Effect of modifying o2 diffusivity and delivery on glomerular and t
ubular function in hypoxic isolated perfused kidneys.
Baines, A. D., G. Adamson, P. Wojciechowski, D. Pliura, P. Ho, and R.
Kluger.
Departments of Clinical Biochemistry and Chemistry University of
Toronto and Hemosol Inc.
APStracts 5:0013F, 1998.
Is O2 diffusivity within renal capillaries rate limiting for O2
delivery to hypoxic renal tubules? Equations, based on diffusion
theory, developed in this paper predict that soluble hemoglobin (Hb)
increases O2 diffusivity by a factor = 1+(442.Hb%/(P50+PO2)). To
examine the effect of P50 and Hb concentration on renal function we
perfused isolated rat kidneys with Hb-P35 (P50 = 35 mm Hg) and Hb-P11
(P50 = 11 mm Hg). Venous PO2 was lower with Hb-P11 (10+/-1 vs 16+/-1
mm Hg with arterial PO2 = 35 mm Hg and 28+/-2 vs 40+/-2 mm Hg with
arterial PO2 =140 mm Hg. p<0.001). Perfusate P50 did not influence
vascular resistance, GFR, O2 consumption, Na reabsorption, protein
excretion or free water clearance. Percent glucose and phosphate
excretion were lower with Hb-P11 than with Hb-P35 (p <0.001). Urine
glucose was 0.17 mmol/L with Hb-P11 and 0.77 mmol/L with Hb-P35
(p<0.001). 2% Hb-P35 doubled O2 delivery and lowered glucose and
phosphate excretion to the level obtained with 1% Hb-P11. Thus Hb-P11
delivered O2 twice as effectively as Hb-P35 to high affinity Na
-glucose and phosphate cotransporters in the late proximal tubule (S3
segment). Hb-P11 may also have shunted O2 from the outer cortex to
the outer medulla and facilitated O2 diffusion where PO2 was low. We
conclude that diffusivity is a limiting factor in delivery of O2 to
hypoxic tubules.
Received 25 June 1997; accepted in final form 5 January 1998.
APS Manuscript Number F207-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 28 January 1998