Modulation of human endothelial thrombomodulin by neutrophils and their release products.

Pulmonary microvascular injury, one of the earliest events in adult respiratory distress syndrome (ARDS), is caused by the release of injurious products from stimulated neutrophils and other inflammatory cells in the lung microvessels. An increased level of the endothelial cell-surface anticoagulant protein thrombomodulin (TM) in plasma from patients with ARDS as shown in this study may be one consequence of this, and our objective in this investigation was to define the mechanisms by which TM is modulated by neutrophils, using an endothelial tissue culture system. Human neutrophils in contact with endothelium caused a fourfold reduction in cell-surface TM activity, but only after prior neutrophil priming and activation.

The long-term effects of metoprolol and epanolol on tissue-type plasminogen activator and plasminogen activator inhibitor 1 in patients with ischaemic heart disease.

This double-blind, randomized parallel group study investigated the effect of 6 months beta-adrenoceptor antagonist therapy with either metoprolol (beta 1-selective without intrinsic sympathomimetic activity [ISA]) or epanolol (beta 1-selective with ISA) on markers of endogenous fibrinolysis in 20 patients with chronic stable angina receiving concurrent treatment with nifedipine. Neither drug had an effect on tissue-type plasminogen activator or plasminogen activator inhibitor type 1 (PAI-1). A significant correlation between fasting insulin and PAI-1 has previously been described and was confirmed in this study.

Effect of terminal (dry) heat treatment on non-enveloped viruses in coagulation factor concentrates.

Terminal dry heat treatment effectively inactivated hepatitis A virus (HAV) and canine parvovirus added to high-purity factor VIII. After 24 h at 80 degrees C, HAV infectivity was reduced by > or = 4.3 log10 TCID50, as measured in a newly developed infectivity assay.