Cellular Mechanisms of Diabetic Vascular Hypertrophy

Vranes, Dimitria; Cooper, Mark E.; Dilley, Rodney J.

doi:10.1006/mvre.1998.2107

Cited by 58 publications

(43 citation statements)

References 32 publications

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“…In this study, vascular remodeling associated with DM reached the tunica adventitia, changing the pattern of collagen fibers and reducing their thickness from that seen in the control group (orange birefringence), to thinner fibers (greenish birefringence). Changes in the pattern of collagen fibers have been previously demonstrated in the mesenteric artery of streptozotocin-induced diabetic rats (11). Rearrangement of collagen fibers in the extracellular matrix, in both the wall of the DAP and periarterial region, suggests that it occurred simultaneously to vascular hypertrophy associated with DM.…”

Section: Discussionmentioning

confidence: 78%

“…Diabetes can cause arterial wall thickening, as reported in the mesenteric artery, renal artery, and aorta (11,12,25). However, this has not been previously described in penile arteries.…”

Section: Discussionmentioning

confidence: 90%

“…Vascular diseases such as microangiopathy, atherosclerosis, and hypertension are often observed in patients with DM. A relationship between these vascular conditions and the occurrence of morphological changes in the mesenteric artery (11,12) and aorta in rats (13) has been demonstrated.…”

Section: Introductionmentioning

confidence: 86%

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Sinusoidal Constriction and Vascular Hypertrophy in the Diabetes-Induced Rabbit Penis

et al. 2013

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Objective: To assess the morphological changes of penile vascular structures and the corpus cavernosum area in alloxan-induced diabetic rabbits. Materials and Methods: Twenty male rabbits (2 months old) were divided into two groups with 10 rabbits each, the control group (CG) and the diabetic group (DG). The animals from DG received an intravenous injection of alloxan (100mg/kg) to induce the diabetes. Ten weeks after the induction of diabetes, all animals were euthanized. Two fragments of the penile shaft were harvested and samples were processed and paraffin embedded. Sections (5µm) were cut and stained for histological and immunohistochemical markers. Results: Nuclear protrusion toward the lumen, and cytoplasmic vacuolization were observed in the tunica intima of the dorsal artery of the penis in DG. The thicknesses of the tunica media increased significantly in DG (p = 0.0350). It was also observed a significant increase in the area of the tunica media (p = 0.0179). There was no significant change in smooth muscle cell density in the tunica media of the dorsal artery of the penis (p = 0.0855). The collagen fiber pattern of the tunica adventitia of the dorsal artery of the penis was different between the control and diabetic groups. There was a significant decrease in the area occupied by the cavernous sinuses in DG (p = 0.0013). Conclusion: Alloxan-induced diabetes mellitus in rabbits promotes important changes in penile vascular structures, thereby decreasing blood supply and affecting penile hemodynamics, leading to erectile dysfunction.

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Section: Discussionmentioning

confidence: 78%

“…Diabetes can cause arterial wall thickening, as reported in the mesenteric artery, renal artery, and aorta (11,12,25). However, this has not been previously described in penile arteries.…”

Section: Discussionmentioning

confidence: 90%

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Sinusoidal Constriction and Vascular Hypertrophy in the Diabetes-Induced Rabbit Penis

et al. 2013

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“…The vascular hypertrophy associated with diabetes has already been documented by other studies (Vranes et al, 1995b(Vranes et al, , 1999. The pro-angiogenic consequences of ip injected STZ have been previously described (Norrby et al, 1990b) and related to mast cell degranulation and histamine release.…”

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confidence: 60%

Alterations of the Rat Mesentery Vasculature in Experimental Diabetes

Arshi

Bendayan

Ghitescu

2000

Laboratory Investigation

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SUMMARY:The alteration induced by diabetes on vascular permeability to serum albumin was investigated in the mesentery of streptozotocin-induced hyperglycemic rats. Double-tagged ( 125 I and dinitrophenol-haptenated) heterologous albumin was intravenously administered in normal and hyperglycemic animals, and the extravasation of the tracer was evaluated by radioactivity measurements and by morphometry at the ultrastructural level using quantitative protein A-colloidal gold immunocytochemistry. The results demonstrate that diabetes induces a significant increase in the permeability of the mesentery vessels to albumin. This increase is due to a more efficient transport of macromolecules by endothelial plasmalemmal vesicles and not to leakier interendothelial junctions. Passage across the endothelial basement membranes did not appear to be restricted in either the control or diabetic condition. However, in diabetes, the mesothelial basement membrane appeared to become modified and to restrain the passage of albumin toward the peritoneal cavity. After 3 months of diabetes, the rats presented a net increase in the average diameter of the blood vessels localized in the mesentery arcada (macrovascular hyperplasy) and a notable angiogenesis, manifested at the level of the microvasculature in the mesenteric windows. (Lab Invest 2000, 80:1171-1184.T he association of diabetes with vascular dysfunctions gradually evolving toward incapacitating or life-threatening vascular pathologies is undisputed. Extensive clinical observations and studies on animal models have amply documented that hyperglycemia accelerates and worsens atherosclerosis in large arteries (Colwell et al, 1988;Shantaram, 1999;Steiner 1997) and affects, although in different ways, the microvessels of selected vascular beds, such as those of the retina (Bazan et al, 1997;Cunha-Vaz, 1983;Porta, 1996;Ruggiero et al, 1997), kidney (Flyvbjerg, 1997;Mauer et al, 1984;Nyengaard and Bendtsen, 1993;Vlassara et al, 1994), and nerves (Cameron and Cotter, 1997;Malik et al, 1993; Tesfay et al, 1994). Particular attention has been directed to the study of diabetes-induced retinopathies and nephropathies, because of their obvious clinical implications. On the other hand, the impact of diabetes on other vascular beds has been generally overlooked. Therefore, it is not known whether diabetic microangiopathy concerns all blood vessels, creating a sort of "dysfunctional background" exacerbated in particular tissues by local factors to a full blown vascular pathology, or the vasculature of many organs is simply spared by the deleterious effects of hyperglycemia/ hypoinsulinemia. The latter hypothesis would fall in line with the ever-growing body of evidence pointing to important physiological and biochemical dissimilarities between various vascular segments (Boegehold, 1998;Rajotte et al, 1998;Thorin and Shreeve, 1998).Several morphologic features and physiologic parameters appear as leit motifs of diabetic microangiopathies. Among these, the thickening of the basement membran...

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“…Alterations in vascular structure, characterized by extracellular matrix deposits in the capillary and arteriolar basement membranes, contribute to the pathogenesis of vascular complications of diabetes [3][4][5][6][7]. As shown by the Diabetes Control and Complications Trial (DCCT) and the UK Prospective Diabetes Study (UKPDS), hyperglycemia is an important factor in the development of diabetic complications [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%