Acute endothelium-mediated vasodilation is not impaired at the onset of diabetes

Michael W Brands, Sharyn M. Fitzgerald

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Vascular injury and impaired vascular function are central to the increased mortality associated with diabetes. Hyperglycemia in diabetes has been suggested to play a role in this process, in part by impairing the function of the vascular endothelium. It has been difficult, however, to isolate the direct effect of glucose in both humans and in animal models of diabetes. This was evaluated in the present study in 7 rats that were Chronically instrumented with a Transonic flow probe at the iliac bifurcation of the abdominal aorta, a nonoccluding catheter inserted immediately anterior to the flow probe, and a femoral vein catheter. Acute infusions of acetylcholine and sodium nitroprusside (1 and 10 μg/min IA) increased hindquarter blood flow significantly by approximately 27 and 10 mL/min over baseline, respectively, at the high dose. Streptozotocin (70 mg/kg IV) was administered, but normoglycemia was maintained with continuous intravenous insulin infusion to control for potential streptozotocin side effects. Diabetes was induced 5 to 7 days later by stopping the insulin infusion. Hindlimb blood flow (measured 24 hours per day) decreased during the diabetic period and was accompanied by an increase in mean arterial pressure, suggesting a vasoconstrictor response. However, the responses to acetylcholine and sodium nitroprusside were not altered significantly on either day 2 or day 6 of the diabetic period. This suggests that neither endothelium-mediated vasorelaxation nor responsiveness to nitric oxide is impaired during the initial phase of diabetes and that diabetic hyperglycemia does not have a significant, direct effect to impair endothelium-mediated relaxation in insulin-dependent diabetes mellitus. The mechanism for the change in baseline blood flow and its potential influence on endothelial function, however, are not known.

Original languageEnglish (US)
Pages (from-to)541-547
Number of pages7
JournalHypertension
Volume32
Issue number3
DOIs
StatePublished - Jan 1 1998
Externally publishedYes

Fingerprint

Vasodilation
Endothelium
Nitroprusside
Streptozocin
Hyperglycemia
Acetylcholine
Catheters
Insulin
Femoral Vein
Vascular System Injuries
Abdominal Aorta
Vascular Endothelium
Vasoconstrictor Agents
Hindlimb
Type 1 Diabetes Mellitus
Intravenous Infusions
Blood Vessels
Arterial Pressure
Nitric Oxide
Animal Models

Keywords

  • Blood flow
  • Diabetes
  • Endothelium-derived relaxing factor
  • Glucose
  • Nitric oxide
  • Vasodilation

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Acute endothelium-mediated vasodilation is not impaired at the onset of diabetes. / Brands, Michael W; Fitzgerald, Sharyn M.

In: Hypertension, Vol. 32, No. 3, 01.01.1998, p. 541-547.

Research output: Contribution to journalArticle

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