Adjunctive Selectin Blockade Successfully Reduces Infarct Size Beyond Thrombolysis in the Electrolytic Canine Coronary Artery Model

Silver, Mitchell; Sutton, Joseph M.; Hook, Sharon E.; Lee, Philmo; Malycky, Janis L.; Phillips, M. L.; Ellis, Stephen G.; Topol, Eric J.; Nicolini, Fabio

doi:10.1161/01.cir.92.3.492

Cited by 48 publications

(19 citation statements)

References 40 publications

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“…A selectin inhibitor administered as an adjunct to thrombolytic therapy was reported to reduce infarct size in a canine model of coronary thrombosis. 40 Treatment with an anti-P-selectin antibody protected the feline heart in a model of myocardial ischemia and reperfusion injury. 41 Finally, 2 anti-P-selectin antibodies decreased vein wall inflammation and thrombus formation in a baboon model of deep vein thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Soluble Form of PSGL-1 Accelerates Thrombolysis and Prevents Reocclusion in a Porcine Model

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Recombinant Soluble Form of PSGL-1 Accelerates Thrombolysis and Prevents Reocclusion in a Porcine Model

et al. 1999

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“…24 -26 Analogues of this carbohydratebinding site, a sLe x oligosaccharide containing fucose and sialic acid moieties [NeuAC2,3Gal␤1,4(Fuc␣1,3)GlcNAc␤1,3Gal␤-O(CH2)5COOCH3] such as CY-1503, inhibit neutrophil adhesion to endothelial selectins in vitro 25,26 and in experimental models of myocardial ischemia and reperfusion in vivo. [27][28][29][30] Recently, it has been shown that a carbohydrate analogue of sLe x reduced cyclic flow variations in injured canine coronary arteries 31 and attenuated intimal hyperplasia after balloon arterial injury in rabbits. 32 However, none of those studies have examined platelet and neutrophil adhesion and interactions with the damaged denuded arteries, which may be the first target of sLe x analogues during the acute response to arterial injury.…”

mentioning

confidence: 99%

Selectin Blockade Reduces Neutrophil Interaction With Platelets at the Site of Deep Arterial Injury by Angioplasty in Pigs

Merhi

Provost

Chauvet

et al. 1999

ATVB

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Abstract-The adhesion of neutrophils to damaged arterial surfaces is increased in the presence of platelets by a mechanism implicating platelet P-selectin. Such interactions may enhance thrombus formation and the vascular response to injury. In this study, we investigated the effects of a selectin blocker (CY-1503), an analogue of sialyl Lewis x , on platelet and neutrophil interactions after arterial injury produced by angioplasty in pigs.51 Cr-platelet deposition and 111In-neutrophil adhesion were quantified on intact, mildly and deeply injured carotid arterial segments, produced by balloon dilation, in control (saline, nϭ8) and treated (CY-1503, 15 mg/kg IV, nϭ7) pigs. The hematological parameters, the aggregation of whole blood in response to adenosine diphosphate, and the activating clotting time, as well as the heart rate and mean arterial blood pressure, were similar among groups and were not influenced significantly by CY-1503. The level of platelet and neutrophil adhesion increased significantly with the severity of arterial injury but was not influenced by CY-1503 on intact and mildly injured arterial segments. However, at the site of deep arterial injury, CY-1503 treatment was associated with a 58% reduction (PϽ0.01) in neutrophil adhesion, from 446.7Ϯ72.6ϫ10 3

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“…In addition, the adhesion of leukocytes to the region of thrombosis can cause further obstruction to blood flow in an already ischaemic region, resulting in further tissue damage [42]. Indeed, the antagonism of P-selectin in a dog model has been shown to reduce infarct size [43]. In addition, Pselectin antagonism can reduce neointimal formation postballoon angioplasty in animal models [44].…”

Section: P-selectin and Atherosclerosismentioning

confidence: 99%

The Assessment of Platelet Activation in Antiplatelet Drug Development

Tan

Lip²

2005

CMC

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Platelet activation plays an important role in a wide range of pathological conditions. For example, platelet activation has been shown to be involved in the defence against parasitic infection, the pathogenesis of atherosclerotic disease, and various arterial and venous thrombotic diseases. Indeed, there is considerable interest in the manipulation of platelet function for therapeutic gain. It is for these reasons that there is considerable interest in developing assays measuring in vivo platelet activation. Current modalities in the measurement of platelet activation include Enzyme-linked Immunosorbent Assays (ELISA), platelet flow cytometry and electron microscopy. It is proposed that methods in measuring platelet activation can also be classified into 'direct' and 'indirect' modalities, both of which have their distinct advantages and disadvantages. Unfortunately, there is at present no consensus on the ideal method of measuring platelet activation. Thus, studies on platelet activation should ideally include at least one of each of direct and indirect modality of studying platelet activation. This review provides an overview of basic platelet biology and the various methods of measuring platelet activation, with an emphasis on their role in drug development.

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Adjunctive Selectin Blockade Successfully Reduces Infarct Size Beyond Thrombolysis in the Electrolytic Canine Coronary Artery Model

Cited by 48 publications

References 40 publications

Recombinant Soluble Form of PSGL-1 Accelerates Thrombolysis and Prevents Reocclusion in a Porcine Model

Recombinant Soluble Form of PSGL-1 Accelerates Thrombolysis and Prevents Reocclusion in a Porcine Model

Selectin Blockade Reduces Neutrophil Interaction With Platelets at the Site of Deep Arterial Injury by Angioplasty in Pigs

The Assessment of Platelet Activation in Antiplatelet Drug Development

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