Interaction Between Glycosaminoglycans, Platelets, and Leukocytes

Cerletti, Chiara; Rajtar, G; Marchi, E.; Gaetano, G de

doi:10.1055/s-2007-1001909

Cited by 24 publications

(21 citation statements)

References 38 publications

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“…These data agree with previously reported findings (Rajtar et al, 1993;Cerletti et al, 1994) that indicated that KRX-101 inhibits thrombin-induced platelet activation. Interestingly, evaluation of the effects of KRX-101 on coagulation, using the aPTT, demonstrated that at the dose used in our study, there was little or no change in hemostasis.…”

Section: Discussionsupporting

confidence: 94%

Sulodexide Attenuates Myocardial Ischemia/Reperfusion Injury and the Deposition of C-Reactive Protein in Areas of Infarction without Affecting Hemostasis

Lauver

Booth

White

et al. 2004

J Pharmacol Exp Ther

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Several glycosaminoglycans (GAGs) have been demonstrated to protect the ischemic heart against reperfusion injury, in part, by modulating activation of the complement cascade. The present study assessed the cardioprotective effects of sulodexide (KRX-101), a mixture of GAGs composed of 80% lowmolecular mass heparin and 20% dermatan sulfate. KRX-101 differs from other GAGs (e.g., heparin) in that it has limited anticoagulant efficacy and can be administered orally. The experimental protocol was designed to determine whether KRX-101 could protect the ischemic myocardium. Anesthetized New Zealand white rabbits underwent 30 min of coronary artery occlusion. Intravenous doses of KRX-101 (0.5 mg/kg, n ϭ 10) or drug diluent (n ϭ 10) were administered at the end of regional ischemia and at each hour of reperfusion. Infarct size, as a percentage of the area at risk, was calculated for both groups. Myocardial infarct size was 31.3 Ϯ 4.1% in the vehicleand 17.3 Ϯ 3.2% in the KRX-101-treated animals (p Ͻ 0.05 versus vehicle). Activated partial thromboplastin times determined at baseline (preischemia) and at each hour of reperfusion (n ϭ 4) were not significantly different between vehicle-and KRX-101-treated groups (p ϭ N.S.). Myocardial injury was further assessed by measuring serum levels of cardiac-specific troponin I. KRX-101 administration significantly reduced (p Ͻ 0.05) the serum concentration of troponin I during reperfusion. The results suggest that KRX-101 may be an effective adjunctive agent in myocardial revascularization procedures, without the risk of increased bleeding.

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Section: Discussionsupporting

confidence: 94%

Sulodexide Attenuates Myocardial Ischemia/Reperfusion Injury and the Deposition of C-Reactive Protein in Areas of Infarction without Affecting Hemostasis

Lauver

Booth

White

et al. 2004

J Pharmacol Exp Ther

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“…These data agree with previously reported findings (13,63) that indicated that sulodexide inhibits thrombin-induced platelet activation. Interestingly, evaluation of the effects of sulodexide on coagulation, using the aPTT, demonstrated that at the dose found to be cytoprotective in the reperfused heart sulodexide produced little or no change in hemostasis (48).…”

Section: Prevention Of Reperfusion Injurysupporting

confidence: 94%

Sulodexide: A Renewed Interest in This Glycosaminoglycan

Lauver

Lucchesi

2006

Cardiovascular Drug Reviews

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Glycosaminoglycans (GAGs) are the most abundant group of heteropolysaccharides found in the body. These long unbranched molecules contain a repeating disaccharide unit. GAGs are located primarily in the extracellular matrix or on the surface of cells. These molecules serve as lubricants in the joints while at the same time providing structural rigidity to cells. Sulodexide is a highly purified glycosaminoglycan composed of a fast mobility heparin fraction as well as dermatan sulfate. Sulodexide differs from other glycosaminoglycans, like heparin, by having a longer half-life and a reduced effect on systemic clotting and bleeding. In addition, sulodexide demonstrates a lipolytic activity that is increased in comparison to heparin. Oral administration of sulodexide results in the release of tissue plasminogen activator and an increase in fibrinolytic activities. An increasing body of research has demonstrated the safety and efficacy of sulodexide in a wide range of vascular pathologies.

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“…Human cerebral cortex cathepsin G generates amyloidogenic fragments from APP [151]. Heparin inhibits cathepsin G [152] and chymotrypsin [153] which decreases the production of the BA peptide. Serine proteases are all highly positively charged at physiologic pH [121] and bind to and are inhibited by highly negatively charged heparin [154].…”

Section: Serine Proteasesmentioning

confidence: 99%

Pathogenic Factors in Vascular Dementia and Alzheimer’s Disease

Engelberg¹

2004

Dement Geriatr Cogn Disord

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The following areas are discussed in this review: atherogenesis; cerebrovascular factors; hypoperfusion; β-amyloid production; β-amyloid fibril formation; β-sheets; metal cations; reactive oxygen species/free radicals; chronic inflammatory factors; endogenous plasma heparin; lipoprotein lipase; polyamines; protein kinase C; casein kinases; phospholipase A₂; serine proteases; myeloperoxidase; cyclooxygenase 2; cysteine proteases; caspases; proprotein convertases; aspartic proteases; cyclin proteinases; thrombin; tau hyperphosphorylation; advanced glycosylation end products; activator protein 1; calcium; apolipoprotein E Ε4; histamine; blood-brain barrier; glutamate; transglutaminase; insulin-like growth factor 1.

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Interaction Between Glycosaminoglycans, Platelets, and Leukocytes

Cited by 24 publications

References 38 publications

Sulodexide Attenuates Myocardial Ischemia/Reperfusion Injury and the Deposition of C-Reactive Protein in Areas of Infarction without Affecting Hemostasis

Sulodexide Attenuates Myocardial Ischemia/Reperfusion Injury and the Deposition of C-Reactive Protein in Areas of Infarction without Affecting Hemostasis

Sulodexide: A Renewed Interest in This Glycosaminoglycan

Pathogenic Factors in Vascular Dementia and Alzheimer’s Disease

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