Abstract
Dr. Lindahl has referred to my concept of macromolecular heparin as a multichain, whose structural integrity depends on a polysaccharide core. In 1971, I postulated that macromolecular heparin must be depolymerized to become biologically active (6). Later, I found that macromolecular heparin is a potent inhibitor of heart lipoprotein lipase (LPL) in vitro (7). Injected macromolecular heparin has a relatively low potency as an initiator of LPL activity in the blood. This activity appears in the blood rather slowly, compared with that of low-molecular-weight heparin (i.e., commercial heparin or enzymatically depolymerized macromolecular heparin) (7). These facts support the concept that depolymerization precedes the release of biologically active heparin from the mast cells. Endogenous heparin in the blood should therefore be of low molecular weight, and I would now like to demonstrate that this is so.
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