Thromb Haemost 1994; 72(06): 942-946
DOI: 10.1055/s-0038-1648988
Original Article
Schattauer GmbH Stuttgart

Effects of Unfractionated and Low Molecular Weight Heparins on Platelet Thromboxane Biosynthesis “In Vivo”

Raffaele Landolfi
Hemostasis Research Center and Departments of Internal Medicine, Pharmacology and Surgery, Catholic University of Rome; Department of Pharmacology, University of Chieti, Italy
,
Erica De Candia
Hemostasis Research Center and Departments of Internal Medicine, Pharmacology and Surgery, Catholic University of Rome; Department of Pharmacology, University of Chieti, Italy
,
Bianca Rocca
Hemostasis Research Center and Departments of Internal Medicine, Pharmacology and Surgery, Catholic University of Rome; Department of Pharmacology, University of Chieti, Italy
,
Giovanni Ciabattoni
Hemostasis Research Center and Departments of Internal Medicine, Pharmacology and Surgery, Catholic University of Rome; Department of Pharmacology, University of Chieti, Italy
,
Armando Antinori
Hemostasis Research Center and Departments of Internal Medicine, Pharmacology and Surgery, Catholic University of Rome; Department of Pharmacology, University of Chieti, Italy
,
Riccardo Masetti
Hemostasis Research Center and Departments of Internal Medicine, Pharmacology and Surgery, Catholic University of Rome; Department of Pharmacology, University of Chieti, Italy
,
Carlo Patrono
Hemostasis Research Center and Departments of Internal Medicine, Pharmacology and Surgery, Catholic University of Rome; Department of Pharmacology, University of Chieti, Italy
› Author Affiliations
Further Information

Publication History

Received 10 May 1994

Accepted after revision 18 August 1994

Publication Date:
06 July 2018 (online)

Summary

Several “in vitro” and “in vivo” studies indicate that heparin administration may affect platelet function. In this study we investigated the effects of prophylactic heparin on thromboxane (Tx)A2 biosynthesis “in vivo”, as assessed by the urinary excretion of major enzymatic metabolites 11-dehydro-TxB2 and 2,3-dinor-TxB2. Twenty-four patients who were candidates for cholecystectomy because of uncomplicated lithiasis were randomly assigned to receive placebo, unfractionated heparin, low molecular weight heparin or unfractionaed heparin plus 100 mg aspirin. Measurements of daily excretion of Tx metabolites were performed before and during the treatment. In the groups assigned to placebo and to low molecular weight heparin there was no statistically significant modification of Tx metabolite excretion while patients receiving unfractionated heparin had a significant increase of both metabolites (11-dehydro-TxB2: 3844 ± 1388 vs 2092 ±777, p <0.05; 2,3-dinor-TxB2: 2737 ± 808 vs 1535 ± 771 pg/mg creatinine, p <0.05). In patients randomized to receive low-dose aspirin plus unfractionated heparin the excretion of the two metabolites was largely suppressed thus suggesting that platelets are the primary source of enhanced thromboxane biosynthesis associated with heparin administration. These data indicate that unfractionated heparin causes platelet activation “in vivo” and suggest that the use of low molecular weight heparin may avoid this complication.

 
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