When Does Nutrition Impact Respiratory Function?

Nutrition therapy is an essential aspect of patient care and an important determinant of outcomes in the ICU. Nutrition can impact respiratory function in a myriad of ways. Under- and overfeeding are two well-established ways by which nutrition impinges on respiratory function. Route of feeding, method of feeding, and carbohydrate composition of the diet are also other key factors regarding nutrition that influence outcomes in ICU patients. Recent studies are now elucidating the role of immune therapy in patients with acute respiratory distress syndrome. In the ICU, nutrition dogmas, such as the necessity of checking gastric residual volumes or utilizing full-calorie enteric feeds, as opposed to trophic feeds, are constantly being challenged by innovative clinical studies. Basic research brings the prospect of testing new approaches for ICU patients, such as the use of antioxidants to prevent diaphragm weakness in these patients. In this review article, we evaluate the recent observational and randomized control trials to critically appraise the evidence regarding nutrition in the ICU.     

Human fluids alter DNA-acquisition in Acinetobacter baumannii

Transformation is one of the mechanisms of acquisition of foreign genetic material leading to the emergence of multidrug resistant (MDR) bacteria. Recently, human serum albumin (HSA) was shown to specifically increase transformation frequency in the nosocomial pathogen Acinetobacter baumannii. To further assess the relevance of HSA as a possible modulator of A. baumannii transformation in host-pathogen interactions, in this work we examined the effect of different human fluids. We observed a significant increase in transformation frequencies in the presence of pleural fluid, whole blood cells and liquid ascites, and to a lesser extent with urine. The observed effects correlate with both HSA and bacterial content found in the assayed patient fluids. Taken together, these results are in agreement with our previous findings that highlight HSA as a possible host signal with the ability to trigger natural transformation in A. baumannii.     

Inspiratory Muscle Training Potentiates the Beneficial Effects of Proportional Assisted Ventilation on Exertional Dyspnea and Exercise Tolerance in COPD: A Proof-of-Concept Randomized and Controlled Trial

Abstract

During pulmonary rehabilitation, a subset of subjects with COPD requires adjunct therapy to achieve high-intensity training. Both noninvasive ventilation (NIV) and inspiratory muscle training (IMT) are available to assist these subjects. We aimed to prime the respiratory muscles before NIV with IMT, anticipating additive effects for maximal exercise tolerance (T _lim) and dyspnea/leg fatigue relief throughout the exercise as primary outcomes. Changes in the respiratory pattern were secondary outcomes. COPD subjects performed a total of four identical constant work rate tests on a cycle ergometer at 75% of maximum work rate, under control ventilation (SHAM, 4?cm H₂O) or proportional assisted ventilation (PAV, individually adjusted), before and after 10 sessions of high-intensity IMT (three times/week) during 30?days. Two-way RM ANOVA with appropriate corrections were performed. Final analysis in nine subjects showed improved T _lim (Δ = 111?s) and lower minute-ventilation (Δ = 4?L^.min^?1) at exhaustion, when comparing the IMT effects within the PAV modality (p?=?0.001 and p?=?0.036, respectively) and improved T _lim for PAV vs. SHAM (PAV main-effect, p?=?0.001; IMT main-effect, p?=?0.006; PAV vs. IMT interaction, p?=?0.034). In addition, IMT?+?PAV association, compared to PAV alone, resulted in lower respiratory frequency (IMT main-effect, p?=?0.009; time main-effect, p?<?0.0001; IMT vs. time interaction, p?=?0.242) and lower inspiratory time related to duty cycle (IMT main-effect, p?=?0.018; time main-effect, p?=?0.0001; IMT vs. time interaction, p?=?0.004) throughout exercise. The addition of IMT prior to a PAV-supported aerobic bout potentiates exercise tolerance and dyspnea relief and induces favourable changes in ventilatory pattern in severe COPD during high-intensity training (Brazilian Registry of Clinical Trials, number RBR-6n3dzz).     

Ethanol withdrawal increases blood pressure and vascular oxidative stress: a role for angiotensin type 1 receptors

We evaluated the possible mechanisms underlying the oxidative stress induced by ethanol withdrawal. With this purpose, we verified the role of AT₁ receptors in such response. Male Wistar rats were treated with ethanol 3%–9% (vol./vol.) for 21 days. Ethanol withdrawal was induced by abrupt discontinuation of the treatment. Experiments were performed 48 hours after ethanol discontinuation. Increased plasma levels of angiotensin II were detected after ethanol withdrawal. Losartan (10 mg/kg; p.o. gavage), a selective AT₁ receptor antagonist, impeded the increase in blood pressure induced by ethanol withdrawal. Increased lipoperoxidation and superoxide anion (O₂^?) levels were detected in aortas after ethanol withdrawal, and losartan prevented these responses. Decreased hydrogen peroxide and nitrate/nitrite concentration were detected in aortas after ethanol withdrawal, and losartan prevented these effects. Nitrotyrosine immunostaining in the rat aorta was increased after ethanol withdrawal, and AT₁ blockade impeded this response. Increased expression of PKCδ and p47^phox was detected after ethanol withdrawal, and treatment with losartan prevented these responses. Our study provides novel evidence that ethanol withdrawal increases vascular oxidative stress and blood pressure through AT₁-dependent mechanisms. These findings highlight the importance of angiotensin II in ethanol withdrawal–induced increase in blood pressure and vascular oxidative damage.