Changes in the aortic endothelium and plasma von Willebrand factor levels during the onset and progression of insulin-dependent diabetes in BB rats

1998 ◽  
Vol 139 (2) ◽  
pp. 291-299 ◽  
Author(s):  
José C.O Ribau ◽  
Mark W.C Hatton ◽  
Mary Richardson
1991 ◽  
Vol 80 (5) ◽  
pp. 525-531 ◽  
Author(s):  
B. M. Fisher ◽  
J. D. Quin ◽  
A. Rumley ◽  
S. E. Lennie ◽  
M. Small ◽  
...  

1. The effects of acute hypoglycaemia on haemostasis, fibrinolysis, blood viscosity and erythrocyte aggregation were examined after acute insulin-induced hypoglycaemia in six normal male subjects and in six male patients with poorly controlled insulin-dependent diabetes. In the control subjects hypoglycaemia caused a significant increase in the concentration of von Willebrand factor, with no change in the concentrations of fibrinogen and cross-linked fibrin degradation products. Fibrinolysis was enhanced, as indicated by significant increases in tissue plasminogen activator concentration and the fibrin plate lysis area, with a fall in plasminogen-activator inhibitor activity, suggesting complex formation. Whole-blood and plasma viscosity increased significantly after hypoglycaemia, but there was no significant change in erythrocyte aggregation tendency. 2. In diabetic patients the increase in the concentration of von Willebrand factor was significantly greater than in the control group (analysis of variance, P < 0.02). The basal concentration of tissue plasminogen activator was reduced at 3.7 ± 0.7 mg/l (mean ± sem) in the diabetic group compared with 8.5 ± 1.3 mg/l in the control group (Student's t-test, P < 0.01), but thereafter the increase in response to hypoglycaemia was similar. The changes in the other variables were not significantly different from the changes in the control group. 3. During acute hypoglycaemia in poorly controlled diabetic patients there is promotion of haemostasis with a greater increase in the concentration of von Willebrand factor, which, in association with the increase in viscosity, might reduce perfusion in diabetic microangiopathy, leading to aggravation of the microvascular complications of diabetes.


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