title: Renal function and metabolism during endotoxemia in rats: role of hypoperfusion.
abstract: Renal failure often complicates endotoxin shock. This might be due to renal hypoperfusion, but endotoxemia could also have additional effects. We studied in anesthetized rats renal plasma flow (RPF), glomerular filtration rate (GFR), and metabolism (ATP, CrP = creatine phosphate, energy charge = [ATP + 0.5 ADP]/[ATP + ADP + AMP], lactate, glucose) during endotoxin shock (Escherichia coli endotoxin, 10 mg/kg for 60 min; n = 10) and "balloon shock" (balloon inflated in vena cava below renal vein to cause comparable decreases in cardiac output and RPF as in endotoxin-treated rats; n = 10). A third group of rats served as controls (n = 10). At t = 0 infusion of endotoxin was started. At t = 90 min, when cardiac output was low and serum lactate was high (indicating shock), GFR and RPF were obtained from plasma disappearance rates (from t = 90 to t = 135 min) of 125I-thalamate and 131I-hippurate, respectively. Experiments ended at t = 135 min. In both shock groups RPF decreased (by ca. - 75% compared with control rats), but filtration fraction only increased (by 72%) in the "balloon shock" rats. In renal biopsies lactate concentration increased more (by 407 vs. 167%) and ATP decreased more (by -63 vs. - 35%) during endotoxin shock than during "balloon shock"; the endotoxin-treated rats also showed a significant decrease in CrP (by - 58%), energy charge (by - 31%), and glucose concentration (by - 34%), and an increase in the number of leukocytes in the glomeruli (by 730%). Renal function and metabolism thus was more affected in this hypodynamic form of endotoxin shock than in "balloon shock." This may be caused by the effects of endotoxin on sticking of leukocytes and renal metabolism.
authors.affiliation: Laboratory for Physiology, Free University, Amsterdam, The Netherlands.
authors.forename: A A
authors.initials: AA
authors.lastname: van Lambalgen
authors.forename: A A
authors.initials: AA
authors.lastname: van Kraats
authors.forename: G C
authors.initials: GC
authors.lastname: van den Bos
authors.forename: H V
authors.initials: HV
authors.lastname: Stel
authors.forename: J
authors.initials: J
authors.lastname: Straub
authors.forename: A J
authors.initials: AJ
authors.lastname: Donker
authors.forename: L G
authors.initials: LG
authors.lastname: Thijs
mesh_terms: D000244:Adenosine Diphosphate / Q000032:analysis; D000249:Adenosine Monophosphate / Q000032:analysis; D000818:Animals; D001786:Blood Glucose; D006439:Hemodynamics; D006626:Hippurates / Q000378:metabolism; D007483:Iothalamic Acid / Q000378:metabolism; D007511:Ischemia / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology*; D007773:Lactates / Q000097:blood; D008297:Male; D010725:Phosphocreatine / Q000032:analysis; D051381:Rats; D011919:Rats, Inbred Strains; D012772:Shock, Septic / Q000503:physiopathology*
chemical_list: D001786:Blood Glucose; D006626:Hippurates; D007773:Lactates; D010725:Phosphocreatine; D007483:Iothalamic Acid; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; C030514:hippuric acid