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 125 I-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 125 I-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.

Background: It is believed that the effectiveness of colloids as plasma volume expanders is dependent on the endothelial permeability for macromolecules. The objective of this study was to test the hypothesis that the plasma volume expanding effect of 5% albumin relative to that of a crystalloid solution is reduced if microvascular permeability is increased. Methods: A control group was resuscitated with either 5% albumin (8 ml/kg) or Ringer’s acetate (36 ml/kg) immediately after a hemorrhage of 8 ml/kg (n = 29). In a second group, permeability was increased by inducing sepsis through cecal ligation and incision (n = 28). Three hours after cecal ligation and incision, the animals were resuscitated with either 5% albumin in a ratio of 1:1 relative to the volume of lost plasma, or Ringer’s acetate in a ratio of 4.5:1. Results: In the hemorrhage group, plasma volumes at 15 min after resuscitation with albumin or Ringer’s acetate had increased by 9.8 ± 2.6 ml/kg (mean ± SD) and 7.4 ± 2.9 ml/kg and were similar at 2 and 4 h. Plasma volume 3 h after cecal ligation and incision had decreased by approximately 7 ml/kg, and at 15 min after resuscitation with albumin or Ringer’s acetate it had increased by 5.7 ± 2.9 and 2.4 ± 3.0 ml/kg, respectively ( P < 0.05). At 2 and 4 h after resuscitation, plasma volumes did not differ between the groups. Conclusion: This study does not support the hypothesis that the plasma-volume-expanding effect of albumin relative to that of crystalloids is decreased under conditions characterized by increased permeability.

Volume kinetics is a method used for analyzing and simulating the distribution and elimination of infusion fluids. Approximately 50 studies describe the disposition of 0.9% saline, acetated and lactated Ringer's solution, based on repeated measurements of the hemoglobin concentration and (sometimes) the urinary excretion. The slow distribution to the peripheral compartment results in a 50-75% larger plasma dilution during an infusion of crystalloid fluid than would be expected if distribution had been immediate. A drop in the arterial pressure during induction of anesthesia reduces the rate of distribution even further. The renal clearance of the infused fluid during surgery is only 10-20% when compared with that in conscious volunteers. Some of this temporary decrease can be attributed to the anesthesia and probably also to preoperative psychologic stress or dehydration. Crystalloid fluid might be allocated to "nonfunctional" fluid spaces in which it is unavailable for excretion. This amounts to approximately 20-25% during minor (thyroid) surgery.

Background The distribution and elimination of 0.9% saline given by intravenous infusion has not been compared between the conscious state and during inhalational anesthesia. Methods Six adult sheep received an intravenous infusion of 25 ml/kg of 0.9% saline over 20 min in the conscious state and also during isoflurane anesthesia and mechanical ventilation. The distribution and elimination of infused fluid were studied by volume kinetics based on serial analysis of hemoglobin dilution in arterial blood and by mass balance that incorporated volume calculations derived from volume kinetic analysis and measurements of urinary volumes. Results The mass balance calculations indicated only minor differences in the time course of plasma volume expansion between the conscious and anesthetized states. However, isoflurane anesthesia markedly reduced urinary volume (median, 9 vs. 863 ml; P < 0.03). In conscious sheep, the central and peripheral volume expansion predicted by volume kinetics agreed well with the calculations based on mass balance. However, during isoflurane anesthesia and mechanical ventilation, calculation using volume kinetic analysis of the variable kr, an elimination factor that, in conscious humans and sheep, is closely related to urinary excretion, represented both urinary excretion and peripheral accumulation of fluid. This suggests that the previous assumption that kr approximates urinary excretion of infused fluid requires modification, i.e., kr simply reflects net fluid movement out of plasma. Conclusions In both conscious and anesthetized, mechanically ventilated sheep, infusion of 0.9% saline resulted in minimal expansion of plasma volume over a 3-h interval. In conscious sheep, infused 0.9% saline was rapidly eliminated from the plasma volume by urinary excretion; in contrast, the combination of isoflurane anesthesia and mechanical ventilation reduced urinary excretion and promoted peripheral accumulation of fluid.

Background The impact of acute preoperative volume loading with colloids on blood volume has not been investigated sufficiently. Methods Before surgery, in 20 patients undergoing major gynecologic procedures, volume loading was performed during anesthesia by infusing approximately 20 ml/kg of colloid at a rate of 90 ml/min (group I: 5% albumin solution; group II: 6% hetastarch solution; n = 10 each). Plasma volume (indocyanine green dilution technique), erythrocyte volume (labeling erythrocytes with fluorescein), hematocrit, total protein, and hetastarch plasma concentrations (group II) were measured before and 30 min after the end of infusion. Results More than 1,350 ml of colloid (approximately 50% of the baseline plasma volume) were infused within 15 min. Thirty minutes after the infusion had been completed, blood volume was only 524 +/- 328 ml (group I) and 603 +/- 314 ml (group II) higher than before volume loading. The large vessel hematocrit (measured by centrifugation) dropped more than the whole body hematocrit, which was derived from double-label measurements of blood volume. Conclusions The double-label measurements of blood volume performed showed that 30 min after the infusion of approximately 20 ml/kg of 5% albumin or 6% hetastarch solution (within 15 min), only mean 38 +/- 21% and 43 +/- 26%, respectively, of the volume applied remained in the intravascular space. Different, i.e., earlier or later, measuring points, different infusion volumes, infusion rates, plasma substitutes, or possibly different tracers for plasma volume measurement might lead to different results concerning the kinetics of fluid or colloid extravasation.

Background Noninvasive techniques used to determine the changes in cerebral blood volume in response to carbon dioxide are hampered by their limited spatial or temporal resolution or both. Using steady state contrast-enhanced magnetic resonance imaging, the authors determined regional changes in cerebral plasma volume (CPV) induced by hypercapnia in halothane-anesthetized rats. Methods Cerebral plasma volume was determined during normocapnia, hypercapnia and recovery in the dorsoparietal neocortex and striatum of each hemisphere, in cerebellum, and in extracerebral tissue of rats with either intact carotid arteries (group 1) or unilateral common carotid ligation (group 2). Another group was studied without injection of a contrast agent (group 3). Results Hypercapnia (partial pressure of carbon dioxide in arterial blood [PaCO2] approximately 65 mmHg) resulted in a significant increase in CPV in the striatum (+42 +/- 8%), neocortex (+34 +/- 6%), and cerebellum (+49 +/- 12%) compared with normocapnic CPV values (group 1). Carotid ligation (group 2) led to a marked reduction of the CPV response to hypercapnia in the ipsilateral striatum (+23 +/- 14%) and neocortex (+27 +/- 17%) compared with the unclamped side (+34 +/- 15% and +38 +/- 16%, respectively). No significant changes in CPV were found in extracerebral tissue. In both groups, the CPV changes were reversed by the carbon dioxide washout period. Negligible changes in contrast imaging were detected during hypercapnia without administration of the contrast agent (group 3). Conclusions The contrast-enhanced magnetic resonance imaging technique is sensitive to detect noninvasively regional CPV changes induced by hypercapnia in rat brain. This could be of clinical interest for determining the cerebrovascular reactivity among different brain regions.