Presence of platelet glycoproteins Ib and IIb-IIIa in inflammatory and noninflammatory synovium.

Rheumatoid synovial tissue and noninflammatory synovial tissue from patients with meniscus lesions were stained using monoclonal antibodies against platelet 150 kDa Ib glycoprotein (gp Ib) and against 140/110 kDa IIb-IIIa glycoprotein complex (gp IIb-IIIa) applied with the avidin-biotin-peroxidase complex method. Gp Ib and gp IIb-IIIa positive intravascular platelet aggregates were not seen, except locally in the capillary blood vessels of one rheumatoid synovial sample. This suggests that the platelets and the clotting sequence are not activated in inflamed synovial tissue. However, in many of the synovial capillaries endothelial immunoreactivity was seen. This reaction could have been due to cross reaction, since the vitronectin receptor beta chain is structurally identical to platelet gp IIIa. The gp IIb-IIIa member of the integrin receptor family plays a role in the transmembrane linkage between its extracellular ligands and intracellular microfibers. Gp IIb-IIIa may thus contribute to normal synovial physiology and to the pathogenesis of chronic synovitis.

[Venous outflow from the intervillous microcirculation in the human placenta]. / Der venöse Abfluss der intervillösen Mikrozirkulation in der menschlichen Plazenta.

This paper presents a morphological description of the venous area of the maternal circulation in the mature placenta. By injection of contrast medium into adjoining fetal cotyledons in 24 placentas the common intercotyledonal venous blood outflow pathways were specifically demonstrated, both radiologically and histologically. The interweaving and density of the terminal villi, the number and location of nuclear bridge formations, the width and course of the intervillous spaces, and the form of the columns and vela are characteristic of the venous outflow areas. The calcium incrustations found in varying degrees are likewise closely associated with venous area of the intervillous microcirculation. The findings are interpreted with regard to their importance for understanding the maternal placental blood flow in relation to the flow unit of the so called placenton.

Histamine receptors of the microvascular endothelium revealed in situ with a histamine-ferritin conjugate: characteristic high-affinity binding sites in venules.

Histamine covalently bound to glutaraldehyde-activated ferritin was prepared as either monomers or as small aggregates of approximately 0.05 to 0.15 micrometer Diam, suitable for electron microscopic detection of histamine cellular binding sites. The histamine-ferritin conjugates (MF) maintain the histamine capability to induce the opening of endothelial junctions in venules. To investigate the distribution of histamine receptors in the vascular endothelium, monomers or aggregates of MF were perfused in situ (mice), and various vascular beds, particularly that of the diaphragm, were fixed and processed for electron microscopy. The conjugate was preferentially bound on restricted areas of luminal endothelial cell plasmalemma especially in regions rich in filaments, and near the junctions between endothelial cells. The density of histamine binding sites was characteristically high in venules; it occurred to a much lesser extent in arterioles, veins, and muscular arteries whereas capillaries and aorta showed the lowest values. A similar distribution was obtained after perfusion of H1 or H2 receptor agonists coupled to ferritin (2-pyridylethylamine-ferritin [PF], or 4-methylhistamine-ferritin [MF], respectively). The binding specificity was assessed through control experiments with either native or activated ferritin or by competition with histamine. The findings suggest that histamine receptors are largely represented in the cell membrane of the vascular endothelium, particularly in venules. Experiments using specific H1 and H2 receptor agonists (PF and MF) and antagonists (mepyramine and cimetidine) indicate that the venular endothelium contains mainly H2 receptors.