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Biomedical subjects

H J Weiss

Publications and source records attributed to H J Weiss.

At least 163 records · Page 9Linked to original sources
PubMed1968

The effect of salicylates on the hemostatic properties of platelets in man.

Ingestion of 1.5 g of aspirin, but not of sodium salicylate, produced a significant prolongation of the bleeding time in six normal male subjects when compared with the effects of a placebo. Similar differences in the effect of the two drugs on platelets was also observed. Aspirin ingestion resulted in impaired platelet aggregation by connective tissue and was associated with a decreased release of platelet adenosine diphosphate (ADP); sodium salicylate had no effect on these values. In vitro, incubation of platelet-rich plasma with an optimum aspirin concentration of 0.50 mmole/liter (0.045 mg/ml) inhibited both the adhesion of platelets to connective tissue and the release of ADP as well as the secondary wave of platelet aggregation produced with ADP or epinephrine; sodium salicylate had no effect on these reactions, which were also normal in patients with von Willebrand's disease. The inhibitory effect produced by ingesting a single 1.8 g dose of aspirin was detectable for 4-7 days at which time salicylate was no longer detectable in the blood, which suggested an irreversible effect on the platelet. Aspirin also inhibited the release of platelet adenosine triphosphate (ATP), but had no effect on the platelet surface charge, available platelet ATP or ADP, or the destruction of ADP by plasma ADPase. These studies lend further support to the hypothesis that ingestion of aspirin, in contrast to sodium salicylate, prolongs the bleeding time by inhibiting the release of platelet ADP, perhaps reflecting the findings in other cell systems which suggest that aspirin alters membrane permeability.

Adenine Nucleotides↗
PubMed1965

A study of the cation- and pH-dependent stability of factors V and VIII in plasma.

The in vitro lability of factors V and VIII in plasma has been studied. In agreement with previous reports, an increase in anticoagulant concentration renders both factors more labile (cation-deficient decay), as does an increase in the pH above 7.3 (alkaline-decay). Calcium appears to be the plasma cation which protects factors V and VIII against in vitro loss of activity. The protection obtained by the addition of other divalent cations depended on the type of plasma used. When resin-EDTA plasma was made cation free by dialysis at 4 degrees C and then incubated at 37 degrees C, the rapid loss of factors V and VIII activity could be prevented by prior addition of strontium, manganese and magnesium. In oxalate plasma, nickel, manganese, cadmium and strontium were effective. The alkaline decay of both factors V and VIII is irreversible. Partial reversibility of the cation-deficient decay was demonstrated for factor V, but not for factor VIII. The temperature coefficient for both the cation-deficient and alkaline decay is 2-3, suggesting an enzymatic rather than a physical reaction. There was no evidence to implicate thrombin, plasmin or trypsin since inhibitors of these enzymes failed to modify either type of decay.

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