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Research Article Free access | 10.1172/JCI109493

Effect of Volume Expansion on Hemodynamics of the Hypoperfused Rat Kidney

Paul A. Johnston, David B. Bernard, John F. Donohoe, Nancy S. Perrin, and Norman G. Levinsky

Evans Memorial Department of Clinical Research, Boston University Medical Center, Boston, Massachusetts 02118

Department of Medicine, Boston University Medical Center, Boston, Massachusetts 02118

Find articles by Johnston, P. in: PubMed | Google Scholar

Evans Memorial Department of Clinical Research, Boston University Medical Center, Boston, Massachusetts 02118

Department of Medicine, Boston University Medical Center, Boston, Massachusetts 02118

Find articles by Bernard, D. in: PubMed | Google Scholar

Evans Memorial Department of Clinical Research, Boston University Medical Center, Boston, Massachusetts 02118

Department of Medicine, Boston University Medical Center, Boston, Massachusetts 02118

Find articles by Donohoe, J. in: PubMed | Google Scholar

Evans Memorial Department of Clinical Research, Boston University Medical Center, Boston, Massachusetts 02118

Department of Medicine, Boston University Medical Center, Boston, Massachusetts 02118

Find articles by Perrin, N. in: PubMed | Google Scholar

Evans Memorial Department of Clinical Research, Boston University Medical Center, Boston, Massachusetts 02118

Department of Medicine, Boston University Medical Center, Boston, Massachusetts 02118

Find articles by Levinsky, N. in: PubMed | Google Scholar

Published August 1, 1979 - More info

Published in Volume 64, Issue 2 on August 1, 1979
J Clin Invest. 1979;64(2):550–558. https://doi.org/10.1172/JCI109493.
© 1979 The American Society for Clinical Investigation
Published August 1, 1979 - Version history
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Abstract

The hemodynamics of the rat kidney were studied during reduction of renal arterial pressure to 35-40 mm Hg (H), and after volume expansion at that pressure with 0.9% NaCl (IS), 1.7% NaCl (HS), 5% mannitol in 0.9% NaCl (MS), 5% mannitol in water (MW), or 50 mM mannitol + 125 mM NaCl. During H, left renal blood flow (RBF) was 0.8±0.1 ml/min. Expansion with IS did not alter RBF, but expansion with HS, MS, MW, and 50 + 125 mM NaCl elevated RBF to 200-250% of hypoperfusion values. Glomerular capillary pressure rose significantly from 15.7±0.7 mm Hg during H to 22.3±1.1, 24.4±0.7, and 26.6±0.7 mm Hg following expansion with HS, MS, or MW, respectively. Efferent arteriolar pressure also rose significantly to 6.9±0.5, 9.7±0.8, and 9.5±0.9 mm Hg, respectively. Preglomerular resistance fell to 18-24% of H values, and postglomerular resistance fell to 58-74% of H values after expansion with HS, MS, or MW. Glomerular filtration (GFR) could not be detected during H or after IS expansion. HS and mannitol-containing solutions restored GFR to 0.10±0.02-0.15±0.02 ml/min, and single nephron glomerular filtration to 6-12 nl/min. Papaverine, acetylcholine, and kinins had no effect on RBF or GFR at a perfusion pressure of 35-40 mm Hg. We conclude that mannitol and HS have the capacity to augment RBF during hypoperfusion by reducing arteriolar resistance. The mechanism of the rise in RBF is uncertain; it may be due to changes in effective osmolality of the extracellular fluid or to a direct action of mannitol on vascular smooth muscle. Other potent vasodilators were ineffective during hypoperfusion. Restoration of GFR occurs as a result of the combined effects of augmented RBF and elevated net filtration pressure.

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