PubMed · 5824736
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Y E Hsia. 1969-10-30. Benzidine: a carcinogen.. https://doi.org/10.1056/nejm196910302811823
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Potential pharmacokinetic and pharmacodynamic interactions between two oral doses of GR32191 (40 and 80 mg), a new thromboxane antagonist, and heparin (5,000 IU bolus + 1,000 IU/h for 3 h) were studied in eighteen healthy male volunteers using two separate double-blind, randomised, placebo-controlled, cross-over studies. Mean (range) bleeding time values were 8.4 min (7.5-9.7) during heparin/placebo, 12.1 min (9.2-18.6) (GR32191/placebo) and 16.3 min (11.5-21.4) (GR32191/heparin) in the 40 mg study, while these values were 8.7 min (5.5-15.5), 16.0 min (9.3 - greater than 36.0) and 23.8 min (10.7 - greater than 36.0), respectively in the 80 mg study. Compared to screening values, the combination of 80 mg of GR32191 and heparin had a greater effect on the bleeding time than the sum of the prolongations after the separate treatments (p = 0.05). In the 40 mg study this was not the case. Pharmacokinetics of heparin (as assessed by plasma anti-Xa and antithrombin activity) and GR32191 were unaltered during co-administration of the two drugs. GR32191 did not influence the effects of heparin on APTT. Heparin slightly diminished the inhibition of collagen induced platelet aggregation by 80 mg of GR32191 and the U-46619 (thromboxane A2-mimetic) induced platelet aggregation remained unchanged. Overall fibrinolytic activity (as evaluated by the fibrin plate test) was similar during all three treatments in the study with 80 mg. The combination of 80 mg of GR32191 and heparin caused a prolongation of the bleeding time which was more than expected on the basis of their individual effects.
Explore the source record for details and available documents.
Suspensions of phorbol myristate acetate-activated polymorphonuclear leukocytes were analyzed with a Coulter Counter STKS hematological analyzer. Phorbol myristate acetate activation induced an increase in polymorphonuclear leukocyte volume and conductivity, while scatter was unchanged. Phorbol myristate acetate-activated neutrophils in a suspension containing nitroblue tetrazolium showed increased scatter. The rise in scatter was phorbol myristate acetate dose dependent, completely inhibited by diphenylene iodonium and partially by dimethyl sulfoxide, two inhibitors of NADPH oxidase. Zymosan-activated polymorphonuclear leukocytes were notably larger with a characteristic position on discriminant function 1 display (volume versus scatter) of the analyzer. Volume and conductivity changes were seemingly inexplicable features of phorbol myristate acetate activation. The rise in scatter was produced by cytoplasmic precipitation of reduced nitroblue tetrazolium and thus by O2-generation in phorbol myristate acetate-activated neutrophils. Zymosan phagocytosis was responsible for the notable rise in polymorphonuclear leukocyte volume. The analysis of activated polymorphonuclear leukocytes by Coulter Counter STKS may provide useful information on their activation and a pragmatic approach for studying function.