Hypovolemia-Induced Cardiovascular Effects on Human Gastric Mucosal Acid and HCO₃⁻ Release

Abstract

Dalenbäck J, Olbe L, Sjövall H. Hypovolemia-induced cardiovascular effects on human gastric mucosal acid and HCO₃⁻ release. Scand J Gastroenterol 1994;29:595-602

Background: The bicarbonate ion seems to play a crucial role in mucosal acid-base regulation by generating a pH gradient that is regarded as a 'first line of defense' against acid back-diffusion. The aim of this study was to determine the effects of hypovolemia on gastric mucosal buffering capacity, as reflected by luminal HCO₃⁻ release, in human volunteers. Methods: Central hypovolemia was induced by lower-body negative pressure (LBNP), and HCO₃⁻ release was measured by using a perfusion system based on continuous recording of the pH and Pco₂ of gastric aspirate. The response to LBNP was related to concomitant cardiovascular effects, to gastric pH, and to the current phase of the migrating motor complex (MMC). Results: At an acid gastric pH, LBNP induced a slight but statistically significant reduction in luminal HC0₃ release (-27 ±10%, p<0.05). The magnitude of the response was significantly correlated with the degree of reflex tachycardia. A larger and less variable response (-78 ± 4%, p < 0.01 versus control group) was seen when luminal pH was increased by ranitidine pretreatment. The effect of LBNP on HCO₃⁻ release was statistically significant only during the early and middle parts of the MMC cycle.

Conclusions: The results indicate that hypotension may reduce gastric mucosal buffering capacity, probably by activation of a sympathetic reflex. The magnitude of this response seems to depend on: 1) the degree of baroreceptor unloading; 2) luminal pH; and 3) the current phase of the MMC.

Key Words:

• Acid secretion
• bicarbonate secretion
• gastric mucosa
• gastric secretion
• hemorrhage
• stress ulceration
• sympathetic nerves