COMPARISON OF THE VASODEPRESSOR EFFECTS OF PROSTACYCLIN AND 6‐OXO‐PROSTAGLANDIN F1α WITH THOSE OF PROSTAGLANDIN E2 IN RATS AND RABBITS
- J. Armstrong, N. Lattimer, S. Moncada, J. Vane
- Biology, MedicineBritish Journal of Pharmacology
- 1 January 1978
In rats and rabbits vasodepressor responses induced by prostacyclin were similar in magnitude after either intravenous or intra‐aortic administration, emphasizing the need to consider prostacyClin in addition to PGE2 as a major determinant influencing blood pressure.
Ticlopidine-, Clopidogrel-, and Prasugrel-Associated Thrombotic Thrombocytopenic Purpura: A 20-Year Review from the Southern Network on Adverse Reactions (SONAR)
- Sony Jacob, Brianne L. Dunn, C. Bennett
- Biology, MedicineSeminars in Thrombosis and Hemostasis
- 30 October 2012
Severe deficiency of ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) was present in 80% and antibodies to 100% of these TTP patients on ticlopidine, 0% of the patients with clopidogrel- associated TTP, and an unknown percentage of patients with prasugrel-associated TTP.
Gene dose effect reveals no Gs-coupled A2A adenosine receptor reserve in murine T-lymphocytes: studies of cells from A2A-receptor-gene-deficient mice.
- J. Armstrong, J. F. Chen, M. Sitkovsky
- BiologyBiochemical Journal
- 15 February 2001
It is concluded that the number of A2ARs is the limiting factor in determining the maximal cAMP response of T-lymphocytes to extracellular adenosine, thereby minimizing the immunosuppressive effects of ExtracellularAdenosine.
Antibiotic-associated colitis: effects of antibiotics on Clostridium difficile and the disease in hamsters.
The results suggest it may be wise to use isolation precautions for patients with colitis caused by C. difficile, as the isolates were often reesistant to tetracycline, cephalosporins, trimethoprim-sulfamethoxazole, clindamycin, erythromycin and aminoglycosides.
Studies on the mode of action for thyroid gland tumor promotion in rats by phenobarbital.
- R. Mcclain, R. Posch, T. Bosakowski, J. Armstrong
- Biology, MedicineToxicology and Applied Pharmacology
- 30 June 1988
Urethane inhibits cardiovascular responses mediated by the stimulation of alpha-2 adrenoceptors in the rat.
- J. Armstrong, F. LEFÈVRE‐BORG, B. Scatton, I. Cavero
- Biology, MedicineJournal of Pharmacology and Experimental…
- 1 November 1982
Urethane inhibits cardiovascular responses that are mediated by peripheral and central alpha-2 adrenoceptors and decreases the pressor responses evoked by clonidine, oxymetazoline and norepinephrine which stimulate both alpha-1 and alpha- 2 adrenoceptor agonists.
Neuroprotective efficacy of lifarizine (RS‐87476) in a simplified rat survival model of 2 vessel occlusion
- Douglas E. McBean, Victoria Winters, A. Wilson, C. B. Oswald, Brian J. Alps, J. Armstrong
- Biology, MedicineBritish Journal of Pharmacology
- 1 December 1995
Data show that the newly modified rat two vessel occlusion model produced a quantifiable level of ischaemic damage and that the novel agent lifarizine is neuroprotective in the model.
α‐Adrenoceptor subtypes in dog saphenous vein that mediate contraction and inositol phosphate production
- P. Hicks, M. Barras, G. Herman, P. Mauduit, J. Armstrong, B. Rossignol
- Biology, ChemistryBritish Journal of Pharmacology
- 1 January 1991
Contractile responses to the α‐adrenoceptor agonists phenylephrine, cirazoline or BHT‐920 in dog isolated saphenous vein rings, using the antagonists yohimbine (Yoh), idazoxan (Idaz), prazosin (Praz), WB‐4101 (WB) and nitrendipine or zero Ca2+ medium are studied.
Synthesis of acetyl, docosahexaenoyl-glycerophosphocholine and its characterization using nuclear magnetic resonance
- A. Polette, C. Deshayes, B. Chantegrel, M. Croset, J. Armstrong, M. Lagarde
- Chemistry, BiologyLipids
- 1 December 1999
It is concluded that 1-acetyl,2-DHA-GPC might be considered as a stable form of 1-lyso, 2- DHA- GPC for its delivery to tissues, if the latter exhibits acetyl hydrolase activity.
Genetic hypertension in rats is accompanied by a defect in renal prostaglandin catabolism
- J. Armstrong, G. J. Blackwell, R. Flower, J. Mcgiff, K. Mullane, J. Vane
- Biology, MedicineNature
- 15 April 1976
Homogenates of kidneys of New Zealand rats inbred for hypertension exhibit lower prostaglandin inactivation by 15-hydroxydehydrogenase than controls, and this biochemical deject could be the inherited abnormality primarily responsible for the development of hypertension in these animals.
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