Vessels In Diabetic Patients Research Articles

Influence of Flickering Light on the Retinal Vessels in Diabetic Patients

Stimulation of the retina with flickering light increases retinal vessel diameters in humans. Nitric oxide is a mediator of the retinal vasodilation to flicker. The reduction of vasodilation is considered an endothelial dysfunction. We investigated the response of retinal vessels to flickering light in diabetic patients in different stages of diabetic retinopathy. We studied 53 healthy volunteers, 68 type 1 diabetic patients, and 172 type 2 diabetic patients. The diameter of retinal vessels was measured continuously online with the Dynamic Vessel Analyzer (DVA). Diabetic retinopathy was classified using Early Treatment Diabetic Retinopathy Study criteria. Changes in vasodilation are expressed as percent change over baseline values. After adjustments for age, sex, and antihypertensive treatment, the response of retinal arterioles to diffuse luminance flicker was significantly diminished in patients with type 1 diabetes compared with healthy volunteers. The vasodilation of retinal arterioles and venules decreased continuously with increasing stages of diabetic retinopathy. The retinal arterial diameter change was 3.6 +/- 2.1% in the control group, 2.6 +/- 2.5% in the no diabetic retinopathy group, 2.0 +/- 2.7% in the mild nonproliferative diabetic retinopathy (NPDR) group, 1.6 +/- 2.2% in the moderate NPDR group, 1.8 +/- 1.9% in severe NPDR group, and 0.8 +/- 1.6% in proliferative diabetic retinopathy group. Flicker responses of retinal vessels are abnormally reduced in diabetic patients. This decreased response deteriorated with increasing stages of retinopathy. The response was already reduced before clinical appearance of retinopathy. The noninvasive testing of retinal autoregulation with DVA might prove to be of value in early detection of diabetic vessel pathological changes.

Contribution of Aldose Reductase to Diabetic Hyperproliferation of Vascular Smooth Muscle Cells

The objective of this study was to determine whether the polyol pathway enzyme aldose reductase mediates diabetes abnormalities in vascular smooth muscle cell (SMC) growth. Aldose reductase inhibitors (tolrestat or sorbinil) or antisense aldose reductase mRNA prevented hyperproliferation of cultured rat aortic SMCs induced by high glucose. Cell cycle progression in the presence of high glucose was blocked by tolrestat, which induced a G0-G1 phase growth arrest. In situ, diabetes increased SMC growth and intimal hyperplasia in balloon-injured carotid arteries of streptozotocin-treated rats, when examined 7 or 14 days after injury. Treatment with tolrestat (15 mg x kg(-1) x day(-1)) diminished intimal hyperplasia and decreased SMC content of the lesion by 25%. Although tolrestat treatment increased immunoreactivity of the lesion with antibodies raised against protein adducts of the lipid peroxidation product 4-hydroxy trans-2-nonenal, no compensatory increase in lesion fibrosis was observed. Collectively, these results suggest that inhibition of aldose reductase prevents glucose-induced stimulation of SMC growth in culture and in situ. Even though inhibition of aldose reductase increases vascular oxidative stress, this approach may be useful in preventing abnormal SMC growth in vessels of diabetic patients.

Comparison with coronary stent and cutting balloon in small coronary vessels in diabetic patients

Comparison with coronary stent and cutting balloon in small coronary vessels in diabetic patients

Fatty acid composition of phospholipids and neutral lipids from human diabetic small arteries and veins by a new TLC method

It has been suggested that lipid peroxidation of polyunsaturated fatty acids (PUFA) may play a role in the pathogenesis of diabetic complications. To test this hypothesis, we aimed to compare PUFA composition of small arteries and veins (< 500 μm diameter) obtained from diabetic or non-diabetic Guadeloupean patients undergoing arterio-venous shunt surgery before renal dialysis. Small forearm subcutaneous vessels were analysed by a new TLC method which involved inclusion of vascular biopies directly in alveoles made in the TLC gel and lyophilization onto the plate. The TLC plate was then chromatographed and lipids were both extracted and eluted during this step. Fatty acid composition of phospholipid and neutral lipid fractions were determined. Similar fatty acid composition was obtained for arteries and veins from diabetic or non-diabetic subjects. In phospholipids from diabetic vessels, major changes consisted of a 20% decrease of arachidonic acid (20:4 n-6), a 40% decrease of its elongation product 22:4 n-6 and 30% increase of 18:2 n-6. In neutral lipids, 20:4 n-6 was also diminished by 60% whereas oleic acid increased by 15%. This loss of arachidonic acid in small diabetic vessels suggests impaired Δ6-desaturase forming 20:4 n-6 or alternatively increased peroxide formation, in the vascular wall of small vessels in diabetic patients.

Hyperpermeability of abdominal capillary vessels to endothelin-1 in patients with diabetes mellitus.

To elucidate the pathophysiologic significance of circulating endothelin-1 (ET-1) to the vascular lesions in diabetic patients, ET-1 levels in plasma and peritoneal dialysis fluid were measured in 11 patients receiving continuous ambulatory peritoneal dialysis (CAPD) [five with diabetic nephropathy (group A); six with chronic renal failure without diabetes mellitus (group B)]. ET-1 levels were determined by a highly sensitive and specific enzymeimmunoassay. Plasma ET-1 levels in group A were not significantly different from those in group B (3.3 +/- 0.9 versus 3.5 +/- 0.9 pg/ml). However, the amounts of ET-1 in peritoneal dialysis fluid in group A were significantly greater than those in group B (19.2 +/- 13.2 versus 10.4 +/- 6.3 ng/day). These results suggest that abdominal capillary vessels in diabetic patients are hyperpermeable to ET-1.