Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Prostaglandin E, release

Vesce F, Buzzi M, Ferretti ME, Pavan B, Bianciotto A, Jorizzo G, Biondi C. Inhibition of amniotic prostaglandin E release by ampicillin. Am J Obstet Gynecol 1998 178(4) 759-64. [Pg.2766]

Gemsa D, Kramer W, Brenner M et al (1980) Induction of prostaglandin E release from macrophages by colchicine. J Immunol 124 376-380... [Pg.478]

Smooth muscles and vascular smooth muscles Prostaglandins E2 and I2 cause arteriolar dilation in the systemic and pulmonary vascular beds. Prostaglandins and E2, as well as thromboxane B2, constrict the human umbilical cord. Leukotrienes C4 and D4, which release prostaglandin E, decrease peripheral vascular resistance. [Pg.480]

Rather than being reincorporated into inositol phospholipids, DAG can be broken down to release some arachidonate which is the precursor of prostaglandin E which, in turn, can react with plasma membrane receptors linked to adenyl cyclase and cAMP production. IL-3 does not activate phospholipase C but does promote phosphorylation of the glucose transporter by phosphokinase C (Dexter and Spooner, 1987). [Pg.30]

Fatalities from normal doses and overdoses of intravenous NAC have not been reported. This is most probably due to the fact that the body produces this compound naturally and can rapidly metabolize it in the liver. Toxicity is usually limited to anaphylactoid reactions and nausea/vomiting. The average time for the onset of adverse effects following commencement of the infusion of NAC was 30 min (range, 5-70 min). In vivo and in vitro tests indicate that NAC is an inhibitor of allergen tachyphylaxis by inhibition of prostaglandin E synthesis. Adverse reactions are anaphylactoid in type and have been attributed to cause histamine release. [Pg.717]

Misoprostol (Cytotec) Prostaglandin E analog which increases HCO3 and mucin release. Also reduces acid secretion. Prevention of ulcers caused by aspirin and other NSAIDS. Abortion (uterine contraction), diarrhea, abdominal pain, nausea, flatulance. [Pg.92]

Fig. 3. Effect of oxytocin (0,1,10 or 100 ng/mL medium) (O) and oxytocin (0,1,10 or 100 ng/mL medium) in combination with protein kinase A inhibitor Rp-cAMPS ( 1 imo ) on prostaglandin (PG)E release by isolated and cultured porcine ovarian follicles. Values are means + SEM. Significant differences (P< 0.05) between cells cultured with and without exogenous oxytocin. Methods of isolation and culture of ovarian follicles, as well as the prostaglandin E radioimmunoassay are described in (8). [Pg.152]

Nizankowska E, Szczeklik A (1979) Keine Bedenken gegen Solosin bei Acetylsalicylsaure-empfindlichen Asthmatikem. Dtsch Med Wochenschr 104 1388-1389 Noid HE, Schulze TW, Winkelmann RK (1974) Diet plan for patients with salicylate-induced urticaria. Arch Dermatol 109 666-670 O Brien JR (1968) Effects of salicylates on human platelets. Lancet 1 779-781 Okazaki T, Ilea VS, Rosario NA, Reisman RE, Arbesman CE, Lee JB, Middleton E Jr (1977) Regulatory role of prostaglandin E in allergic histamine release with observations on responsiveness of basophil leukocytes and the effect of acetylsalicylic add. J Allergy Clin Immunol 60 360-366... [Pg.296]

Colchicine with its microtubule-disrupting properties limits the chemotactic and phagocytic activity of polymorphonuclear lymphocytes. It also induces the release of prostaglandin E, a suppressor of leukocyte function by increasing the level of cyclic adenosine monophosphate [39]. Furthermore, the ability of colchicine in inhibition of IL-1 production and histamine release makes it an excellent drug for a number of dermatitis-related complexities like psoriasis, Behget s syndrome, recurrent aphthous stomatitis, leukocytoclastic vasculitis and urticarial vasculitis, bullous disease, scleroderma, fibromatosis. Sweet s syndrome, amyloidosis, and many more [40]. [Pg.475]

The essential oil of Bupleurum species markedly suppressed the hind paw swelling induced by carrageenin in mice and rats. The mechanism of anti-inflammatory action however might be related with the inhibitory effect of the synthesis or release of prostaglandin E (PGE) and bradykinin [27]. [Pg.335]

Murray, D. and N. Rushton. 1990. The effect of strain on bone ceU prostaglandin E 2 release A new experimental method. Calcif Tissue Int 47 35-9. [Pg.302]


See other pages where Prostaglandin E, release is mentioned: [Pg.431]    [Pg.2757]    [Pg.114]    [Pg.124]    [Pg.431]    [Pg.2757]    [Pg.114]    [Pg.124]    [Pg.273]    [Pg.254]    [Pg.268]    [Pg.100]    [Pg.113]    [Pg.273]    [Pg.320]    [Pg.98]    [Pg.90]    [Pg.445]    [Pg.205]    [Pg.157]    [Pg.1250]    [Pg.429]    [Pg.484]    [Pg.1434]    [Pg.9]    [Pg.29]    [Pg.31]    [Pg.118]    [Pg.144]    [Pg.173]    [Pg.184]    [Pg.324]    [Pg.399]    [Pg.399]    [Pg.49]    [Pg.2182]    [Pg.80]    [Pg.399]   
See also in sourсe #XX -- [ Pg.20 ]




SEARCH



E-prostaglandins

© 2024 chempedia.info