Effect of controlled ventilation on renal and splanchnic blood flows during severe arterial hypoxia.
The present study was undertaken to evaluate the extent that the lung inflation reflex attenuates vasoconstrictor responses in renal cortex and splanchnic beds during severe arterial hypoxia. Hypoxia was induced by inspiration of a 3-5% oxygen gas mixture in three groups of chloralose-anesthetized dogs: Group I, free breathing; Group II, controlled ventilation; Group III, free breathing with arterial PCO2 held constant. Regional vascular conductances (VC) were calculated from regional blood flows measured with 15-microns radioactive microspheres. In Group I, hypoxia caused marked hyperventilation, which was accompanied by no significant change in VC in renal cortex, and by reductions in VC in spleen (-36%), pancreas (-56%), and duodenum (-28%). In Group II, hypoxia caused reduction in VC in renal cortex (-70%), and reductions in VC in spleen, pancreas, and duodenum similar to those in Group I. In Group III, hypoxia again caused marked hyperventilation, but reductions in VC in renal cortex, spleen, pancreas, and duodenum were similar to those in Group II. Results indicate that during severe arterial hypoxia activation of lung inflation reflex does not attenuate or reverse vasoconstriction in renal cortex, spleen, pancreas, and duodenum.
D000818:Animals; D001783:Blood Flow Velocity; D002245:Carbon Dioxide / Q000097:blood; D002628:Chemoreceptor Cells / Q000502:physiology; D004285:Dogs; D005260:Female; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D008863:Microspheres; D010100:Oxygen / Q000097:blood; D012018:Reflex; D012079:Renal Circulation; D012121:Respiration, Artificial; D013152:Splanchnic Circulation; D014661:Vasoconstriction
D002245:Carbon Dioxide; D010100:Oxygen