{'fraction_non_alphanumeric': 0.023071377072819033, 'fraction_numerical': 0.011535688536409516, 'mean_word_length': 5.83743842364532, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Different effects of the histamine H2 receptor blockers, famotidine and zolantidine, on the human atrium in vitro.

The effects of the histamine H2 receptor blocker famotidine were investigated on the human isolated myocardium, in comparison with zolantidine, a new member of the same family. Experiments were performed on human atrial fragments, taken from patients undergoing reconstructive heart surgery. Electrical pacing was applied and H2 receptor-evoked positive inotropic responses were induced with histamine. Famotidine (0.1-10 microM) shifted the concentration-response curve of histamine to the right in a competitive fashion, without affecting the basal contraction and the noradrenaline-induced positive inotropic activity up to 100 microM. Zolantidine (1-100 microM) antagonized the histamine-induced positive inotropic effect, but the rightward shifts were nonparallel and the maximum response was depressed, probably due to a nonspecific cardiodepressive activity at concentrations above 1 microM. Data obtained in the present study confirm the ability of famotidine to block cardiac histamine H2 receptors, but, in contrast with several studies on healthy volunteers, nonspecific effects on the myocardial contractility cannot be demonstrated. Conversely, zolantidine depresses the myocardial contractility with a mechanism differing from that of slow-channel blockers.