Tham khảo tài liệu 'medical physiology rhoades tanner - part 5', y tế - sức khoẻ, y học thường thức phục vụ nhu cầu học tập, nghiên cứu và làm việc hiệu quả | 282 PART IV BLOOD AND CARDIOVASCULAR PHYSIOLOGY The Microvasculature of Intestinal Villi Has a High Blood Flow and Unusual Exchange Properties The intestinal mucosa receives about 60 to 70 of the total intestinal blood flow. Blood flows of 70 to 100 mL min per 100 g in this specialized tissue are probable and much higher than the average blood flow for the total intestinal wall see Table . This blood flow can exceed the resting blood flow in the heart and brain. The mucosa is composed of individual projections of tissue called villi. The interstitial space of the villi is mildly hyperosmotic 400 mOsm kg H2O at rest as a result of NaCl. During food absorption the interstitial osmolality increases to 600 to 800 mOsm kg H2O near the villus tip compared with 400 mOsm kg H2O near the villus base. The primary cause of high osmolalities in the villi appears to be greater absorption than removal of NaCl and nutrient molecules. There is also a possible countercurrent exchange process in which materials absorbed into the capillary blood diffuse from the venules into the incoming blood in the arterioles. Food Absorption Requires a High Blood Flow to Support the Metabolism of the Mucosal Epithelium Lipid absorption causes a greater increase in intestinal blood flow a condition known as absorptive hyperemia and oxygen consumption than either carbohydrate or amino acid absorption. During absorption of all three classes of nutrients the mucosa releases adenosine and CO2 and oxygen is depleted. The hyperosmotic lymph and venous blood that leave the villus to enter the submucosal tissues around the major resistance vessels are also major contributors to absorptive hyperemia. By an unknown mechanism hyperosmolality resulting from NaCl induces endothelial cells to release NO and dilate the major resistance arterioles in the submucosa. Hyperosmolality resulting from large organic molecules that do not enter endothelial cells does not cause appreciable increases in NO formation .
