Antiplatelet effects of prostacyclin and nitric oxide in patients with type I diabetes and ischemic or edematous retinopathy
The aim of this study was investigate prostacyclin and nitric oxide (NO) and their platelet second messengers cAMP and cGMP, in patients with type I diabetes with or without retinopathy. We compared 20 healthy volunteers and 97 patients with type I diabetes: 24 with no signs of diabetic retinopathy...
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Published in: | Platelets (Edinburgh) Vol. 12; no. 4; pp. 210 - 217 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
Informa UK Ltd
2001
Taylor & Francis |
Subjects: | |
Online Access: | Get full text |
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Summary: | The aim of this study was investigate prostacyclin and nitric oxide (NO) and their platelet second messengers cAMP and cGMP, in patients with type I diabetes with or without retinopathy. We compared 20 healthy volunteers and 97 patients with type I diabetes: 24 with no signs of diabetic retinopathy (DR), 43 with ischemicproliferative DR, and 30 with edematous DR. The following parameters were recorded: platelet aggregometry, nitrites/nitrates, 6-keto-prostaglandin-F 1 f , and intraplatelet cAMP and cGMP. Platelet aggregation was greater in patients with edematous DR. The platelets in patients with diabetes were more resistant to inhibition by prostaglandin E 1 or sodium nitropruside. Nitrite concentration in patients with ischemic-proliferative DR was 80% lower than the value in healthy controls, but there was no significant difference between the control group and patients with edematous DR. In the latter group, stimulation of neutrophils with L-arginine increased nitrite + nitrate production by 44 - 3.6%, whereas in patients with ischemic-proliferative DR, the increase was 9.8 - 0.8%. We conclude that NO production is higher in patients with type I diabetes and edematous retinopathy than in those with ischemic-proliferative retinopathy. This finding, together with the possibly greater production of free radicals, may explain the greater impairment of platelet function in the former patients. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0953-7104 1369-1635 |
DOI: | 10.1080/09537100120058748 |