonstrated sensitivity to BK similar to that of normal vessels, but the maximal vasodilation achieved was greater in collaterals (138 +/- 4.6% of preconstricted tension) than in normal vessels (108 +/- 5.0%, p < 0.05). Both substance P and NTG produced dose-related relaxation that was similar in collateral vessels and normal arteries. These findings demonstrate that endothelium-dependent relaxation is intact in well-developed coronary collateral vessels.

Acetylcholine↗
PubMedDate not supplied

Image feature analysis and computer-aided diagnosis in digital radiography. 2. Computerized determination of vessel sizes in digital subtraction angiography.

We developed an iterative deconvolution technique to determine the size of a "blurred" vessel in a digital subtraction angiographic (DSA) image by taking into account the unsharpness of the DSA system. Initially, a region of interest over a small segment of the contrast-filled vessel was selected in a DSA image, and the center line of the opacified vessel was determined by polynomial curve fitting of the locations of the peak pixel values along the vessel image. The blurred image profile was then obtained from pixel values across the vessel in a direction perpendicular to the center line. This measured profile was compared iteratively with a calculated profile for various size vessels, which was obtained from a cylindrical vessel model and from the line spread function, until the root-mean-square difference between the two profiles was minimized. The size of a cylindrical vessel yielding the matched profile was considered the best estimate of the unknown vessel size. Studies with a blood vessel phantom indicated that vessels larger than 0.5 mm could be measured with an accuracy and precision of approximately 0.1 mm, which is about 1/3 of the pixel size used in our DSA system. Details of our approach and some clinical vessel images with and without simulated stenotic lesions are presented.

Angiography↗
PubMed2004

Norrie gene product is necessary for regression of hyaloid vessels.

PURPOSE: To investigate the nature and origin of the vitreous membranes in mice with knock-out of the Norrie gene product (ND mice). METHODS: Eighty-two eyes of ND mice of different age groups (postnatal day [P]0-13 months) and 95 age-matched wild-type control mice were investigated. In vitreoretinal wholemounts and in sagittal sections, vessels and free cells were visualized by labeling for lectin. In addition, staining with a marker for macrophages (F4/80) and collagen XVIII/endostatin known to be involved in regression of hyaloid vessels was performed for light and electron microscopic investigations. Endostatin expression was confirmed by Western blot analysis. RESULTS: Wild-type controls showed the typical pattern of hyaloid vessels, their regression and concomitantly retinal vasculogenesis and angiogenesis. Hyaloid vessels all stained for endostatin, whereas retinal vessels remained unstained. In ND mice, 1 to 5 days after birth, the hyaloid and retinal vasculatures were comparable to that in control mice. The hyaloid vessels also stained for endostatin. Numerous F4/80-positive cells were present adjacent to the vessels. With increasing age, only a few connecting branches of the hyaloid vessels regressed. Even in old mice most of the hyaloid vessels persisted. The vessels still stained for endostatin. Retinal angiogenesis was impaired. CONCLUSIONS: Retrolental membranes in ND mice consist of persistent hyaloid vessels, indicating that the ND gene product is important for the process of regression of these vessels. The ND gene product neither influences endostatin expression nor the presence of macrophages.

Animals↗
PubMed2003

[Feeder vessel treatment of choroidal neovascularization in age-related macular degeneration].

INTRODUCTION: To report on the results of feeder vessel treatment for choroidal neovascularization in age-related macular degeneration (AMD). MATERIAL AND METHODS: Retrospective study of 40 patients presenting subfoveal classic choroidal neovascularization (CCNV) and/or occult choroidal neovascularization (OCNV) with or without fibrovascular pigment epithelium detachment (PED), based on fluorescein angiography (FA) and indocyanine green angiography (ICG). Visual acuity was measured using Snellen lines and/or ETDRS. The feeder vessels were visualized with high-speed ICG angiography (confocal scanning laser ophthalmoscope, Heidelberg HRA, Heidelberg, Germany). Feeder vessels were identified as very thin vessels with early filling and rapid emptying. Feeder vessel closure was achieved by laser photocoagulation treatment with either minipulse infrared laser therapy (810 nm), microburst, or yellow laser (568 nm). Post-treatment high-speed ICG angiography follow-up was recommended to the patient immediately or the day after the treatment. The number of treatments and location of the feeder vessels in relation to the macula as well as FA, ICG, and visual acuity results were assessed. If necessary, other treatment techniques such as photodynamic therapy (PDT) or transpupillary thermotherapy (TTT) were offered to the patient when leakage was still present. RESULTS: The patients were followed for an average of 6.2 months (2-9 months). Twenty-six women and 14 men (mean age, 72 years; range, 51-95) were included. Eight patients demonstrated classic neovascularization, 32 presented occult neovascularization, including 17 cases of vascularized PED and 15 retrofoveal plaques. The average number of treatments was 1.8 (range, 1-4 treatments). Location of feeder vessels were as follows: nine superior-macular, 18 inferior-macular, six nasal-macular and 11 temporal-macular. Visual acuity improved two lines or more in nine patients (22.5%), decreased 2 lines or less in five patients (12.5%) and was stable in 26 patients (65%). After feeder vessel treatment, seven patients showed improvement of the anatomical aspect of the AMD lesions, with a reduction in leakage. Except for one subretinal hemorrhage, no complications after feeder vessel treatment were observed. CONCLUSION: Feeder vessel treatment is a technique requiring high-speed ICG angiography to detect the feeder vessels located at a distance from the subfoveal OCNV, CCNV, and PED. Although the final visual acuity result was for the most part stabilization, the technique appeared to be safe and reproducible. In patients who were not eligible for other therapies such as PED, feeder vessel treatment seemed to be a reasonable alternative.

Aged↗
PubMed1997

Role of astrocytes in the control of developing retinal vessels.

PURPOSE: To assess the role of astrocytes in controlling the growth of developing retinal vessels. METHODS: Growth of retinal vessels in the neonatal rat retina was examined in three conditions: normal development, cyclic hyperoxia, and normoxia (1 day 70% to 75% oxygen, 1 day room air for up to seven cycles from birth, and room air for up to 16 days), and direct hypoxia (10% oxygen from postnatal day 3 [P3]). Retinas were examined as wholemounts labeled for astrocytes, microglia, and blood vessels and in some experiments for the fragmentation of DNA characteristic of apoptosis. RESULTS: In normoxia, superficial retinal vessels formed to the processes of astrocytes. In cyclic hyperoxia, the depletion of superficial retinal vessels and subsequent neovascularization described by others were confirmed. The neovascularization was preceded by the depletion by apoptotic death of the astrocyte population, first between vessels but eventually breaching the glia limitans along vessels. The earliest forms of neovascularization resembled microaneurysms, each protruding through a defect in the glia limitans of a capillary. Neurons of the ganglion cell layer survived. Direct hypoxia from P3 caused hypertrophy of superficial vessels. Between P3 and P6, some vessels accelerated past the still-spreading astrocytes, often growing out of the retina into the vitreous humor. Direct hypoxia also caused astrocyte degeneration, but capillaries retained astrocyte investment and were not the site of vascular damage. By P8, breaches in the astrocytic glia limitans became prominent but were restricted to large veins. At such breaches, bleeding into the vitreous humor was common. CONCLUSIONS: Retinal vessels normally develop in close association with astrocytes. Where that association is broken, preretinal vessels may grow or bleed into the vitreous humor. Astrocytes play important roles in constraining retinal vessels to the retina and in maintaining their integrity.

Animals↗