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Biomedical subjects

H J Weiss

Publications and source records attributed to H J Weiss.

At least 91 records · Page 5Linked to original sources
PubMed1980

Acquired storage pool deficiency with increased platelet-associated IgG. Report of five cases.

Acquired abnormalities of platelet aggregation have been reported with increasing frequency. We studied five patients (including two with systemic lupus erythematosus and one with compensated chronic idiopathic thrombocytopenic purpura) in whom platelet aggregation responses to collagen, epinephrine and ADP are impaired; in all cases, we found that levels of platelet-associated immunoglobulin G (IgG) were increased. In all five patients substances stored in platelet-dense granules (ATP, ADP, serotonin and calcium) were diminished. The content of the alpha-granule substance, beta-thromboglobulin, was also decreased in most cases, whereas the levels of two secretable acid hydrolase enzymes (beta-glucuronidase and beta-N-acetyl glucosaminidase) were within normal limits. These findings are similar to those observed in subtypes of congenital storage pool deficiency. However, in contrast to the congenital disorder, a membrane-bound (nonsecretable) acid phosphatase was also decreased in the patients with acquired storage pool deficiency. These findings suggest that impaired platelet aggregation on an acquired basis may, in some patients, be due to immune platelet damage resulting in a distinctive type of platelet storage pool deficiency.

Adenosine Monophosphate↗
PubMed1980

Platelet-active drugs in the secondary prevention of cardiovascular events: an overview.

Experimental and clinical evidence strongly suggests that platelets play an important role in a variety of acute cardiovascular events, as well as in the vascular disease with which they are frequently associated. Hence, there is considerable interest in the use of platelet-active drugs in the prevention of these events. A sound pharmacologic basis for the use of platelet-active agents will require further advances in our understanding of the pathophysiology of cardiovascular events and the pharmacology of these drugs.

Aspirin↗
PubMed1980

Effect of shear rate on platelet interaction with subendothelium in citrated and native blood. II. Relationships among platelet adhesion, thrombus dimensions, and fibrin formation.

The adhesion of human platelets to subendothelium of rabbit aorta and the formation of microthrombi (aggregation) were investigated in an annular chamber after perfusion of native or citrated blood at wall shear rates ranging from 650 to 3300 sec-1. Previous studies demonstrated reduced adhesion and increased thrombi with native as compared to citrated blood and suggested that thrombi grow larger and higher in native blood. In the present study, thrombus dimensions were quantified by newly developed stereological techniques. The thrombus volume per surface area of subendothelium increased with increasing shear rate and was significantly greater in native blood. At 1300 sec-1 thrombi less than 5 and less than 10 micrometers in height were more frequent in citrated blood, and those greater than 20 micrometers were much more frequent in native blood. Maximum thrombus heights were 62 +/- 7 and 71 +/- 5 micrometers in native and 17 +/- 2 and 28 +/- 4 in citrated blood at shear rates of 650 and 1300 sec-1, respectively. Surface coverage with fibrin was 30%, 11%, and 0% at shear rates of 650, 1300, and 3300 sec-1, respectively. In addition, the effects of approximately 15 and approximately 45 mM citrate (final concentration in plasma) were studied at shear rates of 200, 650, and 2600 sec-1. At a citrate concentration of approximately 45 mM aggregation was abolished, and adhesion was strongly inhibited at the highest shear rate. We conclude that citrate (1) inhibits platelet attachment kinetics, thus acting to reduce adhesion, and (2) inhibits platelet aggregation and thrombus stability, thus reducing thrombus heights, which (3) may indirectly lead to increased adhesion.

Animals↗
PubMed1980

Release of human platelet factor V activity is induced by both collagen and ADP and is inhibited by aspirin.

Factor V activity in suspensions of human platelets washed by albumin density gradient separation increased in response to stimulation by both collagen and adenosine diphosphate (ADP). The appearance of factor V activity extracellularly had the characteristics of platelet secretion and was partially inhibited by aspirin and by the antimetabolites 2-deoxyglucose and antimycin A. Some increase in factor V activity was also observed in platelet suspensions during the initial response to ADP; this activity was not detected extracellularly, but remained associated with the platelets. Patients with storage pool deficiency (SPD) whose platelets are deficient only in dense granule substances released normal amounts of factor V activity, whereas decreased amounts were released in a patient whose platelets have both dense and alpha granule deficiencies. These findings suggest that a portion of platelet factor V is associated with, and released from, alpha granules.

Adenosine Diphosphate↗
PubMed1979

Isolated deficiency of platelet procoagulant activity.

This is a study of a 34 year old woman with a moderate to severe bleeding disorder in whom impaired platelet procoagulant activity (PPA) was found by several methods, including tests of factor 3 availability (PF-3a), prothrombin consumption and contact activation. No deficiencies of platelet adhesion, aggregation, secretion, metabolism or granule-bound substances were detectable. Under adequate platelet coverage, this woman underwent two surgical procedures without difficulty. These findings demonstrate the role of PPA in hemostasis and indicate that a defect in PPA can be an isolated occurrence. The abnormalities in PF-3a found in this patient could be due to the diminished number of factor V binding sites, resulting in impaired factor Xa binding, found in separate studies by Majerus et al.

Adult↗
PubMed1979

Prostacyclin (prostaglandin I2, PGI2) inhibits platelet adhesion and thrombus formation on subendothelium.

Prostaglandin I2 (prostacyclin, PGI2), a substance synthesized in the wall of blood vessels, has been previously shown to inhibit the aggregation of platelets in stirred platelet-rich plasma. We used a method in which segments of deendothelialized rabbit aorta are perfused at arterial shear rates with human blood and found that both platelet adhesion and thrombus formation on subendothelium was inhibited in blood containing 10 nM PGI2. PGI2 appears to reduce adhesion by inhibiting platelet spreading. These findings suggest that PGI2 could regulate the deposition of platelets on vascular surfaces.

Animals↗
PubMed1979

Platelet membrane glycoproteins in thrombasthenia, Bernard-Soulier syndrome, and storage pool disease.

Quantitative polyacrylamide gel electrophoresis has been carried out on patients with Bernard-Soulier syndrome, Glanzmann's thrombasthenia, and storage pool defect in order to clarify the abnormalities in their platelet membrane glycoproteins. Normal individuals had values (expressed as PAS staining units/mg of membrane protein) of 5.11 +/- 0.63 for glycoprotein 1 (Mr 150,000), 2.35 +/- 0.35 for glycoprotein II (Mr 120,000), 0.89 +/- 0.22 for glycoprotein III (Mr 100,000), and 1.34 +/- 0.64 for glycoprotein IV (Mr 85,000). Total PAS staining of these four major bands was 9.70 +/- 1.26 PAS units/mg of membane protein. Patients with Bernard-Soulier syndrome completely lacked glycocalicin and had about one half (1.90 PAS units/mg) of the glycoprotein I of normal controls. These was no significant reduction in glycoproteins II, III, and IV, but total PASstaining was reduced to 4.40 units/mg, reflecting the importance of the contribution of glycoprotein I to this parameter. Thrombasthenic platelets gave values for glycoprotein II of 0.66, which were about 25% of controls, and the values for glycoprotein III (0.34) were about 40% of controls. Patients with storage pool disease gave values within the normal range with the exception of one family which showed, in addition, small platelets and an associated lipid defect. In thic case of glycoprotein (2.71) was significantly elevated.

Blood Platelet Disorders↗
PubMed1978

Dissociation of factor VIII in the presence of proteolytic inhibitors.

When gel filtration of factor VIII is performed with buffers of high ionic strength (1.0 M NaCl or 0.25 M CaCl2), the procoagulant activity elutes with proteins of relatively low molecular weight. It has been suggested that in the presence of proteolytic inhibitors, the procoagulant activity would appear at the void volume. To test this hypothesis, chromatography with buffers of high ionic strength was performed in the presence of benzamidine hydrochloride, soy bean trypsin inhibitor, heparin, DFP, and aprotinin. Under all of these conditions, the procoagulant activity continued to elute with proteins of low molecular weight. Similar findings were obtained after chromatographing cryoprecipitate prepared from the plasma of a normal subject who had received heparin. Thus, at present there is no direct evidence to suggest that proteolysis is involved in the dissociation of factor VIII by buffers of high ionic strength.

Aprotinin↗