Platelet sensitivity to adenosine diphosphate and to prostacyclin in diabetic patients.

Onodera, Hidetoshi; Hirata, Toru; Sugawara, Hiroto; Sugai, Kuniaki; Yoda, Binkoh; Toyota, Takayoshi; Gotō, Yoshio

doi:10.1620/tjem.137.423

Cited by 16 publications

(10 citation statements)

References 15 publications

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“…The sensitivity of platelet aggregation by ADP is increased in diabetic patients, and this may contribute to microangiopathy [99]. Platelets of T2D patients were characterised by high ATP content [100].…”

Section: Purinergic Signalling In Diabetesmentioning

confidence: 99%

Purinergic signalling and diabetes

Burnstock

Novak

2013

Purinergic Signalling

108

127

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The pancreas is an organ with a central role in nutrient breakdown, nutrient sensing and release of hormones regulating whole body nutrient homeostasis. In diabetes mellitus, the balance is broken—cells can be starving in the midst of plenty. There are indications that the incidence of diabetes type 1 and 2, and possibly pancreatogenic diabetes, is rising globally. Events leading to insulin secretion and action are complex, but there is emerging evidence that intracellular nucleotides and nucleotides are not only important as intracellular energy molecules but also as extracellular signalling molecules in purinergic signalling cascades. This signalling takes place at the level of the pancreas, where the close apposition of various cells—endocrine, exocrine, stromal and immune cells—contributes to the integrated function. Following an introduction to diabetes, the pancreas and purinergic signalling, we will focus on the role of purinergic signalling and its changes associated with diabetes in the pancreas and selected tissues/organ systems affected by hyperglycaemia and other stress molecules of diabetes. Since this is the first review of this kind, a comprehensive historical angle is taken, and common and divergent roles of receptors for nucleotides and nucleosides in different organ systems will be given. This integrated picture will aid our understanding of the challenges of the potential and currently used drugs targeted to specific organ/cells or disorders associated with diabetes.

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Section: Purinergic Signalling In Diabetesmentioning

confidence: 99%

Purinergic signalling and diabetes

Burnstock

Novak

2013

Purinergic Signalling

108

127

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“…Thus, the early loss of microvascular pericytes in diabetes, with the concomitant decrease in pericyte prostacy clin, may promote the formation of microvas cular platelet thrombi seen in diabetic mi croangiopathy. In addition, it has been re ported that platelets from diabetic patients show a diminished sensitivity to the anti aggregatory effects of prostacyclin [23] that is correlated with the severity of retinopathv [24], Thus, diminished platelet responsiveness to prostacyclin, hyperaggregability of platelets due to increased thromboxane synthesis, and decreased synthesis of prostacyclin by vascu lar cells would all act together to increase the incidence of thromboembolic complications in diabetes. There is experimental evidence for such complications.…”

Section: Retinal Blood Flow Following Aspirin In Diabeticsmentioning

confidence: 99%

Retinal Blood Flow Increases following Short-Term Aspirin Usage in Type I Diabetics with No or Minimal Retinopathy

Yoshida²,

Ogasawara³

et al. 1996

Ophthalmic Res

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In a double-masked, randomized, placebo-controlled, two period crossover study, we measured the effect of aspirin on retinal blood flow in 8 type I diabetic patients, 5 with no observable retinopathy, and 3 with 1–10 observable micro aneurysms and no other signs of retinopathy. Each patient ingested 1 capsule/day of either aspirin (650 mg) or placebo for 14 days. Following a 1-month washout period, the treatment was reversed. The bidirectional laser Doppler technique and monochromatic photography were used to measure the blood flow rate in a major temporal retinal artery in 1 eye of each patient at baseline and on the 14th day of each treatment period. Retinal blood flow increased following aspirin in 7 of the 8 patients. Using a standard crossover analysis we found a mean aspirin-placebo treatment difference of 21 ± 17% (mean ± 95% CI), which was statistically significant (p = 0.03). Retinal blood flow increased following aspirin by 44 ± 10% (mean ± SEM) in the 5 patients with no retinopathy (p = 0.04), but only by 8 ± 10% (n.s.) in the 3 patients with minimal retinopathy.

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“…Diabetics have increased platelet adhesiveness [36], increased platelet aggregation [18,33], increased fibrinogen turnover [6], and abnormalities of prostanglandin metabolism that may predispose toward clotting [2,30,32,43]. Although it is not clear whether these changes are primary or secondary, it does seem likely that the potential to exacerbate endothelial damage would be high in any vascular bed.…”

Section: Number Of Endothelial Cell Nuclear Indentation (Open Arr¢~wsmentioning

confidence: 99%

Diabetic choroidal and iris vasculature scanning electron microscopy findings

1989

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Scanning Electron Microscopy (SEM) was used to study vascular casts of twenty-four autopsy eyes taken from patients with long-standing insulin-dependent Diabetes Mellitus. These casts were compared to casts of ten 'normal' autopsy eyes from patients without a history of diabetes or other vascular disease. The SEM findings in the choroidal vessels of the diabetic eyes included: increased tortuosity, focal vascular dilations and narrowings, hypercellularity, vascular loops and microaneurysm formation, 'drop-out' of choriocapillaries, and sinus-like structure formation between choroidal lobules in the equatorial area. In the iris, neovascularization was evident in the vascular casts in cases with clinically recognized rubeosis iridis. These findings indicate that there is significant involvement of the uveal tract in diabetic eyes. The present study strongly supports the Hidayat and Fine light microscopic observation that the diabetic choroid demonstrates significant vascular changes (e.g. narrowed vessels with possible 'drop-out' of capillaries and neovascularization). Changes in the diabetic choroid, especially in the choriocapillaris, may be a contributing factor in diabetic retinopathy, resulting in decreased oxygenation of the outer layer of the retina. Short reviews and updated information of diabetic eye disease provide some additional insights into the vascular problems in the eye.

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Platelet sensitivity to adenosine diphosphate and to prostacyclin in diabetic patients.

Cited by 16 publications

References 15 publications

Purinergic signalling and diabetes

Purinergic signalling and diabetes

Retinal Blood Flow Increases following Short-Term Aspirin Usage in Type I Diabetics with No or Minimal Retinopathy

Diabetic choroidal and iris vasculature scanning electron microscopy findings

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