16-16-dimethylprostaglandin-e and Disease-Models--Animal

16-16-dimethylprostaglandin-e has been researched along with Disease-Models--Animal* in 2 studies

Other Studies

2 other study(ies) available for 16-16-dimethylprostaglandin-e and Disease-Models--Animal

ArticleYear
Effect of prostaglandin E in multiple experimental models. VII. Effect on resistance to sepsis.
    Burns : journal of the International Society for Burn Injuries, 1990, Volume: 16, Issue:1

    The immunosuppression seen following burn injury has frequently been attributed to elevated prostaglandin E levels. We evaluated the contribution of elevated prostaglandin E levels on susceptibility to infectious complications utilizing multiple mouse models. The administration of 100 micrograms/kg of the long-acting derivative of prostaglandin E, 16,16-dimethyl-prostaglandin E, was found to improve survival in C3/HEN mice challenged with 1 x 10(8) Escherichia coli organisms intraperitoneally. The administration of indomethacin was found to decrease survival in the same model. With C3/HEJ (endotoxin-resistant) mice, indomethacin was found to increase mortality rates in animals challenged with 1 x 10(8), 1 x 10(9) or 1 x 10(10) Escherichia coli organisms. These findings suggest that elevated prostaglandin E levels seen in burn patients may not be responsible for the postburn increased susceptibility to infectious complications.

    Topics: Animals; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Immune Tolerance; Indomethacin; Male; Mice; Mice, Inbred C3H; Prostaglandins E, Synthetic; Random Allocation

1990
16-16 dimethyl prostaglandin E2 reduces 5-fluorouracil-induced and mitomycin C-induced gastric mucosal injury in the dog.
    Cancer, 1984, Jul-01, Volume: 54, Issue:1

    Gastric complications occur in 5% to 20% of patients treated with hepatic artery infusion of chemotherapeutic agents for hepatic metastatic lesions. Often these complications are due to catheter dislodgement from the common hepatic artery into the left gastric artery. These studies were designed to answer the following questions: (1) Will chronic infusion of 5-fluorouracil into the left gastric artery produce mucosal injury in dogs; and (2) if so, will 16-16 dimethyl prostaglandin E2 afford protection against such injury? Mongrel dogs, 20 kg, were prepared with a polyethylene catheter in the left gastric artery and a Thomas cannula in the antrum 5 days prior to the study. Daily intraarterial infusions of either 5-fluorouracil, 6.7 mgM-2 X h-1, (N = 5) or 5-fluorouracil + 16-16 dimethyl prostaglandin E2, 2 micrograms X kg-1 X h-1, (N = 5) were given 12 hours a day for 5 days. In 2 dogs, 0.15 M NaCl was infused for 12 hours a day for 5 days as controls. Daily endoscopic evaluation of the gastric mucosa was made through the Thomas cannula by an unbiased observer and scored 0 to +5 based on degree of erythema, edema, friability, exudate, and gross ulceration. Results of these studies demonstrated that this dose of 5-fluorouracil had no effect on histamine-stimulated acid output. This dose of 16-16 dimethyl prostaglandin E2 inhibited histamine-stimulated maximal acid output 65%. From the observations made it was concluded that infusion of this chemotherapeutic regimen into the left gastric artery produced significant mucosal injury, simultaneous intraarterial infusion of 16-16 dimethyl prostaglandin E2 provided significant protection against this damage, and, since 16-16 dimethyl prostaglandin E2, at this dose, inhibits stimulated gastric acid secretion, it cannot be determined whether this observed mucosal protection is due to its antisecretory effect or some other mechanism.

    Topics: Animals; Disease Models, Animal; Dogs; Female; Fluorouracil; Gastric Acid; Gastric Mucosa; Infusions, Intra-Arterial; Male; Mitomycin; Mitomycins; Prostaglandins E, Synthetic

1984
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