Gastric blood flow plays an important role in sustaining the normal physiologic functions of the stomach, and it helps to protect the gastric mucosa against ulcer formation. Intrinsic regulatory mechanisms have evolved to ensure that blood flow is adjusted to meet the energy-demanding processes of gastric secretion and motility. Gastric blood flow also helps to maintain a barrier against back-diffusion of luminal acid, thereby preventing mucosal damage and ulceration. Impairment of gastric blood flow renders the mucosa vulnerable to the damaging actions of gastric juice as well as ingested agents, such as ethanol, aspirin, and bacteria (e.g., Helicobacter pylori).
The parallel-coupled capillary networks of the gastric muscular layer and the mucosa are under separate control, responding independently to tissue metabolism, other local factors, and extrinsic neural input. Between meals, blood flow in the mucosal layer is about six times higher than that of the muscle layer, and approximately 75 percent of total gastric blood flow is distributed to the mucosa, with 25 percent directed to the muscle layer. This intramural distribution of blood flow is altered when either of the two layers becomes functionally active—that is, when the mucosa is stimulated to produce acid, mucosal blood flow (and its percent of total flow) preferentially increases.
Gastric blood flow is controlled by neural, humoral, and metabolic factors. Sympathetic activation elicits reductions in total gastric blood flow and mucosal flow through arteri-olar constriction. Parasympathetic nerves exert a tonic vasodilatory influence on gastric arterioles, with vagotomy resulting in a reduction in blood flow. Gastrin and histamine, both powerful stimulants of gastric acid secretion, increase mucosal blood flow. Oxygen consumption by the stomach increases in proportion to acid production. Changes in both blood flow and oxygen extraction assist in meeting the demand for additional oxygen in the acid-secreting stomach. When gastric blood flow is reduced, however, acid secretion and blood flow may fall in parallel, owing to the fact that the rate of oxygen delivery to the parietal cells is limited by blood flow.
The gastric microcirculation contributes to gastric ulcer formation in several ways. Capillary transport of parietal cell-derived bicarbonate normally plays an important role in protecting the surface epithelium against acid-induced injury and ulceration. The mucosal capillaries originating near the gastric pits transport bicarbonate toward the mucosal surface, where it can diffuse into the interstitial compartment beneath the surface epithelial cells. The latter cells transport bicarbonate into the gastric lumen where it can buffer luminal acid. As a consequence, there is an inverse relationship between gastric mucosal injury and the rate of vascular bicarbonate delivery to the mucosal surface.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.