Renal function and intrarenal hemodynamics in acutely hypoxic and hypercapnic rats.
On the basis of microsphere distribution, inert gas washout, and standard clearance data, the effects of acute hypoxia and hypercapnia on the kidney were studied in anesthetized, mechanically ventilated rats. Moderate hypoxia (mean PO2, 48 mm Hg) did not significantly change diuresis, GFR, and tubular sodium rejection. Due to a decrease in renal vascular resistance (R) from 40.1 to 31.8 mm Hg ml-1 min, mean renal blood flow stayed constant in spite of a significant drop in mean arterial blood pressure. Hypoxic changes in R were not accompanied by significant changes in intrarenal distribution of blood flow (IDBF). In severe hypoxia (PO2 less than 45 mm Hg) with oliguria and marked arterial hypotension, R was the lowest of all groups (28.8 mm Hg ml-1 min). Hypercapnia did not significantly change the renal excretory parameters, although an increase in R (without change in IDBF), together with a decrease in MAP caused a marked drop in mean renal blood flow. From these studies we conclude: 1) in the anestheized rat, acute hypoxia caused significant changes in intrarenal hemodynamics without changes in excretory function, 2) hypoxic renal vasodilation persists even in severe hypotension with oliguria and anuria, 3) in acute hypoxia and hypercapnia, changes in renal blood flow and renal vascular resistance are not accompanied by significant changes in IDBF.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D006935:Hypercapnia / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply / Q000503:physiopathology*; D007672:Kidney Cortex / Q000098:blood supply; D008297:Male; D008863:Microspheres; D010100:Oxygen / Q000097:blood; D051381:Rats; D012039:Regional Blood Flow; D014018:Tissue Distribution; D014666:Vasomotor System / Q000503:physiopathology
D002245:Carbon Dioxide; D010100:Oxygen