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Vol. 282, Issue 1, 208-219, 1997
Department of Internal Medicine, Carolinas Medical Center,
Charlotte, North Carolina (T.K.); Departments of
Medicine (Y.-C.H.,
C.A.P.) and
Pharmacology (R.W.), Duke University, Durham, North
Carolina; Departments of
Environmental Health Sciences (A.F.) and
Medicine (D.J.), Johns Hopkins University, Baltimore, Maryland;
Scientific Protein Laboratories, Wanaukee, Wisconsin (E.M.) and the
Department of Medicine, University of Utah, Salt Lake City, Utah
(J.H.).
Heparin has potential use as an antiinflammatory treatment in many lung
diseases but its therapeutic use is limited by inherent anticoagulant
activity. The anticoagulant nature of heparin can be eliminated by a
number of chemical treatments, but often not without loss of other
important pharmacological activities. Lyophilization of porcine mucosal
heparin under extreme alkaline conditions (pH 
13) produces a
nonanticoagulant heparin remarkable for the selective loss of only 2-O
and 3-O sulfates, leaving 6-O and N-sulfates intact. In contrast to the
commonly used nonanticoagulant analog N-desulfated, N-reacetylated
heparin, selectively O-desulfated heparin retains potent activity as an
inhibitor of the cationic neutrophil proteases human leukocyte elastase
and cathepsin G, both in vitro and in vivo.
Selectively O-desulfated heparin also inhibits complement lysis of
erythrocytes, prevents ischemia-reperfusion injury of the lung, remains
a potent antiproliferative treatment for cultured airway smooth muscle
and normalizes altered neuronal M2 muscarinic receptor
sensitivity and bronchial hyperreactivity after antigen challenge.
These retained pharmacologic properties suggest possible use of this
new nonanticoagulant heparin for the treatment of a variety of lung
disorders.
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