prostaglandin-d2 and Hypotension

prostaglandin-d2 has been researched along with Hypotension* in 4 studies

Other Studies

4 other study(ies) available for prostaglandin-d2 and Hypotension

ArticleYear
Effects of 15-deoxy-Delta12,14-prostaglandin-J2 during hyperdynamic porcine endotoxemia.
    Intensive care medicine, 2006, Volume: 32, Issue:5

    To investigate the hemodynamic and metabolic effects of the peroxisome proliferator-activated receptor (PPAR)-gamma ligand and nuclear-factor (NF)-kappa B inhibitor 15-deoxy-Delta12,14-prostaglandin-J2 (15d-PGJ2) during long-term, hyperdynamic porcine endotoxemia.. Prospective, randomized, controlled experimental study with repeated measures.. Investigational animal laboratory.. 19 anesthetized, mechanically ventilated and instrumented pigs.. At 12 h of continuous intravenous endotoxin and hydroxyethylstarch to keep mean arterial pressure (MAP)>60 mmHg, swine randomly received vehicle (control group, n=10) or 15-deoxy-Delta12,14-prostaglandin-J2 (15d-PGJ2 group, n=9; 1 microg kg(-1) min(-1) loading dose during 1 h; thereafter,0.25 microg kg(-1) min(-1) for 11 h).. Hemodynamic, metabolic and organ function parameters were assessed together with parameters of nitric oxide production and oxidative stress. 15d-PGJ2 prevented the endotoxin-induced progressive hypotension, due to a positive inotropic effect, which resulted in a significantly higher blood pressure during the treatment phase and prevented the rise in hepatic vein alanine-aminotransferase activity. It did not affect, however, any other parameter of organ function nor of nitric oxide production, proinflammatory cytokine release or lipid peroxidation (8-isoprostane).. 15d-PGJ2 stabilized systemic hemodynamics, due to improved myocardial performance, and resulted in an only transient effect on alanine-aminotransferase activity, without further beneficial effect on endotoxin-induced metabolic and organ function derangements. Low tissue 15d-PGJ2 concentrations and/or the delayed drug administration may explain these findings.

    Topics: Animals; Cyclopentanes; Endotoxemia; Europe; Hypotension; Immunologic Factors; Oxidative Stress; Prospective Studies; Prostaglandin D2; Prostaglandins; Random Allocation; Respiration, Artificial; Swine

2006
Aspirin idiosyncrasy in systemic mast cell disease: a new look at mediator release during aspirin desensitization.
    Mayo Clinic proceedings, 1995, Volume: 70, Issue:5

    To report the clinical responses and mediator-release profiles of an aspirin-sensitive man with systemic mast cell disease during aspirin desensitization.. We quantified the release of six mediators during aspirin desensitization.. Although aspirin was administered cautiously with an initial dose of 20 mg, successful aspirin desensitization necessitated complete monitoring and resuscitation capabilities of a medical intensive-care unit for 4.5 days because of frequent, severe anaphylactoid responses. To our knowledge, this is the first report of a pronounced increase in plasma levels of the vasodilator peptide calcitonin gene-related peptide during episodes of aspirin-induced hypotension. Increases in plasma levels of calcitonin and serum levels of tryptase paralleled those of calcitonin gene-related peptide, but plasma levels of calcitonin remained increased for up to 18 hours. Urinary excretion of histamine and 1-methyl-4-imidazoleacetic acid also showed precipitous, although delayed, increases. Excretion of the prostaglandin D2 metabolite 11 beta-prostaglandin F2 alpha followed a bimodal pattern during aspirin desensitization; after severe hypotensive responses, the maximal value was more than 490,000 pg/mL, but the level decreased to less than 100 pg/mL after therapeutic serum levels of salicylate were attained.. These data suggest that the hypotensive responses to aspirin in some patients with systemic mast cell disease may result from the combined effects of several mediators.

    Topics: Adult; Aspirin; Calcitonin; Calcitonin Gene-Related Peptide; Chymases; Desensitization, Immunologic; Epinephrine; Humans; Hypotension; Imidazoles; Inflammation Mediators; Male; Mastocytosis; Prostaglandin D2; Serine Endopeptidases; Tryptases

1995
Hazards in operative management of patients with systemic mastocytosis.
    Annals of surgery, 1983, Volume: 197, Issue:5

    During the past two years, six patients with systemic mastocytosis have required general or regional anesthesia for operative correction of various surgical problems. Mastocytosis constitutes an extremely difficult problem in diagnosis and management. A large experience with patients with mastocytosis in the Vanderbilt Medical Center in the last decade has enhanced awareness of this disorder and increased its early recognition. The hazardous problems of systemic mastocytosis and the difficulties of its diagnosis and management are summarized and focussed on the increased hazard of those patients with this disease who require various surgical operations. Close collaboration between anesthesiologists, surgeons, and internists in this medical center in the past two years has made it possible to carry six of these patients through anesthesia, operation, and the postoperative period safely and without fatality.

    Topics: Adult; Chlorpheniramine; Cimetidine; Face; Female; Histamine Release; Humans; Hypotension; Intraoperative Care; Middle Aged; Prostaglandin Antagonists; Prostaglandin D2; Prostaglandins D; Surgical Procedures, Operative; Syncope; Urticaria Pigmentosa

1983
The flush syndrome: an expression of systemic mastocytosis with increased prostaglandin D2 production.
    The Netherlands journal of medicine, 1983, Volume: 26, Issue:1

    Topics: Adult; Aspirin; Erythema; Humans; Hypotension; Male; Prostaglandin D2; Prostaglandins; Prostaglandins D; Shock; Syndrome; Urticaria Pigmentosa

1983