Hypovolemia-induced cardiovascular effects on human gastric mucosal acid and HCO3- release.

Abstract

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. 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). At an acid gastric pH, LBNP induced a slight but statistically significant reduction in luminal HCO3- 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. 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.