Heparin-induced vasodilation in human hand veins

Objective To investigate whether heparin produces vasodilation in human veins and to explore the underlying mechanisms. Methods Eleven healthy volunteers were studied with the dorsal hand vein compliance technique. Dose‐response curves to heparin and enoxaparin were generated. Dose‐response curves t...

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Published in:Clinical pharmacology and therapeutics 1999-09, Vol.66 (3), p.232-238
Main Authors: Tangphao, Oranee, Chalon, Stephan, Moreno, Heitor J., Abiose, Ademola K., Blaschke, Terrence F., Hoffman, Brian B.
Format: Article
Language:English
Subjects:
Adult
Anticoagulants - administration & dosage
Anticoagulants - pharmacology
Biological and medical sciences
Blood. Blood coagulation. Reticuloendothelial system
Dose-Response Relationship, Drug
Enoxaparin - pharmacology
Female
Hand - blood supply
Heparin - administration & dosage
Heparin - pharmacology
Humans
Male
Medical sciences
Pharmacology. Drug treatments
Reference Values
Vasodilation - drug effects
Veins - drug effects
Volunteers
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Summary:Objective To investigate whether heparin produces vasodilation in human veins and to explore the underlying mechanisms. Methods Eleven healthy volunteers were studied with the dorsal hand vein compliance technique. Dose‐response curves to heparin and enoxaparin were generated. Dose‐response curves to heparin were also constructed before and after heparin was infused with the nitric oxide synthase inhibitor NG‐monomethyl‐l‐arginine (L‐NMMA) or combined histamine H1‐ and H2‐receptor blockade. Results Heparin but not enoxaparin caused significant dose‐dependent relaxation with an average apparent maximal response (at an infusion rate of 20 IU/min) of 47% ± 23%. L‐NMMA attenuated heparin‐induced relaxation (P < .001). The combination of H1‐ and H2‐receptor antagonists attenuated heparin‐induced relaxation to a lesser extent (P < .05). Heparin‐induced relaxation decreased by 52%, 73%, and 35% in the presence of L‐NMMA, indomethacin (INN, indometacin) plus L‐NMMA, and combined H1‐ and H2‐receptor blockade, respectively. Conclusion Heparin is an endothelium‐dependent venodilator in humans. The mechanism of heparin‐induced relaxation involves an increased availability of nitric oxide, possibly partially related to local release of histamine. Clinical Pharmacology & Therapeutics (1999) 66, 232–238; doi:
ISSN:0009-9236
1532-6535
DOI:10.1016/S0009-9236(99)70030-5