R. G. Mason

A.K. Naghdi's [1] closed-form Green's function for a semicircular plate, clamped around the curved edge and simply supported along its diameter, is re-derived by the method of images.

The renewed interest in endothelial function is based partly on success with tissue culture of endothelial cells. Endothelium functions primarily in the control of blood vessel wall permeability and in the provision of a blood-compatible lining surface. Recent findings indicate that endothelial cells are active metabolically in ways that may help prevent thrombosis. Endothelium actively degrades several different vasoactive compounds that circulate in blood and that can serve as platelet-aggregating agents. Endothelium also contains an inhibitor of platelet function and an activator of plasminogen, both of which can be released from the cell in response to appropriate stimuli. While intact endothelium functions primarily in prevention of thrombosis, damaged endothelium can contribute greatly to thrombus formation. Release of prostaglandins, adenine nucleotides, and other intracellular components from damaged endothelium can enhance platelet aggregation. Damaged endothelium may not function effectively in removal of vasoactive agents and may not release effective quantities of the inhibitor of platelet function or the activator of plasminogen. Altered endothelium exhibits tissue-factor activity, which can activate the extrinsic blood coagulation-system cascade. Finally, altered endothelial cells may contract and expose basement membrane to blood, thus enhancing thrombosis.

Abstract The plasminogen levels and the reactivities of plasmas in two commonly used blood coagulation tests have been compared for man and seven mammals. The plasmas of three nonhuman primates in general reacted as did human plasma in tests for plasminogen activation and in reactivity in the partial thromboplastin time test. The dog had the highest level of plasminogen, and the goat the lowest, of the eight species tested. Overall, the pig appeared to have the most reactive blood coagulation mechanism, clotting the fastest and lysing the slowest, while man's was among the least reactive in clotting and intermediate in lytic activity of those tested. Aside from the nonhuman primates, the calf's clotting and lytic mechanisms resembled those of man more nearly than did those of the other mammals tested. The influence of these species differences on selection of animals for in vivo evaluation of blood vascular prosthetic materials and devices is discussed.

Heparin, when added to citrated platelet-rich plasma (PRP), caused potentiation of platelet aggregation and the release reaction induced by the aggregating agents adenosine diphosphate (ADP), arachidonic acid, collagen, and epinephrine. At low concentrations (4.7 x 10(-5) M) arachidonic acid failed to cause aggregation of platelets in citrated PRP. However, in the presence of heparin, the same concentration of arachidonic acid caused aggregation. Examination of PRP for the presence of thromboxane A2 (TxA2) by use of a bioassay revealed that heparin also stimulated release of TxA2. This finding indicated that platelets released more TxA2 when they were challenged by low concentrations of arachidonic acid in the presence of heparin than in its absence. Platelets were labeled with 3H-arachidonic acid and 14C-serotonin, and attempts were made to determine whether heparin stimulated the platelet release reaction first with subsequent increased production of TxA2, or alternatively, whether heparin stimulated TxA2 production first with subsequent enhancement of the release reaction. In view of the demonstrated simultaneous release of 14C-serotonin and 3H-arachidonic acid metabolites, it appeared that either release of 14C and 3H occurs concurrently or, even if one of these events is dependent on the other, both events take place in rapid succession. Timed sequential studies revealed that in the presence of arachidonic acid, the addition of heparin hastened the apparently simultaneous release of both 14C and 3H.

SummaryThe extent to which platelets adhere to glass is dependent on fibrinogen concentration. Platelet adhesion increased progressively in a linear fashion when increasing concentrations of purified fibrinogen (0.5-14.0 mg/100 ml) were added to the blood of a patient with congenital afibrinogenemia.