In this model of endotoxemia, fluid resuscitation corrected both serosal intestinal and sublingual microcirculation but was unable to restore intestinal mucosal perfusion. Intramucosal acidosis might be due to persistent villi hypoperfusion.

Alterations in sublingual, intestinal microcirculation, and arterial lactate simultaneously arose from the first step of bleeding. The microcirculatory changes were identified either by semi-quantitative flow index or by quantitative red blood cell velocity measurements.

Sodium intake in Argentina has been estimated to be at least double the dose of 2000 mg/day recommended by WHO, mostly coming from processed foods. Argentina is one of the few countries in the world that have regulated sodium content in certain food products. This study presents an assessment of sodium content in a selection of food groups and categories as reported in the nutrient information panels. We surveyed 3674 food products, and the sodium content of 864 and 1375 of them was compared to the maximum levels according to the Argentinean law and the regional targets, respectively. All food categories presented high variability of sodium content. Over 90% of the products included in the national sodium reduction law were found to be compliant. Food groups with high median sodium, such as condiments, sauces and spreads, and fish and fish products, are not included in the national law. In turn, comparisons with the lower regional targets indicated that almost 50% of the products analyzed had sodium contents above the recommended values. This evidence suggests that enhancing sodium reduction in processed foods may be a necessity for public health objectives and it is also technically feasible in Argentina.

BackgroundThe identification of anaerobic metabolism in critically ill patients is a challenging task. Observational studies have suggested that the ratio of venoarterial PCO2 (Pv–aCO2) to arteriovenous oxygen content difference (Ca–vO2) might be a good surrogate for respiratory quotient (RQ). Yet Pv–aCO2/Ca–vO2 might be increased by other factors, regardless of anaerobic metabolism. At present, comparisons between Pv–aCO2/Ca–vO2 and RQ have not been performed. We sought to compare these variables during stepwise hemorrhage and hemodilution. Since anemia predictably produces augmented Pv–aCO2 and decreased Ca–vO2, our hypothesis was that Pv–aCO2/Ca–vO2 might be an inadequate surrogate for RQ.MethodsThis is a subanalysis of a previously published study. In anesthetized and mechanically ventilated sheep (n = 16), we compared the effects of progressive hemodilution and hemorrhage by means of expired gases analysis.ResultsThere were comparable reductions in oxygen consumption and increases in RQ in the last step of hemodilution and hemorrhage. The increase in Pv–aCO2/Ca–vO2 was higher in hemodilution than in hemorrhage (1.9 ± 0.2 to 10.0 ± 0.9 vs. 1.7 ± 0.2 to 2.5 ± 0.1, P < 0.0001). The increase in Pv–aCO2 was lower in hemodilution (6 ± 0 to 10 ± 1 vs. 6 ± 0 to 17 ± 1 mmHg, P < 0.0001). Venoarterial CO2 content difference and Ca–vO2 decreased in hemodilution and increased in hemorrhage (2.6 ± 0.3 to 1.2 ± 0.1 vs. 2.8 ± 0.2 to 6.9 ± 0.5, and 3.4 ± 0.3 to 1.0 ± 0.3 vs. 3.6 ± 0.3 to 6.8 ± 0.3 mL/dL, P < 0.0001 for both). In hemodilution, Pv–aCO2/Ca–vO2 increased before the fall in oxygen consumption and the increase in RQ. Pv–aCO2/Ca–vO2 was strongly correlated with Hb (R 2 = 0.79, P < 0.00001) and moderately with RQ (R 2 = 0.41, P < 0.0001). A multiple linear regression model found Hb, RQ, base excess, and mixed venous oxygen saturation and PCO2 as Pv–aCO2/Ca–vO2 determinants (adjusted R 2 = 0.86, P < 0.000001).ConclusionsIn hemodilution, Pv–aCO2/Ca–vO2 was considerably increased, irrespective of the presence of anaerobic metabolism. Pv–aCO2/Ca–vO2 is a complex variable, which depends on several factors. As such, it was a misleading indicator of anaerobic metabolism in hemodilution.

A. Dubin ( ) ) calle 42 No.

The alterations in O2 extraction in hemodilution have been linked to fast red blood cell (RBC) velocity, which might affect the complete release of O2 from Hb. Fast RBC velocity might also explain the normal mucosal-arterial Pco2 (ΔPco2). Yet sublingual and intestinal microcirculation have not been completely characterized in extreme hemodilution. Our hypothesis was that the unchanged ΔPco2 in hemodilution depends on the preservation of villi microcirculation. For this purpose, pentobarbital-anesthetized and mechanically ventilated sheep were submitted to stepwise hemodilution (n = 8), hemorrhage (n = 8), or no intervention (sham, n = 8). In both hypoxic groups, equivalent reductions in O2 consumption (V̇o2) were targeted. Microcirculation was assessed by videomicroscopy, intestinal ΔPco2 by air tonometry, and V̇o2 by expired gases analysis. Although cardiac output and superior mesenteric flow increased in hemodilution, from the very first step (Hb = 5.0 g/dl), villi functional vascular density and RBC velocity decreased (21.7 ± 0.9 vs. 15.9 ± 1.0 mm/mm(2) and 1,033 ± 75 vs. 850 ± 79 μm/s, P < 0.01). In the last stage (Hb = 1.2 g/dl), these variables were lower in hemodiution than in hemorrhage (11.1 ± 0.5 vs. 15.4 ± 0.9 mm/mm(2) and 544 ± 26 vs. 686 ± 70 μm/s, P < 0.01), and were associated with lower intestinal fractional O2 extraction (0.61 ± 0.04 vs. 0.79 ± 0.02, P < 0.01) but preserved ΔPco2 (5 ± 2 vs. 25 ± 4 mmHg, P < 0.01). Therefore, alterations in O2 extraction in hemodilution seemed related to microvascular shunting, not to fast RBC velocity. The severe microvascular abnormalities suggest that normal ΔPco2 was not dependent on CO2 washout by the villi microcirculation. Increased perfusion in deeper intestinal layers might be an alternative explanation.

BackgroundThe microvascular reperfusion injury after retransfusion has not been completely characterized. Specifically, the question of heterogeneity among different microvascular beds needs to be addressed. In addition, the identification of anaerobic metabolism is elusive. The venoarterial PCO2 to arteriovenous oxygen content difference ratio (Pv-aCO2/Ca-vO2) might be a surrogate for respiratory quotient, but this has not been validated. Therefore, our goal was to characterize sublingual and intestinal (mucosal and serosal) microvascular injury after blood resuscitation in hemorrhagic shock and its relation with O2 and CO2 metabolism.MethodsAnesthetized and mechanically ventilated sheep were assigned to stepwise bleeding and blood retransfusion (n = 10) and sham (n = 7) groups. We performed analysis of expired gases, arterial and mixed venous blood gases, and intestinal and sublingual videomicroscopy.ResultsIn the bleeding group during the last step of hemorrhage, and compared to the sham group, there were decreases in oxygen consumption (3.7 [2.8–4.6] vs. 6.8 [5.8–8.0] mL min−1 kg−1, P < 0.001) and increases in respiratory quotient (0.96 [0.91–1.06] vs. 0.72 [0.69–0.77], P < 0.001). Retransfusion normalized these variables. The Pv-aCO2/Ca-vO2 increased in the last step of bleeding (2.4 [2.0–2.8] vs. 1.1 [1.0–1.3], P < 0.001) and remained elevated after retransfusion, compared to the sham group (1.8 [1.5–2.0] vs. 1.1 [0.9–1.3], P < 0.001). Pv-aCO2/Ca-vO2 had a weak correlation with respiratory quotient (Spearman R = 0.42, P < 0.001). All the intestinal and sublingual microcirculatory variables were affected during hemorrhage and improved after retransfusion. The recovery was only complete for intestinal red blood cell velocity and sublingual total and perfused vascular densities.ConclusionsAlthough there were some minor differences, intestinal and sublingual microcirculation behaved similarly. Therefore, sublingual mucosa might be an adequate window to track intestinal microvascular reperfusion injury. Additionally, Pv-aCO2/Ca-vO2 was poorly correlated with respiratory quotient, and its physiologic behavior was different. Thus, it might be a misleading surrogate for anaerobic metabolism.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-017-0136-3) contains supplementary material, which is available to authorized users.

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