Relationship of Histamine-Stimulated Gastric Secretion to Gastric Blood Flow and Oxygen Consumption

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Abstract
Alterations in left gastric artery flow and gastric arteriovenous oxygen saturation difference were studied in 20 dogs following stimulation of gastric secretion by either intravenous or intra-arterial (left gastric artery) histamine infusions. Intravenous histamine produced a transient rise in gastric blood flow which fell to or below control levels during the time of active gastric secretion. Gastric venous oxygen saturation was regularly much higher (80%) than central venous saturation (63%) in the resting stomach. During gastric secretion induced by intravenous histamine, gastric venous oxygen saturation fell to near central venous levels. Cardiac output was unchanged during intravenous histamine infusion although arterial pressure was reduced 15 to 20%. Arterial oxygen saturation remained constant throughout all experiments. Carotid artery flow showed a sustained increase during intravenous histamine infusion. Intra-arterial histamine (left gastric artery) produced a sustained increase in gastric artery flow throughout the infusion period, with no change in carotid flow or arterial pressure. This effect and excellent secretory response were seen with as little as 1/100 the dosage of histamine required for intravenous response. Gastric venous oxygen saturation increased (4 of 5 experiments) accompanying gastric secretion induced by intra-arterial histamine. Following cessation of intra-arterial histamine Infusion, gastric secretion continued elevated for a short time. This secretory phase was accompanied by a sharp decrease in gastric blood flow below control levels and accompanying decrease in gastric venous oxygen saturation. The energy (oxygen) required for gastric secretion can come either from an increase in gastric blood flow or from an increase in oxygen extraction. Which of these predominates under physiologic or pathologic conditions requires further study.