Ten healthy volunteers were studied before, during, and after treatment with omeprazole 30 mg daily for two weeks. On the 14th night mean nocturnal (2100-0700) intragastric acidity was significantly decreased by 75%
Analysis of egg albumen foams by electrophoresis showed that the basic protein lysozyme (PI 10.7) was strongly retained. Addition of low concentrations (0.01-0.10% wiv) of the basic proteins clupeine (PI 12) and lysozyme to solutions (0.50% wiv) of several acidic proteins (PI 4.7-6.0) greatly improved their foaming properties at pH values between the isoelectric points. Sucrose strongly enhanced the action of the basic proteins, while not significantly affecting the foaming of the acidic proteins alone. Basic proteins did not enhance the foaming of ovalbumin and egg albumen in the absence of sucrose. Clupeine enhanced foaming more effectively than lysozyme under all conditions studied. Lysozyme was least effective near the isoelectric point of the acidic protein, where electrostatic interactions were weakest. Sodium chloride ( 0 . 1~) had a detrimental effect on the action of lysozyme.
SUMMARY A six week course of cimetidine (1 g/day) healed peptic ulcers in 20 of 23 patients (14 with duodenal ulcer, nine with gastric ulcer). Reduction of basal acid output by 73% and peak acid output by 36% led to a rise in concentrations of intragastric aerobic bacteria and nitrate-reducing bacteria. While the mean intragastric concentration of nitrate was unchanged by treatment, there were statistically significant rises in nitrite and N-nitrosamine concentrations. The conversion from nitrates to nitrites was closely related to the occurrence of nitrate-reducing bacteria. In three patients the intragastric milieu had returned to normal two months after cimetidine treatment had been discontinued. Mean nitrite and N-nitrosamine concentrations did not return to pre-treatment levels in the group of eight patients who remained on maintenance cimetidine (0.4 g at night-time) for three months after the full dose treatment. This study shows that cimetidine treatment can create an intragastric milieu resembling that of atrophic gastritis. Large scale and long-term studies are necessary to establish whether these findings have any clinical significance.
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