Newly Published
Critical Care Medicine  |   December 2017
Microvascular Permeability after an Acute and Chronic Salt Load in Healthy Subjects: A Randomized Open-label Crossover Intervention Study
Author Notes
  • From the Divisions of Nephrology (N.M.G.R., R.H.G.O.E., L.V.) and Vascular Medicine (B.-J.H.v.d.B.); the Departments of Internal Medicine (N.M.G.R., R.H.G.O.E., B.-J.H.v.d.B., L.V.), Nuclear Medicine (Y.C., H.J.V.), and Clinical Chemistry (J.P.v.S.); and the Laboratory of Genetic Metabolic Diseases (N.v.L.), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
  • The results have been presented in abstract form at the 52nd ERA-EDTA Congress in London, United Kingdom (May 28–31, 2015) and at the 25th European Meeting on Hypertension and Cardiovascular Protection in Milan, Italy (June 12–15, 2015).
    The results have been presented in abstract form at the 52nd ERA-EDTA Congress in London, United Kingdom (May 28–31, 2015) and at the 25th European Meeting on Hypertension and Cardiovascular Protection in Milan, Italy (June 12–15, 2015).×
  • Submitted for publication January 22, 2017. Accepted for publication October 17, 2017.
    Submitted for publication January 22, 2017. Accepted for publication October 17, 2017.×
  • Acknowledgments: The authors thank the subjects for participation in this study. The assistance of Nicole Y. Scheper–van den Berg (Division of Nephrology, Academic Medical Center, University of Amsterdam, The Netherlands) is gratefully acknowledged.
    Acknowledgments: The authors thank the subjects for participation in this study. The assistance of Nicole Y. Scheper–van den Berg (Division of Nephrology, Academic Medical Center, University of Amsterdam, The Netherlands) is gratefully acknowledged.×
  • Research Support: Supported by the Dutch Kidney Foundation (Kolff grant No. KJPB 11.22; to Dr. Vogt) and The Netherlands Organization for Scientific Research (Clinical Fellowship grant No. 90700310; to Dr. Vogt).
    Research Support: Supported by the Dutch Kidney Foundation (Kolff grant No. KJPB 11.22; to Dr. Vogt) and The Netherlands Organization for Scientific Research (Clinical Fellowship grant No. 90700310; to Dr. Vogt).×
  • Competing Interests: The authors declare no competing interests.
    Competing Interests: The authors declare no competing interests.×
  • Reproducible Science: Full protocol available at: n.m.rorije@amc.uva.nl. Raw data available at: n.m.rorije@amc.uva.nl.
    Reproducible Science: Full protocol available at: n.m.rorije@amc.uva.nl. Raw data available at: n.m.rorije@amc.uva.nl.×
  • Correspondence: Address correspondence to Dr. Rorije: Academic Medical Center, Meibergdreef 9, Room F4-215, 1105 AZ Amsterdam, The Netherlands. n.m.rorije@amc.uva.nl. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Critical Care Medicine / Cardiovascular Anesthesia / Critical Care
Critical Care Medicine   |   December 2017
Microvascular Permeability after an Acute and Chronic Salt Load in Healthy Subjects: A Randomized Open-label Crossover Intervention Study
Anesthesiology Newly Published on December 7, 2017. doi:10.1097/ALN.0000000000001989
Anesthesiology Newly Published on December 7, 2017. doi:10.1097/ALN.0000000000001989
Abstract

Background: Sodium-induced microcirculatory changes, endothelial surface layer alterations in particular, may play an important role in sodium-mediated blood pressure elevation. However, effects of acute and chronic sodium loading on the endothelial surface layer and microcirculation in humans have not been established. The objective of this study was to assess sodium-induced changes in blood pressure and body weight as primary outcomes and also in microvascular permeability, sublingual microcirculatory dimensions, and urinary glycosaminoglycan excretion in healthy subjects.

Methods: Twelve normotensive males followed both a low-sodium diet (less than 50 mmol/day) and a high-sodium diet (more than 200 mmol/day) for 8 days in randomized order, separated by a crossover period. After the low-sodium diet, hypertonic saline (5 mmol sodium/liter body water) was administered intravenously in 30 min.

Results: Both sodium interventions did not change blood pressure. Body weight increased with 2.5 (95% CI, 1.7 to 3.2) kg (P < 0.001) after dietary sodium loading. Acute intravenous sodium loading resulted in increased transcapillary escape rate of 125I-labeled albumin (2.7 [0.1 to 5.3] % cpm · g−1 · h–1; P = 0.04), whereas chronic dietary sodium loading did not affect transcapillary escape rate of 125I-labeled albumin (−0.03 [−3.3 to 3.2] % cpm · g−1 · h–1; P = 1.00), despite similar increases of plasma sodium and osmolality. Acute intravenous sodium loading coincided with significantly increased plasma volume, as assessed by the distribution volume of albumin, and significantly decreased urinary excretion of heparan sulfate and chondroitin sulfate. These changes were not observed after dietary sodium loading.

Conclusions: Our results suggest that intravenous sodium loading has direct adverse effects on the endothelial surface layer, independent of blood pressure.