title: The Gastrointestinal Circulation: Physiology and Pathophysiology.
abstract: The gastrointestinal (GI) circulation receives a large fraction of cardiac output and this increases following ingestion of a meal. While blood flow regulation is not the intense phenomenon noted in other vascular beds, the combined responses of blood flow, and capillary oxygen exchange help ensure a level of tissue oxygenation that is commensurate with organ metabolism and function. This is evidenced in the vascular responses of the stomach to increased acid production and in intestine during periods of enhanced nutrient absorption. Complimenting the metabolic vasoregulation is a strong myogenic response that contributes to basal vascular tone and to the responses elicited by changes in intravascular pressure. The GI circulation also contributes to a mucosal defense mechanism that protects against excessive damage to the epithelial lining following ingestion of toxins and/or noxious agents. Profound reductions in GI blood flow are evidenced in certain physiological (strenuous exercise) and pathological (hemorrhage) conditions, while some disease states (e.g., chronic portal hypertension) are associated with a hyperdynamic circulation. The sacrificial nature of GI blood flow is essential for ensuring adequate perfusion of vital organs during periods of whole body stress. The restoration of blood flow (reperfusion) to GI organs following ischemia elicits an exaggerated tissue injury response that reflects the potential of this organ system to generate reactive oxygen species and to mount an inflammatory response. Human and animal studies of inflammatory bowel disease have also revealed a contribution of the vasculature to the initiation and perpetuation of the tissue inflammation and associated injury response.
authors.affiliation: Department of Molecular and Cellular Physiology, LSU Health Science Center-Shreveport, Shreveport, Louisiana, USA.
authors.forename: D Neil
authors.initials: DN
authors.lastname: Granger
authors.affiliation: Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
authors.forename: Lena
authors.initials: L
authors.lastname: Holm
authors.affiliation: Department of Physiological Sciences, College of Medicine, Alfaisal University, Riyadh, Saudi Arabia.
authors.forename: Peter
authors.initials: P
authors.lastname: Kvietys
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000378:metabolism / Q000502:physiology; D041981:Gastrointestinal Tract / Q000098:blood supply* / Q000502:physiology / Q000503:physiopathology; D006801:Humans; D006940:Hyperemia / Q000209:etiology*; D055806:Microvessels / Q000378:metabolism / Q000502:physiology; D010101:Oxygen Consumption; D014661:Vasoconstriction