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Biomedical subjects

A R Buckley

Publications and source records attributed to A R Buckley.

At least 19 recordsLinked to original sources
PubMed1999

Radiofrequency ablation followed by resection of malignant liver tumors.

BACKGROUND: Radiofrequency ablation (RFA) has recently been used to treat liver tumors, but few clinical reports have described the pathological characteristics of radiofrequency ablation in human specimens. This study delineates the gross pathologic and histochemical changes induced by RFA in benign and malignant human liver tissue and confirms the tumor necrosis described in early clinical reports. METHODS: Ten patients with metastatic tumors of the liver received a single treatment of ultrasound-guided percutaneous RFA to 12 tumors. Hepatic resection was carried out within 6 weeks of RFA. Specimens were stained with standard hematoxylin and eosin stain followed by oxidative stain to determine if there was evidence of viable tumor within the zone of ablation. RESULTS: Nine of the 12 ablations were resected. Microscopic examination within the zone of ablation showed successful ablation in 8 of the 9 resected ablations. CONCLUSIONS: Percutaneous RFA creates well-circumscribed areas of tumor necrosis with apparent cell death using an oxidative stain. Further investigation is encouraged to determine the clinical effectiveness of radiofrequency ablation in the complete destruction of liver tumors for palliative or curative intent.

Aged↗
PubMed1999

Ascorbic acid recycling in Nb2 lymphoma cells: implications for tumor progression.

Analysis of cultured rat "Nb2 lymphoma" cell lines, showing different degrees of malignant progression, can lead to identification of phenotypic changes associated with this phenomenon in T-cell cancers. In the present study we have compared the metastatic sublines, Nb2-11 and Nb2-SFJCD1, with regard to ascorbate and glutathione recycling, important processes in cellular protection from oxidative stresses. Whereas the Nb2-11 subline is prolactin (PRL)-dependent, the genetically related Nb2-SFJCD1 subline is growth factor-independent and shows more chromosomal alterations, indicative of more advanced progression. The Nb2-SFJCD1 cells, compared to the Nb2-11 cells, were less sensitive to toxic effects of dehydroascorbate, a potentially toxic oxidation product of ascorbate. Results were consistent with a significantly higher production of reducing equivalents (e.g., NADPH, GSH) and an accelerated reduction of dehydroascorbate by homogenates of Nb2-SFJCD1 cells. However, the increased resistance was apparently not directly related to the cellular uptake and reduction of dehydroascorbate by whole cells, which was similar in both cell lines. Observations indicate that Nb2 lymphoma cells, in their progression to malignancy, can acquire an enhanced capability to protect themselves from oxidative damage assisting them in withstanding the oxidative stress that anti-neoplastic drugs can cause. The adaptation may also be a mechanism that is utilized by tumor cells in suppressing apoptosis and other protective cellular functions facilitating, or potentiating, a tumor cell's ability to become more metastatic. However, the mechanism leading to this augmented capacity of Nb2 lymphoma cells to resist oxidative stress in not known and is the subject for further study.

Animals↗
PubMed1999

Prolactin regulation of pim-1 expression: positive and negative promoter elements.

The lactogen-dependent rat Nb2 lymphoma is a useful model to investigate PRL signaling pathways that lead to regulation of gene transcription. A primary mechanism coupled to PRL receptor (PRLR) activation in Nb2 cells involves phosphorylation by Jak-family tyrosine kinases of one or more signal transducers and activators of transcription (Stat) factors which subsequently bind to gamma-interferon activation sequences (GAS) within promoter regions of target genes. However, it is presently unclear whether this mechanism is operative as a means for regulating PRL-induced gene expression to the exclusion of other signaling pathways. Previously, we reported that PRL directly stimulated rapid expression of the protooncogene, pim-1, at the mRNA and protein levels in lactogen-dependent Nb2-11 cells. In the present study, experiments were conducted to evaluate signaling mechanisms by which PRL regulates transcription of pim-1. Toward this end, a 1,268-bp segment upstream of the transcription initiation site of the 5'-pim-1 promoter and a series of deletion mutants were ligated upstream of the chloramphenicol acetylase transferase (CAT) gene in an expression vector that was introduced into FDC/Nb2 cells, a premyeloid line that stably expresses the intermediate form of the PRLR. Analysis of PRL-treated cultures indicated that two elements [distal (DE), -427 to -336 bp and proximal (PE), - 104 to -1] but not several GAS or GAS-like sequences were required for hormone activation of the pim-1 promoter. Moreover, treatment of Nb2-11 cells with PRL activated protein binding to these elements assessed by gel mobility shift assay. Deoxyribonuclease I (DNase I) protection experiments revealed a motif containing a nuclear factor-1 (NF-1, -224 to -217 bp) half-site that was hydrolyzed when exposed to extracts from PRL-treated cells but protected by proteins from unstimulated cells. Gel mobility shift analysis of this sequence showed decreased protein binding after PRL stimulation. It is concluded that the PRLR initiates pim-1 transcription by a mechanism that involves transcriptional activation by factors that stimulate the DE- and PE-sites and derepress a NF-1-containing element. Moreover, this mechanism appears to be independent of an interaction between Stat transcription factors and GAS-like elements present within the promoter.

Animals↗
PubMed1999

Proteolysis of human prolactin: resistance to cathepsin D and formation of a nonangiostatic, C-terminal 16K fragment by thrombin.

The N-terminal 16K fragments of rat and human PRLs possess angiostatic activity. 16K PRL has also been detected in vivo in both humans and rats. Based on an in vitro study, cathepsin D, an acid protease, has been implicated in the generation of rat 16K PRL. However, the proteolytic cleavage of human PRL has not been demonstrated. Our objective was to identify an enzyme that is capable of forming an angiostatic human 16K PRL. To confirm the angiostatic action of rat 16K PRL, the fragment was generated by incubating 23K PRL with rat mammary microsomal fraction at pH 3.2. Upon incubation with human umbilical vein endothelial cells (HUVEC), rat 16K PRL, but not 23K PRL, inhibited basal- and basic fibroblast growth factor-stimulated cell proliferation. Intact rat and human PRLs were then incubated with cathepsin D or acidified microsomal pellets of MCF-7 human breast cancer cells. Analysis by SDS-PAGE showed cleavage of rat, but not human, PRL. Next, hormones were incubated with thrombin at pH 7.4. As shown by SDS-PAGE, digestion of both human and rat PRL by thrombin resulted in the formation of 16K fragments. PRL contained within human amniotic fluid was also cleaved by thrombin. Enzyme specificity was supported by prevention of cleavage by the thrombin inhibitor hirudin. When tested with HUVEC, the human 16K PRL was devoid of angiostatic activity. The activity of this fragment in the Nb2 lymphoma bioassay was 10- to 15-fold lower than that of 23K PRL. Mass spectrometry revealed that the fragment has a mass of 16,878.30+/-15.8 Daltons. Subsequent N-terminal sequencing showed that the thrombin cleavage occurred between amino acid residues 53 (Lys) and 54 (Ala), resulting in the formation of a C-terminal, not an N-terminal, 16K fragment. We conclude that, unlike rat PRL, human PRL is resistant to cleavage by cathepsin D. Thrombin at a physiological pH can generate a C-terminal 16K fragment of human PRL that is not angiostatic and retains little mitogenic activity. We suggest that the precise nature of endogenous 16K PRL fragments that are present in human tissues and body fluids should be carefully examined.

Animals↗
PubMed1999

Proteolysis of heat shock transcription factor is associated with apoptosis in rat Nb2 lymphoma cells.

Previously, we reported that prolactin (PRL)-dependent Nb2 lymphoma cells exhibit an aberrant heat shock response because of cysteine protease-mediated fragmentation of the heat shock transcription factor (HSF). Moreover, exposure of the cells to PRL abrogated heat-induced HSF proteolysis. The present study was conducted to investigate whether HSF proteolysis is a component of the apoptotic process in this model. Initially, the effect of heat stress (41 degrees C for 1 h) on apoptosis, determined by agarose gel electrophoresis and flow cytometric analysis, was evaluated in PRL-dependent Nb2-11 cells and in an autonomous subline (Nb2-SFJCD1). Heat was found to induce HSF proteolysis concomitant with activation of apoptosis in each cell line; treatment with PRL blocked these effects. To determine whether HSF proteolysis occurred as a generalized phenomenon associated with apoptosis, the effects of other activators of this process were evaluated. Vinblastine, cycloheximide, and thapsigargin stimulated fragmentation of HSF and hydrolysis of DNA in each cell line. The addition of PRL blocked the effects of vinblastine but was ineffective in cells treated with either cycloheximide or thapsigargin. Iodoacetamide, a cysteine protease inhibitor that blocks HSF fragmentation, also inhibited apoptosis. In addition, Z-VAD, a general caspase antagonist, blocked vinblastine-induced fragmentation of HSF and DNA, suggesting that the enzyme responsible for proteolysis of the transcription factor was likely a caspase family member. The results suggest that proteolysis of HSF reflects the action of one or more caspases activated as a consequence of stimulation of cell death. It is concluded that HSF may represent a previously unrecognized substrate for caspases or other cysteine proteases activated during apoptosis.

Alkylating Agents↗
PubMed1998

Changes in glutathione redox cycling and oxidative stress response in the malignant progression of NB2 lymphoma cells.

Differential analysis of closely related Nb2-lymphoma cell lines can be used for identification of changes in biochemical properties associated with the malignant progression of certain T-cell cancers. As tumors progress, they tend to show metabolic alterations such as an increased resistance to oxidative stress, a characteristic that may be correlated with changes in intrinsic antioxidant levels (e.g., glutathione) and in activities of associated enzymes such as the glutathione redox pathway. Whether increases in malignancy of Nb2 cells were associated with changes in cellular glutathione levels and activities of glutathione-metabolizing enzymes was addressed. To evaluate this relationship, 3 cell lines, showing increased malignancy, were used: Nb2-U17 (hormone-dependent, non-metastatic), Nb2-11 (hormone-dependent, metastatic), Nb2-SFJCD1 (growth factor-independent, metastatic). Compared to Nb2-U17 and Nb2-11 cells, the highly progressed Nb2-SFJCD1 lymphoma cells maintain low basal glutathione levels. However, the Nb2-SFJCD1 cells display an enhanced capacity to produce glutathione when challenged with an oxidative stress and show a significantly higher resistance to H2O2-induced apoptosis.

Animals↗
PubMed1998

Prolactin stimulates phosphorylation of the human T-cell antigen receptor complex and ZAP-70 tyrosine kinase: a potential mechanism for its immunomodulation.

Prolactin (PRL) is an immunomodulatory hormone which promotes T-cell activation and proliferation. However, the intracellular mechanisms of this action in normal lymphocytes are unknown. Because the PRL receptor (PRLR) activates several signals also activated by the T-cell antigen receptor (TCR)/CD3 complex, we evaluated whether signaling "cross-talk" occurs between these distinct receptors. Using human thymocytes, human peripheral blood lymphocytes and the rat Nb2 lymphoma T-cell, we found that PRL induced rapid phosphorylation of multiple, TCR/CD3 complex proteins, an event required for lymphocyte activation. Two of these phosphorylated proteins were identified to be CD3 epsilon and ZAP-70 tyrosine kinase, molecules essential for TCR function. Further, PRL induced tyrosyl phosphorylation of ZAP-70 in each population of T-lymphocytes tested, demonstrating for the first time that ZAP-70 is a target of PRL action. Taken together, our results suggest that the PRLR directly affects T-lymphocyte activation by means of signaling cross-talk with the TCR/CD3 complex.

Adjuvants, Immunologic↗
PubMed1998

Heat-induced proteolysis of HSF causes premature deactivation of the heat shock response in Nb2 lymphoma cells.

Nb2-11 cells, a prolactin (PRL)-dependent T-lymphoma cell line, display an unusual response to heat stress characterized by the lack of expression of inducible hsp70 mRNA transcripts and a reduction in the levels of constitutively expressed heat shock protein (HSP) genes. This aberrant heat shock response appears to result from heat-induced proteolytic fragmentation of heat shock factor (HSF). In this report, we have investigated processes that promote HSF fragmentation and identified characteristics of a protease that may be responsible for this effect. Cycloheximide did not affect HSF fragmentation of heat-shocked Nb2-11 cells suggesting that proteases responsible for this proteolysis are constitutively expressed and become activated by the heat shock conditions. PRL protected Nb2-11 cells from heat-induced fragmentation whereas sodium butyrate (NaBT) rendered a fragmentation-resistant cell line (Nb2-SFJCD1 cells) sensitive to HSF proteolysis. Heat-induced HSF fragmentation in Nb2-11 cells was not affected by pretreating cultures with several serine protease inhibitors. However, a dose-dependent decrease in HSF fragmentation was achieved by pretreating cultures with iodoacetamide, a cysteine protease inhibitor that is active in apoptosis. Apparently, the heat shock response in Nb2 cells is attenuated by a mechanism that involves the premature deactivation of HSF by its selective proteolysis. Attenuation of this critical cellular stress response may be an important contributor to the progression of hormone-dependent tumors possibly by influencing apoptotic processes known to regulate the activity of these cells.

Animals↗
PubMed1998

Prolactin-regulated apoptosis of Nb2 lymphoma cells: pim-1, bcl-2, and bax expression.

Lactogen-dependent Nb2 lymphoma cells, widely employed for studying prolactin (PRL) mitogenic mechanisms, are also useful for investigations of apoptosis in T-lineage lymphocytes. Utilizing PRL-dependent Nb2-11 cultures, apoptosis-regulatory genes were evaluated for participation in dexamethasone- (DEX) provoked cell death or its inhibition by PRL. Treatment of lactogen-starved, G1-arrested Nb2-11 cells with DEX (100 nM) activated apoptosis within 12 h evaluated by flow cytometric analysis of fragmented DNA. This effect was not associated with altered expression of bcl-2, bax, or pim-1. PRL (10 ng/mL), coincubated with DEX-treated cells, completely blocked DEX-induced apoptosis. This inhibition was associated with increased expression of bcl-2 and pim-1 mRNAs, genes reported to suppress apoptosis, within 2-6 h after addition of the hormone. Moreover, the increased transcription of bcl-2 and pim-1 was coupled to increases in their protein levels. The results suggest that bcl-2, bax, and pim-1 do not play a critical role in DEX-induced apoptosis in Nb2 cells. However, expression of bcl-2, together with pim-1, may have a role in mediating the antiapoptotic actions of PRL.

Animals↗
PubMed1998

Prolactin receptor signaling: shared components with the T-cell antigen receptor in Nb2 lymphoma cells.

Previously, we reported that activation of the human prolactin receptor (PRLR) produced a protein phosphorylation pattern strikingly similar to that provoked by Concanavalin A (Con A), an activator of the T-cell antigen receptor (TCR). These results suggested that certain signaling components of the TCR may be shared by the activated PRLR. Additional studies here assessed the levels of TCR expression following PRLR stimulation and the effect of TCR activation on PRL-stimulated proliferation in lactogen-dependent pre-T Nb2-11 lymphoma cells. The results indicated that the TCR was expressed on the surface of approx 4% of exponentially proliferating and prolactin- (PRL) treated cells. In contrast, approx 45% of quiescent cells, cultured in the absence of PRL for 24 h, expressed the TCR at the cell surface, suggesting that lactogen withdrawal may up-regulate TCR cell-surface expression. Moreover, TCR activation with anti-CD3 antibodies attenuated PRL-stimulated Nb2-11 cell proliferation in a concentration-dependent manner. In other experiments, immunoprecipitation and immunoblotting of Nb2-11 lysates revealed that activation of the PRLR resulted in rapid tyrosyl phosphorylation of ZAP-70, a critical TCR-associated tyrosine kinase. In addition, ZAP-70 was found to associate transiently with the putative guanine nucleotide exchange factor and substrate, Vav, in PRL-treated cells. ZAP-70 was also found to associate constitutively with the PRLR; PRL stimulation provoked the transient recruitment of Vav to the complex. These observations suggest that PRL signaling reflects the transient formation of a PRLR-ZAP-70-Vav complex and its immunomodulatory actions involve diverse interactions that affect TCR expression and signaling mechanisms.

CD3 Complex↗
PubMed1997

Increased cystine uptake capability associated with malignant progression of Nb2 lymphoma cells.

Analysis of rat, pre-T cell 'Nb2 lymphoma' sublines, manifesting different degrees of malignant progression, can indicate phenotypic changes potentially useful as therapeutic targets. In this study, the prolactin (cytokine)-dependent Nb2-11 and autonomous Nb2-SFJCD1 sublines were compared for in vitro thiol growth requirements. Whereas Nb2-11 culture growth depended on 2-mercaptoethanol (2-ME; 33-100 microM), Nb2-SFJCD1 cells were 2-ME-independent. This difference stemmed from differential uptake of exogenous L-cystine, critically required for proliferation. Uptake of 35S-L-cystine (10 microCi/ml; 40 microM) showed Nb2-11 cells had low cystine uptake capability; 2-ME enhanced cystine uptake to growth-sustaining levels. Nb2-SFJCD1 cells did not require 2-ME due to intrinsic, 11-fold higher cystine uptake via the x(c)- cystine/glutamate transport system. In absence of 2-ME, monosodium glutamate abrogated Nb2-SFJCD1 proliferation by specifically inhibiting cystine uptake (85% at 10 mM). Elevated glutathione (GSH) levels were not essential for growth of either line as shown with L-buthionine-(S,R)-sulfoximine (0.1-4 mM) treatment. The cyst(e)ine requirement therefore did not primarily involve maintenance of normal GSH levels, reported critical for T lymphocyte replication. These and other results suggest increased cystine uptake capability constitutes another potential step in progression of T cell cancers which is not coupled to cytokine autonomy or metastatic ability development. The x(c)- transport system apparently provides a novel target for T cell cancer therapy. Its inhibition would suppress cystine uptake by certain progressed cells, and also interfere with cystine uptake, and subsequent cysteine release, by eg macrophages, thought to have a role in cysteine delivery to lymphoid cells.

Animals↗
PubMed1996

A comparative study of the effects of timolol and latanoprost on blood flow velocity of the retrobulbar vessels.

PURPOSE: To examine the effects of topical timolol and latanoprost on retrobulbar vessel blood velocity in patients with glaucoma or ocular hypertension. METHODS: Nine patients with primary open-angle glaucoma and six patients with ocular hypertension were enrolled for this study. All patients were treated topically with 0.5% timolol or 0.005% latanoprost, using a double-masked crossover design with a 3-week washout before administration of each drug. Each patient had a baseline color Doppler imaging ultrasound of the central retinal artery, short posterior ciliary arteries, and ophthalmic artery and two other ultrasound examinations during the 1-week treatment with each drug, performed 12 hours after the first dose of the drug and 12 hours after the last dose, 7 days later. RESULTS: Both topical timolol and topical latanoprost significantly reduced the intraocular pressure. The only significant change observed in the retrobulbar blood velocity with timolol was a reduction of end diastolic velocity in the ophthalmic artery 12 hours after the first dose, accompanied by a trend toward a decrease in the peak systolic velocity and an increase in the resistance index in the same vessel. No change in blood velocity was observed with latanoprost. CONCLUSION: Topical timolol and latanoprost significantly reduced the intraocular pressure in ocular hypertensive and glaucoma patients without creating substantial hemodynamic changes in the retrobulbar vessels.

Administration, Topical↗
PubMed1996

Color Doppler imaging in patients with asymmetric glaucoma and unilateral visual field loss.

PURPOSE: To determine whether lower blood velocities and high resistive index in the retrobulbar arteries are primary or secondary to glaucomatous damage in patients with open-angle glaucoma. METHODS: Color Doppler imaging was performed in 32 glaucomatous patients with unilateral visual field loss and in 31 control subjects. Peak systolic velocity and end diastolic velocity were measured, and resistive index was calculated in the central retinal artery and short posterior ciliary arteries. RESULTS: In patients with glaucoma, both the more affected and the contralateral eyes with normal visual fields had significantly lower peak systolic velocity and end diastolic velocity in their central retinal artery and short posterior ciliary arteries than did the control subjects of similar age (P < or = .03). The resistive index of the central retinal artery of both eyes of patients with glaucoma was also significantly higher than in the control subjects (P = .001). When considering the 16 patients who had the greatest visual field asymmetry, the more affected eyes had lower peak systolic velocity and end diastolic velocity in the central retinal artery than the contralateral eyes did (P = .02). CONCLUSIONS: Even eyes with normal visual fields in patients with asymmetric disease had decreased blood velocities in their retrobulbar vessels, suggesting that these circulatory changes probably precede detectable damage. Furthermore, the finding of lower central retinal artery blood velocities in the more affected eye of asymmetric patients suggests that low blood velocities may be one of the lateralizing factors in those patients and that they have a possible role in the pathogenesis of the disease.

Aged↗
PubMed1996

Various glaucomatous optic nerve appearances. A color Doppler imaging study of retrobulbar circulation.

PURPOSE: The purpose of this study was to observe the blood flow velocity in the retrobulbar vessels of patients with glaucoma with different appearances of optic discs. METHODS: Patients with four different disc appearances (focal ischemic discs, myopic glaucomatous discs, senile sclerotic discs, and discs with a generalized enlargement of the cup) were selected from a pool of optic disc photographs. No clinical information from the patients was available during the selection. Color Doppler imaging (CDI) was performed in those patients whose discs clearly belonged to one of the disc patterns. The peak systolic and end diastolic velocity were measured and the resistance index calculated from the central retinal artery, short posterior ciliary arteries and ophthalmic artery. RESULTS: Color Doppler imaging was performed in 24 patients with focal ischemic discs, 26 patients with myopic glaucomatous discs, 16 patients with senile sclerotic discs, and 16 patients with generalized enlargements of the cup. The patients with senile sclerotic discs had statistically significantly lower diastolic velocity and a higher resistance index in their ophthalmic, central retinal and the mean of the short posterior ciliary arteries sampled. These statistical differences persisted for the ophthalmic artery even after correcting the values for the age differences between the groups. CONCLUSIONS: Patients with senile sclerotic discs seem to have greater circulatory abnormalities in their retrobulbar vessels studied with color Doppler imaging that are compatible with a higher downstream resistance in these vessels. These circulatory abnormalities could be related to the pathogenesis of the glaucoma in these patients.

Aged↗
PubMed1996

Rapid modulation of the apoptosis regulatory genes, bcl-2 and bax by prolactin in rat Nb2 lymphoma cells.

The Nb2 rat lymphoma represents a useful model for investigation of molecular events coupled to PRL-induced proliferation. Moreover, recent evidence has also demonstrated the utility of this system to study mechanisms linked to programmed cell death (apoptosis). Thus, glucocorticosteroids activate apoptosis in lactogen-dependent Nb2 cells, whereas the addition of PRL abrogates this effect. The present study was conducted to determine whether PRL stimulation in lactogen-dependent Nb2-11 or autonomous Nb2-SFJCD1 cultures alters expression of bcl-2 or bax, genes that suppress or facilitate apoptosis, respectively. We demonstrate that PRL stimulation in stationary Nb2-11 cultures significantly increased the level of bcl-2 messenger RNA (mRNA) within 3 h (15-fold) and its protein product by 6 h, time points previously shown to correspond with G1 cell cycle progression. In Nb2-SFJCD1 cells, bcl-2 mRNA was found to be constitutively present. Addition of PRL to these lactogen-independent cultures further enhanced its expression at the mRNA and protein levels with a kinetic pattern similar to that observed in the PRL-dependent line. Results from stability studies indicated that increased bcl-2 mRNA evoked by PRL in Nb2 cell lines was most likely not attributable to increased stability of its transcripts. Furthermore, the rapid increase in its expression in PRL-stimulated Nb2-11 cells was not altered by inhibition of protein synthesis suggesting a direct action of the hormone. PRL also increased bax mRNA by 8 h in Nb2-11 cultures. However, hormone stimulation markedly attenuated the level of the Bax protein from 2-6 h. In contrast, bax expression in Nb2-SFJCD1 cultures remained unaltered by the addition of the hormone. These results demonstrate that altered expression of bcl-2 and bax are each associated with PRL-stimulated cell cycle progression in Nb2 cells. Moreover, bcl-2 appears to be an immediate-early gene induced by PRL in the hormone-dependent line and may represent an important regulator of early G1 cell cycle progression most likely by suppressing cell death mechanisms.

Animals↗
PubMed1996

Visual field correlations with color Doppler studies in open angle glaucoma.

PURPOSE: This study was designed to assess the correlation between flow velocity, the resistive index and visual field defects in patients with chronic open angle glaucoma in comparison with a nonglaucomatous control population. METHODS: Color Doppler imaging was used to study flow velocity in the central retinal artery and short posterior ciliary arteries of 76 patients with chronic open angle glaucoma and 28 normal subjects. Velocity and resistive index were correlated with visual field abnormalities. RESULTS: The chronic open angle glaucoma patients showed a statistically significant lowering of the end diastolic velocity and a raised resistive index in all vessels studied. The end diastolic velocity of the central retinal arteries of glaucoma patients were significantly correlated with the Mean Deviation of the visual field (right eye, p = 0.0041; left eye, p = 0.0167). The glaucoma patients showed a statistically significant lowering of the end diastolic velocity and a raised resistive index in all vessels supplying those parts of the optic disc that corresponded to visual hemifield defects. CONCLUSION: Open angle glaucoma is associated with changes in central retinal and ciliary artery flow velocity and resistive index which suggest a compromised circulation in this region.

Adult↗
PubMed1996

Ocular hypertension and primary open-angle glaucoma: a comparative study of their retrobulbar blood flow velocity.

PURPOSE: To compare the orbital blood flow velocities of patients with long-standing ocular hypertension and patients with primary open-angle glaucoma. METHODS: Twenty patients with ocular hypertension were recruited from our clinic and underwent color Doppler imaging evaluation of their retrobulbar vessels. The blood flow velocities and resistance index of their central retinal artery, temporal short posterior ciliary artery, and ophthalmic artery were compared with those of 20 glaucoma patients individually matched for age and level of the highest untreated intraocular pressure ever recorded. RESULTS: Glaucoma patients had significantly lower peak systolic velocity and end-diastolic velocity than did patients with ocular hypertension in their central retinal artery (p < 0.001). No significant difference between the groups was observed in the other vessels studied. CONCLUSIONS: Glaucoma patients had lower blood flow velocity in the central retinal artery compared with that of ocular hypertension patients of similar age and level of untreated intraocular pressure. This might be important in the development of glaucomatous damage in those patients.

Blood Flow Velocity↗