Heparin prevents postischemic endothelial cell dysfunction by a mechanism independent of its anticoagulant activity

Sternbergh, W. C. and Adelman, B. (1993). Heparin prevents postischemic endothelial cell dysfunction by a mechanism independent of its anticoagulant activity. In: 40th Scientific Meeting of the International Society for Cardiovascular Surgery, Chicago, IL, United States, (318-327). 9-10 June 1992. doi:10.1067/mva.1993.42846


Author Sternbergh, W. C.
Adelman, B.
Title of paper Heparin prevents postischemic endothelial cell dysfunction by a mechanism independent of its anticoagulant activity
Conference name 40th Scientific Meeting of the International Society for Cardiovascular Surgery
Conference location Chicago, IL, United States
Conference dates 9-10 June 1992
Journal name Journal of Vascular Surgery   Check publisher's open access policy
Place of Publication Philadelphia, PA, United States
Publisher Mosby
Publication Year 1993
Sub-type Fully published paper
DOI 10.1067/mva.1993.42846
ISSN 0741-5214
Volume 17
Issue 2
Start page 318
End page 327
Total pages 9
Language eng
Formatted Abstract/Summary
Purpose: Heparin may have protective effects on postischemic vascular endothelial cell function that are distinct from its anticoagulant, antiplatelet, or anticomplement activity. We tested this hypothesis in isolated rat hindlimbs.

Methods: Isolated rat hindlimbs underwent 60 minutes of normothermic ischemia and 10 minutes of reperfusion. Potential heparin interaction with plasma-based proteins or cells was eliminated by perfusion of the hindlimbs with a nonrecirculated albumin-enriched crystalloid buffer. Endothelial function was assessed by measurement of endothelium-derived relaxing factor (EDRF) activity. Limbs perfused at constant pressure were subjected to increasing log dose infusions of acetylcholine and nitroprusside to measure endothelial-dependent (EDRF-mediated) and endothelial-independent vasoreactivity, respectively. Fifty limbs were divided into seven groups: two nonischemic groups (one with heparin) and five ischemia/reperfusion groups treated with increasing doses of heparin (0 to 1.0 U/ml perfusate).

Results: The nontreated ischemia/reperfusion group (n = 12) had a 46.2% reduction in endothelial-dependent vasodilation of the rat hindlimb when compared with the nonischemic control (n = 7, p < 0.05). Treatment with heparin 0.5 U/ml (n = 6) nearly abolished this attenuation of endothelial-dependent vasodilation (4.3% reduction, p = not significant vs nonischemic control). The endothelial protective effect of heparin was dose-dependent: groups treated with 0.25 U/ml (n = 6) and 0.1 U/ml heparin (n = 7) showed progressive impairment in postischemic EDRF-mediated vasodilation. Endothelial-independent vasodilation induced by nitroprusside was unchanged by ischemia/reperfusion or heparin treatment, which confirmed that the postischemic damage and its protection by heparin were specific to the endothelium.

Conclusions: Heparin prevented postischemic endothelial cell dysfunction by a mechanism independent of its interactions with plasma-based proteins or cells. This nonanticoagulant protective effect may contribute to the salutary effects of heparinization during acute ischemic events.
Q-Index Code E1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Conference Paper
Collection: School of Medicine Publications
 
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Created: Mon, 14 Mar 2011, 10:04:50 EST