Dipyridamole increases red cell deformability.

So, Sowemimo-Coker; Kovács, Iren B.; Pickles, H; Hedges, A.; Turner, Patricia V.

doi:10.1111/j.1365-2125.1983.tb02188.x

Cited by 10 publications

(5 citation statements)

References 7 publications

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“…For example, it decreases erythrocyte membrane deformability (32) and interferes with cell spreading and pseudopod formation in cultured embryonal cells (33). Through such action it might influence virus binding or release.…”

Section: Discussionmentioning

confidence: 99%

Dipyridamole potentiates the inhibition by 3'-azido-3'-deoxythymidine and other dideoxynucleosides of human immunodeficiency virus replication in monocyte-macrophages.

Szebeni

Wahl

Popovič

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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Dipyridamole (DPM) is commonly used as a coronary vasodilator and inhibitor of platelet aggregation in the treatment of cardiovascular diseases. We report here that DPM potentiates the inhibitory effects of 3'-azido-3'-deoxythymidine (AZT) and 2',3'-dideoxycytidine against human immunodeficiency virus type 1 (HIV-1) in human monocyte-macrophages. At the same concentrations, DPM does not potentiate the toxic effects of AZT on these cells or on human bone marrow (granulocytemonocyte) progenitor cells. Since monocyte-macrophage lineage cells appear to be the major reservoir for HIV-1 in vivo, these finding suggest the possibility of using DPM or its analogues in combination chemotherapy of HIV infections.Dipyridamole (DPM; Persantine) is widely used as an oral agent in the treatment of cardiovascular diseases because of its platelet antiaggregant and vasodilator activities (1). At pharmacologic concentrations it has several different mechanisms of action (1,2). The best-studied to date is an inhibitory effect on carrier-mediated transport of nucleosides across cell membranes (3, 4). Through this mechanism, DPM affects primarily the "salvage" pathways for nucleotide production. Hence, it has been studied for cancer chemotherapy in combination with inhibitors of de novo nucleotide synthesis (5-8). We report here that DPM potentiates the inhibitory effects of 3'-azido-3'-deoxythymidine (AZT) and 2',3'-dideoxycytidine (ddC) against human immunodeficiency virus type 1 (HIV-1) in cultured human monocytemacrophages. AZT is currently accepted therapy for acquired immunodeficiency syndrome (AIDS); ddC is being used in clinical trials, both as a single agent and in alternation with AZT (9-13). These dideoxynucleosides (ddNs) appear to act principally as inhibitors of the viral reverse transcriptase (9-11). MATERIALS AND METHODS 3842The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Section: Discussionmentioning

confidence: 99%

Dipyridamole potentiates the inhibition by 3'-azido-3'-deoxythymidine and other dideoxynucleosides of human immunodeficiency virus replication in monocyte-macrophages.

Szebeni

Wahl

Popovič

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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“…Magnesium may partially improve the impaired microcirculation in preeclampsia by increasing RBC deformability through antagonizing the stimulation of calcium pumps and reducing ATP depletion (Schauf et al, 2004 ). An additional example is dipyridamole, an inhibitor of platelet activation, which may enhance RBC deformability by enhancing glucose uptake and boosting glycolysis, increasing intracellular levels of ATP, and thus maintaining a more efficient calcium pumping to the extracellular milieu (Sowemimo-Coker et al, 1983 ; Saniabadi et al, 1992 ).…”

Section: Hereditary Hemolytic Anemia: Understanding the Molecular Biomentioning

confidence: 99%

Red blood cell vesiculation in hereditary hemolytic anemia

et al. 2013

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Hereditary hemolytic anemia encompasses a heterogeneous group of anemias characterized by decreased red blood cell survival because of inherited membrane, enzyme, or hemoglobin disorders. Affected red blood cells are more fragile, less deformable, and more susceptible to shear stress and oxidative damage, and show increased vesiculation. Red blood cells, as essentially all cells, constitutively release phospholipid extracellular vesicles in vivo and in vitro in a process known as vesiculation. These extracellular vesicles comprise a heterogeneous group of vesicles of different sizes and intracellular origins. They are described in literature as exosomes if they originate from multi-vesicular bodies, or as microvesicles when formed by a one-step budding process directly from the plasma membrane. Extracellular vesicles contain a multitude of bioactive molecules that are implicated in intercellular communication and in different biological and pathophysiological processes. Mature red blood cells release in principle only microvesicles. In hereditary hemolytic anemias, the underlying molecular defect affects and determines red blood cell vesiculation, resulting in shedding microvesicles of different compositions and concentrations. Despite extensive research into red blood cell biochemistry and physiology, little is known about red cell deformability and vesiculation in hereditary hemolytic anemias, and the associated pathophysiological role is incompletely assessed. In this review, we discuss recent progress in understanding extracellular vesicles biology, with focus on red blood cell vesiculation. Also, we review recent scientific findings on the molecular defects of hereditary hemolytic anemias, and their correlation with red blood cell deformability and vesiculation. Integrating bio-analytical findings on abnormalities of red blood cells and their microvesicles will be critical for a better understanding of the pathophysiology of hereditary hemolytic anemias.

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“…0.01. aspirin did so. Phosphodiesterase inhibitors are known to improve red blood cell deformability [40], but this is not the case for aspirin which reduces red cell deformability [41]. Cilostazol, a phosphodiesterase inhibitor, was reported to inhibit platelet activation and coagulation when tested by haemostatometry [14].…”

Section: Discussionmentioning

confidence: 99%

Effects of Clopidogrel on Platelet Activation and Coagulation of Non-Anticoagulated Rat Blood under High Shear Stress

Taka

Okano

Seki

et al. 1999

Pathophysiol Haemos Thromb

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Clopidogrel is a new thienopyridine derivative similar to ticlopidine, which inhibits adenosine diphosphate-induced platelet aggregation. The in vitro effects of clopidogrel on shear-induced platelet activation and coagulation were assessed after oral administration to rats, by subjecting non-anticoagulated blood to haemostatometry. Clopidogrel significantly inhibited shear-induced platelet activation and coagulation 2 h after administration at doses of 7.5 and 15 mg/kg. Both ticlopidine (200 mg/kg) and aspirin (200 mg/kg) inhibited shear-induced platelet activation, but not coagulation. The peak inhibition of plaetelet activation by clopidogrel occurred 2 h after oral administration, but significant inhibition persisted even after 24 h. These results suggest that clopidogrel could be a more potent antithrombotic agent than ticlopidine or aspirin, and also that ADP plays an important role in shear-induced platelet activation.

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Dipyridamole increases red cell deformability.

Cited by 10 publications

References 7 publications

Dipyridamole potentiates the inhibition by 3'-azido-3'-deoxythymidine and other dideoxynucleosides of human immunodeficiency virus replication in monocyte-macrophages.

Dipyridamole potentiates the inhibition by 3'-azido-3'-deoxythymidine and other dideoxynucleosides of human immunodeficiency virus replication in monocyte-macrophages.

Red blood cell vesiculation in hereditary hemolytic anemia

Effects of Clopidogrel on Platelet Activation and Coagulation of Non-Anticoagulated Rat Blood under High Shear Stress

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