Role of solute excretion in prevention of norepinephrine-induced acute renal failure.
Infusion of 0.75 μ g/kgbw/min norepinephrine (NE), for 40 minutes, into one renal artery in anesthetized dogs, induced acute renal failure (ARF). Subsequently there was nearly complete reversal of function within 8 weeks. Isotonic saline volume expansion, or renal vasodilation plus diuresis by acetylcholine (into renal artery: 20 μg/min) did not protect against this type of ARF. Volume expansion with either 5 or 20 percent mannitol partly prevented the fall of GFR 3 hours after NE, this protection being correlated with the magnitude of the osmolar clearance at the time of the insult. IV furosemide (10 mg/kg + 10 mg/kg/h; fluid losses replaced) afforded an even better protection. Proximal tubular necrosis in the "protected" kidneys was as severe as in non-protected kidneys. Glomerular cell morphology (scanning electron microscopy) was not altered by the 40-minute NE infusions. Functional "protection" appeared to depend on solute diuresis at the time of insult.
D000109:Acetylcholine / Q000494:pharmacology; D058186:Acute Kidney Injury / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D004195:Disease Models, Animal; D004231:Diuresis; D004285:Dogs; D005110:Extracellular Space / Q000502:physiology; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D007678:Kidney Glomerulus / Q000473:pathology; D007687:Kidney Tubules, Proximal / Q000473:pathology; D008297:Male; D009638:Norepinephrine; D014664:Vasodilation
D005665:Furosemide; D000109:Acetylcholine; D009638:Norepinephrine