Maximal acid output

Upper and lower limits of normal (95% confidence limits) were derived from data obtained from 100 healthy men and 50 healthy women. There were no lower limits of normal for BAO or for the ratio of BAO to PAO because many normal subjects have a BAO of zero. BAO, basal acid output MAO, maximal acid output PAO, peak acid output. (Reprinted with permission from Feldman M (1989) Gastric secretion in health and disease. In Sleisenger MH and Fordtran JS (eds.) Gastrointestinal Disease Pathophysiology, Diagnosis, Management, vol. I, pp. 713-734. Philadelphia W.B. Saunders Company.)... 

Card and Marks then applied the method of estimating the parietal cell mass to 17 patients with duodenal ulceration, chronic gastric ulceration, or carcinoma of the stomach whose stomachs were removed at operation. Their description of how they sampled the stomachs (Fig. 5-5) presumably applied to the previous work of Marks, Komarov, and Shay. When they plotted the maximal acid output against the parietal cell mass. Card and Marks saw that the data were fitted better by a quadratic than by a linear equation (Fig. 5-6). " ... 

Figure 5-6. Relationship between maximal acid output in response to histamine stimulation and the estimated parietal cell count in the resected portions of 17 human stomachs. (From Card Wl, Marks IN. The relationship between the acid output of the stomach following maximal" histamine stimulation and the parietal cell mass. Clin Sc/19 147-163, 1960.)...

Steady-state inhibition on once-a-day dosing is reached at approximately the third dose. At steady state in humans, once-a-day dosing results in 66% inhibition of maximal acid output after 5 days of drug administration. This is the degree of inhibition expected with a 24-hour half-life of pump recovery and 75% active pumps at the time of drug administration. 

On once-a-day PPI treatment, the inhibition of maximal acid output is approximately 70%. Steady-state inhibition is found on approximately the third... 

An arbitrary maximal acid output (AAAO) of less than 5 mmol per hour has been used to define this term. Even in such situations, however, the gastric... 

Ulcer index of treated animals are compared with controls. Using various doses, dose-response curves can be established for ulcer formation and gastric acid secretion. ID50 values can be calculated by probit analysis, whereby 0 % corresponds to no and 100 % to maximal stimulated gastric acid output. 

Sprinting and marathon running are powered by different fuels to maximize power output. The 100-meter sprint is powered by stored ATP, creatine phosphate, and anaerobic glycolysis. In contrast, the oxidation of both muscle glycogen and fatty acids derived from adipose tissue is essential in the running of a marathon, a highly aerobic process. 

Note that gastrin injection produced the maximal rate of acid output, followed by sham feeding and by talking about food. If the latter responses are to be calculated as percentages of this maximum, the basal rate must be subtracted from all three values first. This manipulation is a simple example of the preliminary corrections that must be applied to experimental data before more complicated questions can be answered correctly. 

Experiments comparing bile fistula rats with intact rats are difficult to interpret. In the bile fistula rat, the enterohepatic circulation of bile acids is interrupted, feedback inhibition by the circulating pool is abolished, and bile acid synthesis is presumably at a maximum. The effects of thyroid hormone are thus superimposed on a system that is operating already at or near maximal capacity. The stimulation of bile acid output by thyroid hormone can thus be seen more readily in the intact rat, where bile acid synthesis is under feedback regulation by the circulating bile acid pool. 

Measurements of gastric acid secretion performed by gastric aspiration include basal, maximal, and peak acid output. Acid output cannot be accurately measured by gastric aspiration in the presence of food in the stomach hence, it is not used to measure meal-stimulated acid output. 

Card WI, Marks IN. The relationship between the acid output of the stomach following maximal histamine stimulation and the parietal cell mass. Clin Sci 19 147-163, 1960. 

It can be seen that steady-state inhibition of stimulated acid output is expected by day 3, as is stabilization of intragastric pH and the degree of inhibition immediately after drug administration. The latter parameter is the most rapidly affected, still providing better acid control than Hz receptor antagonists. To improve the response of add secretion, because the lag is due to the maximal number of pumps active during the dwell time of the drug in blood, the dose should be divided rather than increased. 

As a further difference, it takes several days for omeprazole to reach its steady-state bioavailability [5]. Corresponding data for lansoprazole and pantoprazole are not available, although unchanged values of C ax and area under the time concentration curve (AUC) indicate the absence of relevant increases after the first dose [7, 8]. At face value, this discrepancy would suggest that the latter drugs reach maximum acid inhibitory efficacy with the first dose and, by this, are apt to provide faster pain relief. Hence, it may be surprising that omeprazole as well as lansoprazole and pantoprazole take several days to reach steady-state inhibition of acid secretion [9-11]. For instance, 40 mg of pantoprazole reduced acid output by 51 and 85% after the first and seventh dose, respectively [11]. This type of behavior, however, is predictable from the way the parietal cell organizes its supply with active H, K" -ATPase molecules [12] unless acid secretion is maximally stimulated, a substantial portion of the pump molecules are stored in... 

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