Microvascular Permeability after an Acute and Chronic Salt Load in Healthy Subjects
| Autor: | Bert-Jan H. van den Born, Naomi van Vlies, Liffert Vogt, Jan P. van Straalen, Hein J. Verberne, Youssef Chahid, Nienke M. G. Rorije, Rik H. G. Olde Engberink |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Endothelium business.industry Urinary system Sodium Healthy subjects Hemodynamics chemistry.chemical_element Vascular permeability 030204 cardiovascular system & hematology medicine.disease Microcirculation 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Anesthesiology and Pain Medicine medicine.anatomical_structure chemistry Internal medicine medicine Cardiology Hypernatremia business |
| Zdroj: | Anesthesiology. 128:352-360 |
| ISSN: | 0003-3022 |
| DOI: | 10.1097/aln.0000000000001989 |
| Popis: | 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 eight 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|