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Chronic inflammation and sepsis induced a decrease in contractile performances of extensor digitorum longus along with accelerated kinetics of atracurium possibly induced by modified expression of RyR1 receptors and not acetylcholine-receptors.

Chronic inflammation and sepsis induced modifications of sodium channel properties that could contribute to muscular inexcitability. This inexcitability can be elicited by a modification of properties or type of voltage-gated sodium channels. Our results lead us to explain this inexcitability by an up-regulation of NaV 1.5 sodium channel.

Our study demonstrates poor correlation between hemoglobin measured noninvasively by multiwavelength pulse oximetry and a laboratory hematology analyzer. The difference was greater when the pulse oximetry perfusion index was low, as may occur in shock, hypothermia, or vasoconstriction patients. The multiwavelength pulse oximetry is not sufficiently accurate for clinical use in a cardiovascular intensive care unit.

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The results of the Stewart-Fencl approach for interpretation of acid-base status can vary according to the analyzer used. These differences may have important clinical and research implications..

The goal of this study was to analyze the mortality data following neck dissection and determine the risk factors of early death. The hospital mortality records were analyzed from 3,015 consecutive patients who underwent neck dissection. A case control study analyzed risk factors of death during the first 3 postoperative days. The mortality incidences were 0.50% and 1.33%, respectively, during the first 3 and the first 30 postoperative days. Eleven of the 12 unexplained deaths occurred during the first 3 postoperative days, and most of these patients died suddenly. They were more likely to be alcoholic and to have undergone nerve section. In most of the patients who died after the third postoperative day, death was related to a postoperative complication. Although the mechanisms of sudden death remain unclear, careful follow-up of these patients during the early postoperative days should be performed to reduce the mortality risk by shortening the delay of care.

Sepsis is involved in the decrease of membrane excitability of skeletal muscle, leading to polyneuromyopathy. This effect is mediated by alterations of the properties of voltage-gated sodium channels (Na(V)), but the exact mechanism is still unknown. The aim of the present study was to check whether tumor necrosis factor (TNF-α), a cytokine released during sepsis, exerts a rapid effect on Na(V). Sodium current (I(Na)) was recorded by macropatch clamp in skeletal muscle fibers isolated from rat peroneus longus muscle, in control conditions and after TNF-α addition. Analyses of dose-effect and time-effect relationships were carried out. Effect of chelerythrine, a PKC inhibitor, was also studied to determine the way of action of TNF-α. TNF-α induced a reversible dose- and time-dependent inhibition of I(Na). A maximum inhibition of 75% of the control current was observed. A shift toward more negative potentials of activation and inactivation curves of I(Na) was also noticed. These effects were prevented by chelerythrine pretreatment. TNF-α is a cytokine released in the early stages of sepsis. Besides a possible transcriptional role, i.e., modification of the channel type and/or number, we demonstrated the existence of a rapid, posttranscriptional inhibition of Na(V) by TNF-α. The downregulation of the sodium current could be mediated by a PKC-induced phosphorylation of the sodium channel, thus leading to a significant decrease in muscle excitability.