Vitamin C affects thrombosis/ fibrinolysis system and reactive hyperemia in patients with type 2 diabetes and coronary artery disease.
OBJECTIVE
To examine the effect of vitamin C on forearm vasodilatory response to reactive hyperemia and on plasma level of plasminogen activator inhibitor 1 (PAI-1), von Willebrand factor (vWF), tissue plasminogen activator (tPA), antithrombin III (ATIII), proteins C and S, and factors V (fV) and VII (fVII) in patients with both type 2 diabetes and CAD.


METHODS
A total of 39 patients with type 2 diabetes and CAD were divided into two groups and received vitamin C (2 g/day) or no antioxidant for 4 weeks. Forearm blood flow was determined using venous occlusion gauge-strain plethysmography at baseline and after treatment. Forearm vasodilatory response to reactive hyperemia (RH%) or nitrate (NTG%) was defined as the percent change of flow from baseline to the maximum flow during reactive hyperemia or after administration of nitrate, respectively. Biochemical markers were determined by enzyme-linked immunosorbent assay (ELISA) or other standard methods.


RESULTS
RH% was significantly increased after treatment with vitamin C (from 62.4 +/- 7.2 to 83.1 +/- 9.3%, P = 0.024) but remained unaffected in the control group. Vitamin C decreased plasma levels of fV (from 143 +/- 5.4 to 123 +/- 6.03%, P = 0.038), vWF (from 133.5 +/- 14.5 to 109.5 +/- 11.4%, P = 0.016), and tPA (from 12.3 +/- 0.99 to 8.40 +/- 0.60 ng/ml, P = 0.001), whereas these levels remained unaffected in the control group. The changes in RH%, vWF, and tPA were significantly greater (P = 0.028, 0.036, and 0.007, respectively) in the vitamin C-treated group than in the control group. Levels of ATIII, proteins S and C, fVII, and PAI-1 remained unchanged in all groups.


CONCLUSIONS
Short-term treatment with high doses of vitamin C improved RH% and decreased plasma levels of tPA and vWF in patients with type 2 diabetes and CAD.
D000284:Administration, Oral; D000368:Aged; D000975:Antioxidants / Q000008:administration & dosage*; D000990:Antithrombin III / Q000378:metabolism; D001205:Ascorbic Acid / Q000008:administration & dosage*; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications*; D005165:Factor V / Q000378:metabolism; D005167:Factor VII / Q000378:metabolism; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects; D005542:Forearm / Q000098:blood supply; D006801:Humans; D006940:Hyperemia / Q000097:blood / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011486:Protein C / Q000378:metabolism; D017293:Protein S / Q000378:metabolism; D012039:Regional Blood Flow / Q000187:drug effects; D013927:Thrombosis / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D010959:Tissue Plasminogen Activator / Q000097:blood; D014664:Vasodilation / Q000187:drug effects; D014841:von Willebrand Factor / Q000378:metabolism
D000975:Antioxidants; D017395:Plasminogen Activator Inhibitor 1; D011486:Protein C; D017293:Protein S; D014841:von Willebrand Factor; D000990:Antithrombin III; D005165:Factor V; D005167:Factor VII; D010959:Tissue Plasminogen Activator; D001205:Ascorbic Acid