Retinal Microvascular Patency in the Diabetic Rat

Ben-nun, Joshua; Alder, Valerie A.; Constable, Ian J.

doi:10.1007/s10792-004-5815-x

Cited by 6 publications

(5 citation statements)

References 7 publications

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“…Autoregulation of cerebral blood flow and vasodilation of cerebral arteries are impaired in T1DM patients (Hoffman et al, 2004). Lower extremity and retinal capillary perfusion are also impaired in DM rats and lead to diabetic retinopathy and neuropathy (Arora et al, 2002; Ben-nun et al, 2004). We found that T1DM-MCAo rats exhibit increased vascular density but significantly decreased vascular perimeter and artery diameter compared to WT-MCAo rats.…”

Section: Discussionmentioning

confidence: 99%

Niaspan enhances vascular remodeling after stroke in type 1 diabetic rats

Chopp

Cui

et al. 2011

Experimental Neurology

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We investigated the changes and the molecular mechanisms of cerebral vascular damage and tested the therapeutic effects of Niaspan in type-1 streptozotocin induced diabetic (T1DM) rats after stroke. T1DM-rats were subjected to transient middle cerebral artery occlusion (MCAo) and treated without or with Niaspan. Non-streptozotocin rats (WT) were also subjected to MCAo. Functional outcome, blood–brain-barrier (BBB) leakage, brain hemorrhage, immunostaining, and rat brain microvascular endothelial cell (RBEC) culture were performed. Compared to WT-MCAo-rats, T1DM-MCAo-rats did not show an increase lesion volume, but exhibited significantly increased brain hemorrhage, BBB leakage and vascular damage as well as decreased functional outcome after stroke. Niaspan treatment of stroke in T1DM-MCAo-rats significantly attenuated BBB damage, promoted vascular remodeling and improved functional outcome after stroke. T1DM-MCAo-rats exhibited significantly increased Angiopoietin 2 (Ang2) expression, but decreased Ang1 expression in the ischemic brain compared to WT-MCAo-rats. Niaspan treatment attenuated Ang2, but increased Ang1 expression in the ischemic brain in T1DM-MCAo-rats. In vitro data show that the capillary-like tube formation in the WT-RBECs marginally increased compared to T1DM-RBEC. Niaspan and Ang1 treatment significantly increased tube formation compared to non-treatment control. Inhibition of Ang1 attenuated Niacin-induced tube formation in T1DM-RBECs. Niaspan treatment of stroke in T1DM-rats promotes vascular remodeling and improves functional outcome. The Ang1/Ang2 pathway may contribute to Niaspan induced brain plasticity. Niaspan warrants further investigation as a therapeutic agent for the treatment of stroke in diabetics.

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Section: Discussionmentioning

confidence: 99%

Niaspan enhances vascular remodeling after stroke in type 1 diabetic rats

Chopp

Cui

et al. 2011

Experimental Neurology

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“…Alterations in retinal capillaries are the hallmark of diabetic retinopathy and include multiple occlusions due to increased leukocyte entrapment (Ogura, 2000), increased permeability of the vessel wall with focal leakage occurring primarily at the location between the deep retinal capillary net and the ascending venules (Ben-Nun et al, 2004) and, in the proliferative form, growth of newly-formed vessels (neovascularization).…”

Section: Regulation Of Ocular Blood Flow In Diseasementioning

confidence: 99%

Cellular and physiological mechanisms underlying blood flow regulation in the retina and choroid in health and disease

Kur

Newman

Chan‐Ling

2012

Progress in Retinal and Eye Research

550

455

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We review the cellular and physiological mechanisms responsible for the regulation of blood flow in the retina and choroid in health and disease. Due to the intrinsic light sensitivity of the retina and the direct visual accessibility of fundus blood vessels, the eye offers unique opportunities for the non-invasive investigation of mechanisms of blood flow regulation. The ability of the retinal vasculature to regulate its blood flow is contrasted with the far more restricted ability of the choroidal circulation to regulate its blood flow by virtue of the absence of glial cells, the markedly reduced pericyte ensheathment of the choroidal vasculature, and the lack of intermediate filaments in choroidal pericytes. We review the cellular and molecular components of the neurovascular unit in the retina and choroid, techniques for monitoring retinal and choroidal blood flow, responses of the retinal and choroidal circulation to light stimulation, the role of capillaries, astrocytes and pericytes in regulating blood flow, putative signaling mechanisms mediating neurovascular coupling in the retina, and changes that occur in the retinal and choroidal circulation during diabetic retinopathy, age-related macular degeneration, glaucoma, and Alzheimer's disease. We close by discussing issues that remain to be explored.

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“…astrocytes, may also contribute to the neurotrophic effect. It must also be realized that experimental studies in rodents have potential shortcomings, for instance, animals which lack an inner retinal circulation won't develop real human DR changes (60). Notwithstanding its limitations, this study does provide a better understanding of multiple potential protective mechanisms of EPO in the diabetic retina, and suggest that Müller cells, as primary mediators of these effects, may be important targets in the therapy of DR, and perhaps other neurodegenerative diseases of the retina.…”

Section: Discussionmentioning

confidence: 96%