Responses of innervated and denervated gut to whole-body hypoxia.
As a significant user of O2 at rest (20% of whole body), the gut may be subject to more severe limitation of O2 supply during global hypoxia than more vital areas because of preferential redistribution of blood flow. Accordingly, its accumulation of O2 deficit during hypoxia and its excess O2 use during normoxic recovery might be altered by extrinsic neural activity. We measured blood flow and O2 uptake in whole body (WB) and gut segments while anesthetized dogs were ventilated with 9% O2-91% N2 for 30 min followed by 30-min normoxic recovery. In six dogs extrinsic innervation to the gut segment was left intact and it was severed in another six animals. O2 deficit and excess were the accumulated differences from the normoxic O2 uptake for both gut and WB corrected for O2 stores changes. The intact gut, although only 4% body wt, incurred 22% of WB O2 deficit but contributed only 8% to WB O2 excess. The imbalance (gut excess was only 44% of gut deficit) implied that O2 using functions were curtailed during hypoxia without obligating an energy stores deficit. Denervation did not alter these quantitative relationships. Blood flow responses to transition between normoxia and hypoxia were only transiently altered. Extrinsic innervation apparently plays no major role in gut responses to WB hypoxia.
D000818:Animals; D001794:Blood Pressure; D003714:Denervation; D004064:Digestive System / Q000294:innervation / Q000503:physiopathology*; D004285:Dogs; D000860:Hypoxia / Q000503:physiopathology*; D007421:Intestine, Small / Q000378:metabolism; D007422:Intestines / Q000098:blood supply; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D014655:Vascular Resistance
D010100:Oxygen