Impaired vascular function during short-term poor glycaemic control in Type 1 diabetic patients.
OBJECTIVE
To study the effects of short-term poor glycaemic control on vascular function in Type 1 diabetic patients.


METHODS
Ten Type 1 diabetic patients, with diabetes duration of less than 10 years and normal urinary albumin excretion and ophthalmoscopy, were studied. All patients were examined after 48 h of good vs. poor glycaemic control within a 3-week period. Blood glucose was measured seven times daily for 2 days before each examination. External ultrasound was used to measure the dilatory response of the brachial artery to post-ischaemic increased blood flow (endothelium-dependent dilation) and to nitroglycerin (endothelium-independent dilation). Plasma concentration of von Willebrand factor antigen, adhesion molecules, vascular endothelial growth factor, homocystein and cholesterol were also measured.


RESULTS
The median blood glucose levels in the 48 h before the examinations were [median (range), good vs. poor control]: 6.3 (5.0-7.6) vs. 15.9 (11.3-17.8) (mmol/l). The flow-associated vasodilation (% of baseline) was reduced during poor control: 102.7 (94.7-110.8) vs. 104.0 (99.6-118.5) (P < 0.05) as were the nitroglycerin-induced dilation (% of baseline): 114.5 (103.3-127.9) vs. 120.2 (106.8-148.0) (P < 0.05). P-von Willebrand factor antigen was high during poor control (kIU/l): 1.14 (0.73-1.84) vs. 0.86 (0.72-1.39) (P < 0.05) and so was P-vascular endothelial growth factor (ng/l): 288 (133-773) vs. 254 (90-383) (P < 0.05).


CONCLUSIONS
Short-term (48 h) hyperglycaemia in Type 1 diabetic patients may disturb vascular function, possibly mediated through smooth muscle cell dysfunction as well as endothelial dysfunction. We suggest that prolonged and repeated episodes of hyperglycaemia could possibly lead to permanent vascular dysfunction and thereby development and progression of vascular complications in diabetes.
Department of Nephrology, Rigshospitalet, Copenhagen University Hospital, Denmark.
V R
VR
Sørensen
E R
ER
Mathiesen
P
P
Clausen
A
A
Flyvbjerg
B
B
Feldt-Rasmussen
D000328:Adult; D001786:Blood Glucose / Q000032:analysis*; D001916:Brachial Artery / Q000187:drug effects / Q000502:physiology*; D015815:Cell Adhesion Molecules / Q000097:blood; D002784:Cholesterol / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology*; D004334:Drug Administration Schedule; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D006710:Homocysteine / Q000097:blood; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000503:physiopathology; D007004:Hypoglycemic Agents / Q000008:administration & dosage; D007328:Insulin / Q000008:administration & dosage; D008297:Male; D005996:Nitroglycerin / Q000494:pharmacology; D012039:Regional Blood Flow / Q000502:physiology; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology; D014841:von Willebrand Factor / Q000032:analysis
D001786:Blood Glucose; D015815:Cell Adhesion Molecules; D007004:Hypoglycemic Agents; D007328:Insulin; D042461:Vascular Endothelial Growth Factor A; D014665:Vasodilator Agents; D014841:von Willebrand Factor; D006710:Homocysteine; D002784:Cholesterol; D005996:Nitroglycerin