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The reproducibility of simultaneous, long-term, ambulatory gastric pH recordings in the antrum and corpus was investigated in nine healthy subjects who underwent three separate, 27-h gastric double pH-metries. Intraindividual reproducibility for the entire 27-h recording period was good in the corpus (Kendall's concordance coefficient, W' = 0.6393, p less than 0.025) but not in the antrum (W' = 0.4806, NS). Analysis of predefined time periods showed that non-meal daytime pH was reproducible in the corpus (W' = 0.6531, p less than 0.025) but not in the antrum (W' = 0.3395, NS), whereas mealtime pH was reproducible in the antrum (W' = 0.7159, p less than 0.005) but not in the corpus (W' = 0.4954, NS); nocturnal pH was not reproducible in either the antrum or the corpus. These results reflect the functional separation of corpus and antrum and their differing responses to food. Thus, studies of gastric acidity over long periods should be conducted in the corpus, whereas studies of gastric acidity over shorter, meal-related periods should be conducted with a second electrode in the antrum.

SUMMARY The interaction between smoking and the effect of histamine H2-antagonists on intragastric acidity was examined in a double blind double dummy placebo controlled study. Healthy volunteers, 11 smokers and 10 non-smokers, were given, on four separate days at least one week apart, either placebo or cimetidine 800 mg nocte or ranitidine 2x 150 mg per day or ranitidine 300 mg nocte. Tablets were taken at 2115 and 0900 h. Smokers smoked a cigarette hourly from 0700 to 2300 h. Breakfast, lunch, and dinner were standardised. Intragastric acidity was measured with a combined intragastric glass electrode and a solid state recorder. The subjects were fully ambulatory. The three histamine H2-receptor antagonist regimens were less effective (p=004) in smokers than in non-smokers, but the difference between acidity of smokers and non-smokers was small. Means of medians of pH during a 24-h period with placebo, cimetidine 800 mg, raniditine 2x 150 mg and ranitidine 300 mg were 1-6, 2 3, 3-1, and 2-7 in smokers and 1-5, 2.7, 3*2, and 3-1 in non-smokers, respectively. In a second part of the study seven chronic smokers were reexamined after acutely stopping smoking: inhibition of gastric acidity by histamine H2-receptor antagonists was similar before and after withdrawal. Smoking does not affect intragastric acidity in untreated volunteers and only slightly decreases the effectiveness of histamine H2-receptor antagonists on intragastric acidity. This effect best in part explains the unfavourable effect of smoking on healing of peptic ulcer in patients treated with these drugs.Smoking has an unfavourable effect on the course of peptic ulcer. It may slow down healing, favour relapse, diminish the effectiveness of histamine H2-receptor antagonists in duodenal ulcer'-22 and possibly also in gastric ulcer.2324 The mechanism is unknown. It has been hypothesised that smoking interferes with the antisecretory effect of histamine H2-receptor antagonists,25 but the data to support this hypothesis are scanty25 and controversial.2627 It is not even known if smoking affects gastric acidity.3' In order to clarify the effect of smoking on intragastric acidity, we undertook a double blind crossover trial in healthy volunteers.

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