Cardiovascular reflexes evoked by histamine stimulation of the stomach.

This study examined the potential for histamine to cause cardiovascular reflexes when applied to the serosal or mucosal surface of the stomach. Thus, in chloralose-anesthetized cats, histamine was applied to the serosal surface of the stomach in concentrations ranging from 0.5 to 1,000 micrograms/ml. This resulted in graded increases in mean arterial pressure (MAP), maximal left ventricular pressure over time (dP/dt), and heart rate ranging from 9 +/- 4 to 30 +/- 3 mmHg, 450 +/- 103 to 1,710 +/- 610 mmHg/s, and 2 +/- 1 to 13 +/- 4 beats/min, respectively. Histamine stimulation of the gastric serosa evoked a greater pressor response than that observed when the same concentration of histamine (100 micrograms/ml) was applied to the gastric mucosa (43 +/- 7 vs. 13 +/- 3 mmHg, respectively). In six cats, celiac ganglionectomy abolished the previously observed cardiovascular response to histamine stimulation of the serosal surface of the stomach. When the gastric serosa was treated with the H1-receptor antagonist diphenhydramine (1 mg/ml) (n = 5), the cardiovascular response to histamine was abolished. In five other cats, administration of the H2-antagonist ranitidine (1 mg/ml) had no effect on the histamine-induced responses. When indomethacin (2-5 mg/ml), was applied to the serosal surface of the stomach (n = 6), histamine-induced increases in MAP and dP/dt were attenuated. However, application of PGE2 (1 microgram/ml) restored these two responses. These results suggest that histamine stimulates H1-receptors in the gastric wall to cause reflex cardiovascular responses that are dependent, in part, on the local production of prostaglandins.