Journal of applied physiology
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Volumetric capnography is a standard method to determine pulmonary dead space. Hereby, measured carbon dioxide (CO2) in exhaled gas volume is analyzed using the single-breath diagram for CO2. Unfortunately, most existing CO2 sensors do not work with the low tidal volumes found in small animals. ⋯ Dead space and wasted ventilation during MV increased with tidal volume. This increase was mostly reversible by switching back to SB. Surfactant depletion had no further influence on the dead space increase during MV, but impaired the reversibility of the dead space increase.
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Exhaled breath contains information on systemic and pulmonary metabolism, which may provide a monitoring tool for the development of lung injury. We aimed to determine the effect of intravenous (iv) and intratracheal (IT) lipopolysaccharide (LPS) challenge on the exhaled mixture of volatile metabolites and to assess the similarities between these two models. Male adult Sprague-Dawley rats were anesthetized, tracheotomized, and ventilated for 6 h. ⋯ LPS-induced lung injury rapidly changes exhaled breath metabolite mixtures in two animal models of lung injury. Changes partly overlap between an iv and an IT LPS challenge. This warrants testing the diagnostic accuracy of exhaled breath analysis for acute respiratory distress syndrome in clinical trials, possibly focusing on biological markers described in this study.
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Although it is well established that carbohydrate and lipid metabolism are profoundly altered by cold stress, the effects of short-term cold exposure on protein metabolism in skeletal muscle are still poorly understood. Because cold acclimation requires that an organism adjust its metabolic flux, and muscle amino acids may be an important energy source for heat production, we hypothesize that muscle proteolysis is increased and protein synthesis is decreased under such a stress condition. Herein, cold exposure for 24 h decreased rates of protein synthesis and increased overall proteolysis in both soleus and extensor digitorum longus (EDL) muscles, but it did not affect muscle weight. ⋯ Plasma insulin levels were lower, whereas catecholamines, corticosterone, and thyroid hormones were higher in cold-exposed rats compared with control rats. The present data provide the first direct evidence that short-term cold exposure for 24 h decreases rates of protein synthesis and increases the UPS and Ca(2+)-dependent proteolytic processes, and increases expression of atrogin-1 and MuRF1 in skeletal muscles of young rats. The activation of atrophy induced by acute cold stress seems to be mediated at least in part through the inactivation of Akt/FoxO signaling and activation of AMP-activated protein kinase.
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In human heart failure (HF), reduced cardiac function has, at least partly, been ascribed to altered calcium homeostasis in cardiomyocytes. The effects of the calcium sensitizer levosimendan on diastolic dysfunction caused by reduced removal of calcium from cytosol in early diastole are not well known. In this study, we investigated the effect of long-term levosimendan treatment in a murine model of HF where the sarco(endo)plasmatic reticulum ATPase (Serca) gene is specifically disrupted in the cardiomyocytes, leading to reduced removal of cytosolic calcium. ⋯ Gene-expression analysis, however, revealed an increase in genes related to production of the ECM in animals treated with levosimendan. In conclusion, long-term levosimendan treatment improves both contractility and relaxation in a heart-failure model with marked diastolic dysfunction due to reduced calcium transients. However, altered gene expression related to fibrosis was observed.
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Trauma patients with "compensated" internal hemorrhage may not be identified with standard medical monitors until signs of shock appear, at which point it may be difficult or too late to pursue life-saving interventions. We tested the hypothesis that a novel machine-learning model called the compensatory reserve index (CRI) could differentiate tolerance to acute volume loss of individuals well in advance of changes in stroke volume (SV) or standard vital signs. Two hundred one healthy humans underwent progressive lower body negative pressure (LBNP) until the onset of hemodynamic instability (decompensation). ⋯ Changes in heart rate, blood pressure, and SV did not differentiate HT from LT groups. Machine modeling of the photoplethysmogram response to reduced central blood volume can accurately trend individual-specific progression to hemodynamic decompensation. These findings foretell early identification of blood loss, anticipating hemodynamic instability, and timely application of life-saving interventions.