However, whereas HCH reduced peak free thrombin generation in adult plasma by 81%, HCD was only able to reduce activity by 33%. In the presence of ATH, peak free thrombin generation in adult plasma on the cell surface was reduced by 92% compared with controls (no anticoagulant). We compared the abilities of ATH, covalent HC–heparin complex (HCH), and covalent HC–dermatan sulfate (HCD) to inhibit thrombin generation on FDLE in plasmas from either adults or newborns. However, heparin cofactor II (HC) has been shown to selectively inhibit thrombin, which may be advantageous if other enzyme activities are present in the airspace. We previously showed that covalent antithrombin–heparin complex (ATH) is superior to noncovalent antithrombin (AT) + heparin (H) mixtures at inhibiting plasma thrombin generation on rat fetal distal lung epithelium (FDLE) in vitro. Extravascular coagulation within the lung airspace is a hallmark of respiratory distress syndrome (RDS) in premature infants.
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