Effects of chronic hypoxia on canine gastric secretion.
Interdigestive gastirc acid output and acid secretory response to histamine, insulin  and pentagastrin were studied in five dogs before and after creation of a right to left extracardiac vascular shunt. The arterial PO2 decreased from 81.5 +/- 5.5 mm Hg to 39.8 +/- 6.0 mm Hg postoperatively with no change in arterial pH or PaCO2. Basal (interdigestive) acid output increased from 1.19 +/- 0.26 mEq/hr to 4.97 +/- 0.81 mEq/hr postoperatively. Acid secretory response to insulin was increased after the induction of chronic hypoxia. Increased sensitivity to pentagastric was also observed although parietal cell mass (maximum histamine-stimulated output) was unchanged postoperatively. Changes in acid secretory response and PaO2 were present at one week and were sustained through twelve weeks after shunting. Chronic hypoxia resulted in gastric acid hypersecretion secondary to enhanced sensitivity of the parietal cell to a combination of neural and humoral stimuli.
D000818:Animals; D001769:Blood; D002245:Carbon Dioxide / Q000097:blood; D004285:Dogs; D005750:Gastric Juice / Q000378:metabolism*; D006400:Hematocrit; D006632:Histamine / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000503:physiopathology*; D007328:Insulin / Q000494:pharmacology; D008297:Male; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D010418:Pentagastrin / Q000494:pharmacology; D011667:Pulmonary Veins / Q000601:surgery; D014682:Vena Cava, Inferior / Q000601:surgery
D007328:Insulin; D002245:Carbon Dioxide; D006632:Histamine; D010418:Pentagastrin; D010100:Oxygen