Ocular blood flow and associated functional deviations in diabetic retinopathy

Schmetterer, Leopold; Wolzt, Michael

doi:10.1007/s001250051171

Cited by 216 publications

(154 citation statements)

References 174 publications

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“…In the superior cervical ganglion, which like the brain has a higher metabolic rate, blood flow is reduced by 45 % and PCr is reduced by 38 % in STZ-diabetic rats [48,46]. Likewise, in the retina of diabetic rabbits ATP concentrations can also be reduced [49], but it should be noted that ATP reductions in the retina have not been found consistently [50] and much controversy still exists about the nature of blood flow changes in the retina [51].…”

Section: Discussionmentioning

confidence: 99%

Cerebral metabolism in streptozotocin-diabetic rats: an in vivo magnetic resonance spectroscopy study

et al. 2001

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It is becoming increasingly clear that the brain is another site of diabetic end-organ damage [1]. Some diabetic patients develop cognitive deficits, which are generally moderate in young adults [2] but can be more pronounced in the elderly [3]. Recent epidemiological studies even report an association between diabetes and dementia [3,4]. Given the prevalence of diabetes among the elderly and the effect of cognitive impairment and dementia on the quality of life of patients and health care resources, a better understanding of the effects of diabetes on the brain is needed.Experimentally diabetic rodents develop cerebral deficits similar to those observed in diabetic patients. Streptozotocin (STZ)-diabetic rats have been found to have impaired learning and memory functions [5] and increases in the peak latencies of brainstem audi- Diabetologia (2001) Abstract Aims/hypothesis. It is increasingly evident that the brain is another site of diabetic end-organ damage. The pathogenesis has not been fully explained, but seems to involve an interplay between aberrant glucose metabolism and vascular changes. Vascular changes, such as deficits in cerebral blood flow, could compromise cerebral energy metabolism. We therefore examined cerebral metabolism in streptozotocin-diabetic rats in vivo by means of localised 31 P and 1 H magnetic resonance spectroscopy. Methods. Rats were examined 2 weeks and 4 and 8 months after diabetes induction. A non-diabetic group was examined at baseline and after 8 months.Results. In 31 P spectra the phosphocreatine:ATP, phosphocreatine:inorganic phosphate and ATP:inorganic phosphate ratios and intracellular pH in diabetic rats were similar to controls at all time points. In 1 H spectra a lactate resonance was detected as frequently in controls as in diabetic rats. Compared with baseline and 8-month controls 1 H spectra did, however, show a statistically significant decrease in N-acetylaspartate:total creatine (±14 % and ±23 %) and Nacetylaspartate:choline (±21 % and ±17 %) ratios after 2 weeks and 8 months of diabetes, respectively. Conclusion/interpretation. No statistically significant alterations in cerebral energy metabolism were observed after up to 8 months of streptozotocin-diabetes. These findings indicate that cerebral blood flow disturbances in diabetic rats do not compromise the energy status of the brain to a level detectable by magnetic resonance spectroscopy. Reductions in Nacetylaspartate levels in the brain of STZ-diabetic rats were shown by 1 H spectroscopy, which could present a marker for early metabolic or functional abnormalities in cerebral neurones in diabetes. [Diabetologia (2001) 44: 346±353]

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Section: Discussionmentioning

confidence: 99%

Cerebral metabolism in streptozotocin-diabetic rats: an in vivo magnetic resonance spectroscopy study

et al. 2001

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“…37 Accumulation of sorbitol in retinal cells is dependant on the activity of aldose reductase and this may impinge on a range of pathways and contribute to diabetic retinopathy. 38 Also de novo synthesis of diacylglycerol (DAG) leading to the over-activation of several isoforms of protein kinase C (PKC), 39 excessive production of free radicals leading to oxidative stress, 40,41 changes in blood rheology and haemodynamics, 42,43 and over-activation of the renin-angiotensin system 44 contribute significantly to retinopathy as diabetes progresses. Accumulation of advanced glycation end products (AGEs) and activation of receptors for AGEs are also important pathogenic mechanisms with clear links to diabetic retinopathy.…”

Section: Retinal Hypoperfusion In Diabetes: Links To Early Pathologymentioning

confidence: 99%

Microvascular lesions of diabetic retinopathy: clues towards understanding pathogenesis?

Curtis

Gardiner

Stitt

2009

Eye

311

231

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Retinopathy is a major complication of diabetes mellitus and this condition remains a leading cause of blindness in the working population of developed countries. As diabetic retinopathy progresses a range of neuroglial and microvascular abnormalities develop although it remains unclear how these pathologies relate to each other and their net contribution to retinal damage. From a haemodynamic perspective, evidence suggests that there is an early reduction in retinal perfusion before the onset of diabetic retinopathy followed by a gradual increase in blood flow as the complication progresses. The functional reduction in retinal blood flow observed during early diabetic retinopathy may be additive or synergistic to proinflammatory changes, leucostasis and vasoocclusion and thus be intimately linked to the progressive ischaemic hypoxia and increased blood flow associated with later stages of the disease. In the current review a unifying framework is presented that explains how arteriolar dysfunction and haemodynamic changes may contribute to late stage microvascular pathology and vision loss in human diabetic retinopathy.

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“…Retinal blood flow in clinical diabetic retinopathy has been studied using a number of indirect methods (Schmetterer & Wolzt 1999). These investigations have shown an increase in the retinal blood flow in early stages of retinopathy and a decrease in later stages which is marked when retinopathy has become proliferative and is given laser treatment (Kohner et al 1975, Grunwald et al 1989, Rimmer et al 1989, Arend et al 1991, Patel et al 1992, Konno et al 1996.…”

Section: Analysis Of Clinical Findingsmentioning

confidence: 99%

Diabetic maculopathy caused by disturbances in retinal vasomotion. A new hypothesis

Bek

1999

Acta Ophthalmologica Scandinavica

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Ocular blood flow and associated functional deviations in diabetic retinopathy

Cited by 216 publications

References 174 publications

Cerebral metabolism in streptozotocin-diabetic rats: an in vivo magnetic resonance spectroscopy study

Cerebral metabolism in streptozotocin-diabetic rats: an in vivo magnetic resonance spectroscopy study

Microvascular lesions of diabetic retinopathy: clues towards understanding pathogenesis?

Diabetic maculopathy caused by disturbances in retinal vasomotion. A new hypothesis

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