Equine Gastric Ulcer Syndrome (EGUS) – Keeping Up with Evolution

The mechanical breakdown and mixing of food occurs in the stomach and reduces meals into smaller particle size that can pass into the small intestine. The lining of the equine stomach is divided into an upper squamous mucosa (non-glandular) and the lower glandular mucosa. The squamous mucosa does not absorb or secrete anything, but has the primary role of aiding the mechanical breakdown of ingested foods. The glandular mucosa, on the other hand, produces hydrochloric acid (HCl), pepsin, lipase, gastrin, histamine, somatostatin, and several other physiologic mediators. The glandular mucosa of the stomach has a complex mechanism for protecting itself from its own corrosive agents. The essence of this barrier is a combination of mucus and bicarbonate that is produced by cells of the gastric glands, and through which secreted acid and pepsinogen can easily move out into gastric lumen, but not vice versa (1). Thus, under normal conditions, the pH of the area just adjacent to the glandular mucosal surface is biologically neutral. The two digestive enzymes of note secreted by the equine stomach are pepsin and lipase, which is in concordance with most other mammalian species. Pepsin is proteolytic when in an acidic environment. We really know nothing about the extent to which pepsin contributes to the digestion of ingested dietary protein in the horse. Equine gastric lipase is produced by the zymogen cells primarily in the glandular mucosa (2). Horses produce a large amount of gastric lipase but, as with pepsin, nothing is known about its role in the processing of food. Of related interest is that, on a relative basis, the equine pancreas produces much more lipase than any of the other digestive enzymes it produces. Also interesting, recent studies have shown that horses can effectively assimilate quite large amounts of dietary fat (3, 4), which is broken down by these pancreatic enzymes. Like most other species, horses secrete some gastric acid even when the stomach is empty. When equine gastric contents are continually collected over time, the acid concentration (and thus pH) is quite spontaneously variable (5). Ingestion of food naturally has a significant impact on intra-gastric pH. The pH of intra-gastric contents in the free-feeding adult horses is anything but uniform. Duodenal contents can readily reflux into the stomach of the horse, especially when the stomach is empty. Because of the high sodium and substantial bicarbonate concentration of those contents, they provide an additional buffer of the gastric acid, and thus provide more protection for the gastric mucosa (6). It appears in the adult horse at least, that duodenal reflux is more responsible for this variability than is saliva. This idea is supported by the endoscopic observation that the pyloric sphincter region of the horse is open most of the time. It is reasonable to assume that this backflow is less when the stomach is full, and the general gradient of contents movement is more aborad, but this remains to be determined. The equine stomach takes approximately 12-14 hours to completely empty of solid material (hay) but grain exits rapidly; a recent study demonstrated that one pound of grain consumed on an empty stomach took just 4.5 hours to exit into the intestine. In other words, fiber and roughage lingers in the equine stomach, while a meal of only grain empties rapidly. These observations have important clinical implications with respect to the potential for ulcerogenesis in horses that have empty stomachs, either because of illness-related anorexia or human-imposed management conditions. Ulcers that occur in the glandular portion of the stomach are found most often in the region of the antrum and the pylorus (7), and are often caused by a breakdown in the protective buffers. The squamous mucosa, however, is highly sensitive to HCl; in fact damage (represented by ulceration or discoloration) can occur within 30 minutes of exposure (8). Ulcerogenic stresses that impact the glandular portion are different from those that impact the squamous portion. Ulcerogenic stresses that have been identified in controlled studies include transportation, serious illness, diet, management changes, high doses of non-steroidal anti-inflammatory drugs (NSAIDs), withholding feed from horses, stall confinement (9) and exercise (10, 11, 12). Both prevalence and severity of ulcers increase as the intensity and duration of training increase, which has been demonstrated in racehorse and even in research with horses trained on a treadmill. Risk factors, acting singly or interacting together, contribute to the pressures experienced by a horse, and the expression of these pressures as a gastric ulcer depends on a horse‟s individual characteristics as well as the risk factors themselves.