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PubMed2000

[Development of neovascularization of the optic papilla, retina and iris. Dependence on site and extent of retinal ischemia].

BACKGROUND: Is it possible to find a correlation between the localisation of neovascularisations and the localisation and extension of the retinal ischemia? Ischemia was recognized not as capillary non-perfusion but as impaired retinal perfusion. MATERIALS AND METHODS: Patients with retinal ischemia like in diabetic retinopathy (n = 95), central retinal vein occlusion (n = 9), ischemic ophthalmopathia (n = 8) and branch vein occlusion (n = 5) who had neovascularisations were examined. The localisation of retinal ischemia and the localisation of neovascularisations were diagnosed by fluorescein angiography and biomicroscopy. RESULTS: Neovascularisations at the different places were observed with different frequencies depending on localisation and extension of retinal ischemia. Panretinal ischemia caused by diabetic retinopathy type B was followed by neovascularisations at iris in 69.2% with participation of the anterior chamber angle in 61.1%. In diabetic retinopathy type A with limited retinal ischemia neovascularisations of iris and chamber angle were significantly less frequent (31.7%/25%). On the contrary panretinal ischemia caused by central retinal vein occlusion was followed by neovascularisations elsewhere in 11.1%; in diabetic retinopathy type C with limited retinal ischemia neovascularisations elsewhere were observed only in 66.7%. CONCLUSIONS: There is a relationship between the localisation of the neovascularisations and the localisation and the extension of the retinal ischemia. The differentiation of PDR in different ischemic types is confirmed by different frequencies of the neovascularisation sites depending on the ischemic type. The explanation for the frequent finding of neovascularisations at the disk caused by the peripheral type of diabetic retinopathy is a communication via Cloquet's canal between periperal retina and papilla.

Diabetic Retinopathy↗
PubMed1993

Argon laser scatter photocoagulation in treatment of branch retinal vein occlusion. A prospective clinical trial.

The objective of this prospective study was to ascertain whether scatter argon laser photocoagulation to the involved sector in major branch retinal vein occlusion and ischemic hemicentral retinal vein occlusion (a) prevents development of retinal and/or optic disk neovascularization and vitreous hemorrhage, and (b) affects visual acuity, visual fields and macular retinal lesions. The study was done in 271 eyes allocated to either treated (n = 61 eyes) or untreated (n = 210) groups. In this study, on an average follow-up of 3.6 years, the laser treatment (1) significantly reduced the risk of development of retinal neovascularization and vitreous hemorrhage, (2) did not affect the visual acuity and macular retinal lesions, and (3) produced a significant worsening in the peripheral visual fields compared to the untreated eyes. In view of our findings, we recommend that argon laser photocoagulation treatment should be given only when neovascularization is seen and not otherwise, because in the latter case, its detrimental effects may outweigh its beneficial ones.

Aged↗
PubMed1984

Recurrent subarachnoid bleeding in association with dural substitute. Report of three cases.

Three cases of recurrent subarachnoid bleeding are reported. The hemorrhages occurred at intervals of up to 10 years after posterior fossa craniotomy with closure using grafts of Silastic dural substitute. In one case, reexploration showed that the hemorrhage had arisen from a neomembrane formed at the site of the dural substitute; in the others, circumstantial evidence suggested a similar pathology.

Adolescent↗
PubMed1998

Increased expression of placenta growth factor in proliferative diabetic retinopathy.

Proliferative diabetic retinopathy is thought to be mediated by the hypoxic regulation of angiogenic growth factors, in particular the vascular endothelial growth factor (VEGF) family. The aim of this study was to determine if placental growth factor (PIGF), a recently identified member of the VEGF family, was expressed in diabetic eyes undergoing preretinal neovascularization. Rabbit anti-PIGF antiserum was raised using a 20-amino acid N-terminal sequence to PIGF and did not cross react with VEGF165. Immunohistochemistry was performed on specimens of normal retina (n = 8), diabetic retina in the absence (n = 7) and presence (n = 4) of proliferative retinopathy, scatter laser-treated diabetic retina (n = 7), excised fibrovascular preretinal membranes (n = 12), and nondiabetic fibrocellular epiretinal (n = 7) membranes. PIGF levels were also determined in vitrectomy specimens from patients with either proliferative diabetic retinopathy or macular hole. PIGF immunoreactivity was intensely localized to the endothelial and perivascular regions of newly formed blood vessels of excised fibrovascular preretinal membranes. Intense localization of PIGF protein was also observed in superficial retinal vessels in diabetic retinae adjacent to neovascular preretinal membranes. Localization of PIGF was weak or absent in diabetic retinae that showed no evidence of neovascular proliferation. PIGF protein was also absent in normal retinae, in diabetic retinae that had received extensive treatment with scatter laser photocoagulation, and in nonvascularized epiretinal membranes. PIGF was present in all diabetic vitreous samples (mean 103 pg/ml) but nondetectable in control samples. These results strongly implicate a role for PIGF in the pathogenesis of proliferative diabetic retinopathy.

Adult↗
PubMed1988

Site-directed neovessel formation in vivo.

Angiogenesis is an important component of organogenesis and wound repair and occurs during the pathology of oncogenesis, atherogenesis, and other disease processes. Thus, it is important to understand the physiological mechanisms that control neovascularization, especially with methods that permit the molecular dissection of the phenomenon in vivo. Heparin-binding growth factor-1 was shown to bind to collagen type I and type IV. When complexed with gelatin, heparin-binding growth factor-1 can induce neovascularization at polypeptide concentrations that are consistent with the biological activity of the mitogen in vitro. The adsorption strategy induces rapid blood vessel formation at and between organ- and tissue-specific sites and permits recovery of the site-specific implant for examination and manipulation by molecular methods.

Animals↗
PubMed2001

[Surgery for choroidal subfoveal neovascularization in patients with severe myopia. Retrospective analysis of 17 patients].

UNLABELLED: Treatment of choroidal neovascularization in pathological myopia is still controversial. METHODS: A retrospective analysis of 17 patients with severe myopia (>-6) and subfoveal choroidal neovascularization who underwent surgical removal of choroidal neovascularization, was performed. The patient population consisted of 2 groups: 9 patients younger than 50 years and 8 patients older than 50 years. All the patients underwent vitrectomy with surgical removal of subfoveal choroidal neovascularization. RESULTS: We reviewed the postoperative clinical and angiographic findings. In group I, visual acuity improved in 4 eyes (44%), remained unchanged in 4 eyes (44%) and decreased in one eye. In group II, none of the patients had visual improvement, visual acuity remained unchanged in 6 eyes (71%), and decreased in 2 eyes. CONCLUSION: The visual outcomes in most patients in this series were better than their natural history. Surgical removal of subfoveal choroidal neovascularization associated with severe myopia may provide visual benefit in young patients. A prospective, randomized clinical trial is necessary to determine the place of this surgical procedure.

Adult↗
PubMedDate not supplied

Senile disciform macular degeneration complicated by massive hemorrhagic retinal detachment and angle closure glaucoma.

Six eyes developed angle-closure glaucoma secondary to total hemorrhagic retinal detachment that occurred as a rare complication of senile disciform macular degeneration. The patients were all elderly with known senile macular choroidal degeneration. They had no history of eye surgery and experienced sudden loss of vision followed by pain. Balloons of retinal detachment were pushed tightly against the lens in a characteristic "Y suture" appearance causing shallowing of the anterior chamber and glaucoma. Pathologic examination of three eyes revealed that the choroid was not detached but that a massive subretinal hemorrhage was present. Neovascular tissue in macular disciform lesions was found in every case and was the probable source of hemorrhage. Sheets of avulsed retinal outer segments were seen incarcerated in subretinal blood in two cases, and drainage of this subretinal blood in three cases did not restore useful vision.

Aged↗
PubMed2004

Increased vascular wall thrombogenicity combined with reduced blood flow promotes occlusive thrombus formation in rabbit femoral artery.

OBJECTIVE: Plaque disruption does not always result in complete thrombotic occlusion. The mechanism of arterial thrombus propagation remains unclear. METHODS AND RESULTS: We studied how vascular wall thrombogenicity and blood flow reduction affect thrombus propagation using a rabbit model of single and repeated balloon injury. After balloon injury of the normal femoral artery, the blood flow was reduced to 50%, 25%, or 10% (n=5). Small mural thrombi composed of aggregated platelets were produced, but no occlusive thrombi developed in any flow reduction. Three weeks after the first balloon injury, neointima with tissue factor expression and increased procoagulant activity was developed. Balloon injury of the neointima with the same blood flow reduction (n=5) induced fibrin-rich thrombus formation. Additionally, injury with flow reduced to 25% and 10% promoted thrombus propagation resulting in vessel occlusion within 160+/-18 and 71+/-17 seconds, respectively. An injection of anti-von Willebrand factor (vWF) monoclonal antibody (AJW200; 1.0 mg/kg) prevented occlusive thrombus formation. CONCLUSIONS: Increased vascular wall thrombogenicity together with a substantial blood flow reduction is crucial for occlusive thrombus formation, and vWF plays an important role in thrombus propagation. Reduced blood flow at plaque disruption sites might contribute to thrombus propagation leading to acute coronary syndromes.

Animals↗
PubMed2003

In vivo adenovirus-mediated delivery of a uPA/uPAR antagonist reduces retinal neovascularization in a mouse model of retinopathy.

Diabetic retinopathy and retinopathy of prematurity are among the leading causes of vision impairment throughout the world. Both diseases are characterized by pathological angiogenesis, which severely impairs vision. Extracellular proteinases play important roles in endothelial cell migration during angiogenesis. Amino-terminal fragment (ATF) is an angiostatic molecule that targets the uPA/uPAR system and inhibits endothelial cell migration. The angiostatic effect of ATF has been demonstrated in models of cancer, but has never been assessed in pathological retinal neovascularization. Endostatin also has angiostatic effects on tumor growth and retinal neovascularization. We used an adenoviral vector carrying the murine ATF (AdATFHSA) or endostatin gene coupled to human serum albumin (HSA) (AdEndoHSA) to increase the half-life of the therapeutic protein in the circulation. We induced retinopathy by exposing 7-day-old mice to high levels of oxygen. They were intravitreally injected with the vectors. Local injection of AdATFHSA or AdEndoHSA reduced retinal neovascularization by 78.1 and 79.2%, respectively. Thus, the adenovirus-mediated delivery of ATFHSA or EndoHSA reduces retinal neovascularization in a mouse model of hypoxia-induced neovascularization.

Adenoviruses, Human↗
PubMed1997

Mast cell interactions with the nervous system: relationship to mechanisms of disease.

In summary, mast cell interactions in the nervous system are relevant to both physiological processes (i.e. reproduction) and pathologic states (i.e. inflammatory demyelination, painful disorders, toxic and metabolic disease, and tumor angiogenesis). Their physiologic roles may contribute to gender-related vulnerability to inflammatory disease and may modulate sensitivity to pain. Mast cells are universally involved in tissue repair and they release and respond to trophic factors such as NGF. These cells also produce and react to cytokines, and thus appear to play a role in tissue degeneration as well as repair. In certain neurological diseases, i.e. multiple sclerosis and Guillain-Barré syndrome, the ability of mast cell proteases to degrade specific myelin proteins suggests that these cells are agents, rather than bystanders, in the demyelinative process. Even more intriguing is their recently identified capacity to process bacterial antigen as efficiently as activated macrophages, suggesting that a more critical role than previously suspected might be considered for mast cells in CNS and PNS demyelination. In experimental metabolic disorders such as galactose intoxication and thiamine deficiency, mast cells appear to play a pathogenic role. Thus, in galactose intoxication, altered BNB vascular permeability occurs in conjunction with mast cell proliferation and degranulation, while in thiamine deficiency, increased histamine levels have been reported in the rat thalamus (79) and are associated with cell death and proliferation as well as mast cell degranulation (Powell and Langlais, unpublished observations). Structural interactions between mast cells and a variety of other cells have been observed, as well as close approximation of mast cells to nerve endings in tissues in which mast cells are especially active. Due to their paracrine nature, mast cells can modulate events in their microenvironment through explosive degranulation, piecemeal degranulation, or "transgranulation" as they insert granules into neighboring cells. Lastly, these cells play specific roles in reparative processes, e.g. angiogenesis, and are active in neoplastic states, including von Recklinghausen's disease (neurofibromatosis). Their involvement may have been underestimated in neuropathological studies, to date, by a reliance on staining techniques that are inadequate for identifying degranulated and therefore activated mast cells (4). More exacting histochemical and immunostaining procedures will help to fully realize the extent of their participation in physiological and pathological processes.

Animals↗
PubMed1996

Subfoveal choroidal neovascularization in punctate inner choroidopathy. Surgical management and pathologic findings.

PURPOSES: To evaluate submacular surgery for the management of subfoveal choroidal neovascularization in punctate inner choroidopathy, to describe the histopathology and ultrastructure of the excised subretinal tissue, and to propose a staging system that characterizes the development of choroidal neovascularization with associated subretinal fibrosis. METHODS: The authors reviewed the records of five patients (6 eyes) with punctate inner choroidopathy who underwent submacular surgery for subfoveal choroidal neovascularization. Surgical specimens were examined using light and transmission electron microscopy. RESULTS: Visual improvement was noted postoperatively in all six eyes, with follow-up ranging from 8 to 36 months (median, 14 months). Recurrences (6 in 4 eyes) were common. Five of the six recurrences required additional procedures: three were managed surgically, two with laser photocoagulation, and one with observation. "Bridging" of separate foci of choroidal neovascularization resulted in stellate or "dumbbell-shaped" areas of subretinal fibrosis in four of six eyes. Histopathologic evaluation of the excised tissue showed endothelial-lined vascular channels, retinal pigment epithelium, lymphocytes, plasma cells, fibrocytes, collagen fragments, and rarely, outer retinal elements. CONCLUSIONS: Subfoveal choroidal neovascularization in punctate inner choroidopathy may be managed with submacular surgery. Recurrences are common and may result in substantial loss of vision. Choroidal neovascular membranes with an accompanying fibrotic reaction are responsible for the stellate or dumbbell-shaped areas of subretinal fibrosis. No beneficial effect was demonstrated using corticosteroid treatment of the choroidal neovascularization.

Adult↗
PubMed1990

Argon laser panretinal photocoagulation in ischemic central retinal vein occlusion. A 10-year prospective study.

We conducted a prospective, planned study of argon laser panretinal photocoagulation (PRP) in ischemic central retinal vein occlusion (CRVO) over a 10-year period in 123 eyes. On comparing the lasered eyes versus the nonlasered eyes, there was no statistically significant difference between the two groups in the incidence of development of angle neovascularization (NV), neovascular glaucoma (NVG), retinal and/or optic disc NV, or vitreous hemorrhage, or in visual acuity. Our study, however, did show a statistically significant (P = 0.04) difference in the incidence of iris NV between the two groups, with iris NV less prevalent in the laser group than in the nonlaser group, but only when the PRP was performed within 90 days after the onset of CRVO. The other parameter which showed a statistically significant difference between the two groups was the peripheral visual fields-the laser group suffered a significantly (P less than or equal to 0.03) greater loss than the non-laser group. We discuss the implications of these findings in light of the natural history of ischemic CRVO and of ocular NV. Since the original rationale for advocating PRP in ischemic CRVO was the proven beneficial effect of PRP on ocular NV in proliferative diabetic retinopathy, we also discuss the disparities in the disease process between ischemic CRVO and proliferative diabetic retinopathy and in their responses to PRP.

Aged↗
PubMed1984

Heparan structure and the modulation of angiogenesis.

It is postulated that the angiogenic potential of tissues is influenced by the fine structure of heparan glycosaminoglycans present in the tissues. Possible mechanisms involved are discussed. It is suggested that compounds chemically related to heparans might usefully act as inhibitors of pathological angiogenesis.

Capillaries↗
PubMed2005

Pathological evaluation of angiogenesis in human tumor.

Angiogenesis is the process in which endothelial cells divide and migrate to form new capillaries, which support the continued growth of tumor through blood flow. Cancer-induced angiogenesis in general represents results of increased expression of angiogenic factors such as VEGF or decreased expression of anti-angiogenic factors, or a combination of both events. Numerous reported studies have demonstrated that angiogenesis plays an important role in tumor progression and metastasis of the great majority of human solid tumors. Furthermore, the quantitation of tumor angiogenesis in resected specimens of human tumor or surgical pathology specimens contribute to assessment of biological behavior and/or clinical outcome of the patients with cancer. Therefore, it is very important to assess the status of angiogenesis or cancer-induced vessels in resected tumor or surgical pathology specimens including those before and after the neoadjuvant therapy. It then becomes very important for pathologists involved in this evaluation to determine which methods to use in order to obtain accurate and reproducible results. In this short review, the status of an analysis of angiogenesis in surgical pathology specimens through analyzing vascular density or vasculatiry using immunohistochemical staining of CD34, a specific immunohistochemical marker for endothelial cells and subsequent evaluation of immunoreactivity in surgical pathology specimens will be summarized.

Animals↗