Intimal alterations in rabbit aortas during the first 6 months of alloxan-induced diabetes.

Hadcock, S.J.; Richardson, Mary; Winocour, Peter D.; Hatton, M. W. C.

doi:10.1161/01.atv.11.3.517

Cited by 51 publications

(37 citation statements)

References 25 publications

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“…This pattern of dysfunction is seen in both diabetes mellitus and hypercholesterolaemia and could represent an abnormality of membrane or receptor coupling at this stage of the disease. It should be noted that the alloxan-induced diabetic rabbit model is associated with vascular structural changes after longer periods of hyperglycaemia [22]. Our model is therefore one of early vascular dysfunction.…”

Section: Discussionmentioning

confidence: 78%

Gene transfer of endothelial nitric oxide synthase alters endothelium-dependent relaxations in aortas from diabetic rabbits

et al. 2000

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Cardiovascular disease is responsible for most of the excess mortality associated with diabetes mellitus [1], and impaired endothelium-dependent relaxation has been described in humans and in animal models of the disease [2±6]. A variety of mechanisms have been proposed to explain this observation and, in particular, the role of nitric oxide (NO) has been evaluated. Nitric oxide production has been reported to be either increased [7] or decreased [8] in the presence of high glucose concentrations. Moreover, endothelial dysfunction following hyperglycaemia is associated with increased generation of oxygen free radicals [9] and vasoconstrictor prostanoids [10,11]. The observation that diabetes-induced abnormalities of vascular relaxation are reversed when the vessel segments are exposed to indomethacin in the organ Diabetologia (2000) Abstract Aims/hypothesis. Cardiovascular disease is the leading cause of death in diabetes mellitus. Abnormal endothelium-dependent relaxation is observed both in humans and in animal models of diabetes mellitus and decreased bioavailability of nitric oxide (NO) is thought to be involved in this defect. Therefore, the aim of this study was to test whether adenovirus-mediated gene transfer of endothelial nitric oxide synthase (eNOS) alters vascular reactivity of diabetic vessels. Methods. Vascular reactivity was first assessed in thoracic aortas and carotid arteries from nine alloxan-induced diabetic (plasma glucose, 26.5 ± 1.2 mmol/l; HbA 1 c , 6.4 ± 0.3 %) and nine control rabbits (plasma glucose, 11.1 ± 1.3 mmol/l; HbA 1 c , 2.1 ± 0.1 %). Vascular reactivity was next examined in thoracic aortas of diabetic animals after ex vivo transduction with replication-deficient adenovirus encoding gene for eNOS (AdeNOS) or b-galactosidase (Adbgal).Results. After 10 weeks of hyperglycaemia, endothelium-dependent relaxation to acetylcholine was impaired in diabetic aorta, but was normal in carotid arteries from diabetic rabbits. In contrast, responses of both vessels to calcium ionophore and nitric oxide donor were normal. Histochemical staining for b-galactosidase and immunohistochemistry for eNOS showed transgene expression in the endothelium and adventitia in Adbgal and AdeNOS transduced vessels, respectively. During submaximum contractions with phenylephrine, relaxations to low concentrations of acetylcholine (3 10 ±8 to 10 ±7 mol/l) were augmented in AdeNOS transduced diabetic vessels. Conclusion/interpretation. These findings suggest that adenovirus-mediated gene transfer of eNOS to diabetic aorta alters vascular reactivity. [Diabetologia (2000) 43: 340±347]

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Section: Discussionmentioning

confidence: 78%

Gene transfer of endothelial nitric oxide synthase alters endothelium-dependent relaxations in aortas from diabetic rabbits

et al. 2000

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“…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: 89%

“…Mitochondrial and nuclear changes are indicators of the reversible injury mechanism, vacuolar degeneration (29). Chemically induced hyperglycemia may also cause oxidative stress leading to cellular vacuolization (25).…”

Section: Discussionmentioning

confidence: 99%

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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“…This effect was independent of increases in serum insulin levels. Several studies have assessed the relation between hyperglycaemia and leucocyte binding to endothelial cells [14][15][16][17]. Although these studies used various experimental conditions and have their own meanings depending on the experimental conditions, most in vivo and in vitro studies have shown that hyperglycaemia induces leucocyte adhesion to endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta

et al. 2005

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Aims/hypothesis: Several epidemiological data suggest that patients with postprandial hyperglycaemia are at high risk of cardiovascular disease. The aim of this study was to elucidate the effect of a glucose 'spike' on monocyte adhesion to rat aortic endothelial cells. Materials and methods: Monocyte adhesion to endothelial cells in vivo was quantitated using an en face method for observation of endothelial surface after immunohistochemical staining for CD68 in the thoracic aortas of Sprague-Dawley rats after several kinds of blood glucose rises. Results: The number of monocytes adhering to endothelial cells increased at 30 min after injection of glucose in 8-week-old Sprague-Dawley rats. The increased adhesion returned to the basal level at 120 min after glucose injection, concomitantly with the return of blood glucose levels to normal. The infusion of octreotide to inhibit endogenous insulin secretion did not prevent the glucose-induced increase in monocyte adhesion to endothelial cells. On the other hand, the number of monocytes adhering to endothelial cells did not increase in rats with streptozotocin-induced diabetes and sustained hyperglycaemia. Conclusions/interpretation: Our data demonstrate that a temporary rise in blood glucose levels can in itself promote a reversible increase in monocyte adhesion to arterial endothelial cells.

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Intimal alterations in rabbit aortas during the first 6 months of alloxan-induced diabetes.

Cited by 51 publications

References 25 publications

Gene transfer of endothelial nitric oxide synthase alters endothelium-dependent relaxations in aortas from diabetic rabbits

Gene transfer of endothelial nitric oxide synthase alters endothelium-dependent relaxations in aortas from diabetic rabbits

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

Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta

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