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SUMMARY The effect of acute administration of indomethacin over 24 hours on basal and histamine stimulated gastric acid secretion was evaluated in seven normal male volunteers. Augmented histamine tests (0.015 mg/kg/h) infused with the antihistamine diphenhydramine hydrochloride (25 mg/h) were performed before and after pretreatment with indomethacin or matching placebo capsules. The dose of indomethacin was 75 mg (sustained release capsules) taken 12 and 24 hours before and 50 mg taken one hour before a two hour histamine infusion test. Indomethacin enhanced basal gastric secretion from 3*5±0-5 to 6-4±0-6 mmol/h (p<0.01) and histamine stimulated secretion from 48±6 to 62±5 mmol/2 h (p<005). Indomethacin significantly inhibited systemic prostaglandin biosynthesis as measured by urinary excretion (87±12 vs 41±6 ng PGE/g creatinine/h) and the drug increased platelet aggregation time two, five, and six fold, respectively, induced by ADP, collagen, and adrenaline. The data indicate that therapeutic doses of indomethacin augmented basal and secretagogue stimulated gastric acid secretion in control subjects. The 15 August 1983 alterations or lack of alteration in gastric acid secretion after indomethacin therapy was predicted only from the knowledge of the inhibitory effect of the drug on prostaglandin biosynthesis.We undertook this study to evaluate the effect of indomethacin on basal and histamine stimulated gastric acid secretion in normal subjects. We used therapeutic concentrations of the drug and documented inhibition of systemic endogenous prostaglandin levels in the biological fluids of these control subjects. We found that indomethacin increased both basal and stimulated gastric acid secretion attributable to the drug.

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A number of UV-induced pigmentation mutants of Micrococcus roseus were isolated. The carotenoid pigment composition of a yellow mutant and a pink mutant were determined and compared with the composition of the wild type. The yellow mutant appeared to have the ability to insert oxygen functions on only one end of β-carotene. The pink mutant formed less total carotenoids than the wild type; it formed diketo-carotenoids but no dihydroxy compounds. The results are discussed in relation to xanthophyll synthesis in M. roseus.