Heparin prevents postischemic endothelial cell dysfunction by a mechanism independent of its anticoagulant activity*
- 1 February 1993
- journal article
- Published by Elsevier in Journal of Vascular Surgery
- Vol. 17 (2) , 318-327
- https://doi.org/10.1016/0741-5214(93)90417-k
Abstract
No abstract availableThis publication has 29 references indexed in Scilit:
- Surgical management of severe acute lower extremity ischemiaJournal of Vascular Surgery, 1992
- Functional coronary microvascular injury evident as increased permeability due to brief ischemia and reperfusion.Circulation Research, 1990
- Exogenous magnesium chloride-adenosine triphosphate administration during reperfusion reduces the extent of necrosis in previously ischemic skeletal muscleJournal of Vascular Surgery, 1990
- Replication of the Compartment Syndrome in a Canine Model: Experimental Evaluation of TreatmentJournal of Investigative Surgery, 1990
- Nitric oxide synthesized from L-arginine regulates vascular tone in the coronary circulation of the rabbitBritish Journal of Pharmacology, 1989
- Vasodilator actions of acetylcholine, A23187 and bradykinin in the guinea‐pig isolated perfused heart are independent of prostacyclinBritish Journal of Pharmacology, 1988
- Heparinization reduces endothelial permeability and hydrogen ion accumulation in a canine skeletal muscle ischemia-reperfusion modelJournal of Vascular Surgery, 1988
- Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factorNature, 1987
- The anti-inflammatory action of heparin: Heparin as an antagonist to histamine, bradykinin and prostaglandin E1Thrombosis Research, 1979
- The interaction of platelets with a tritium-labelled heparinThrombosis Research, 1976