Articles: function.
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Minerva anestesiologica · Oct 2014
Dysnatremia on intensive care unit admission is a stronger risk factor when associated with organ dysfunction.
Dysnatremia present at the time of intensive care unit (ICU) admission is associated with mortality. In this study, we investigated the epidemiology of dysnatremia present on ICU admission and the impact of organ dysfunction on the association between dysnatremia and mortality. We hypothesized that dysnatremia comorbid with organ dysfunction is associated with higher risk of mortality. ⋯ Below 125 and above 150 mmol/L sodium levels at ICU admission are risk factors for higher mortality rates in patients with comorbid organ dysfunction. The effect of dysnatremia on mortality is observed when organ dysfunction is present.
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Left atrial pressure and its surrogate, pulmonary capillary wedge pressure (PCWP), are important for determining diastolic function. The role of transthoracic echocardiography (TTE) in assessing diastolic function is well established in awake subjects. The objective was to assess the accuracy of predicting PCWP by TTE and transesophageal echocardiography (TEE) during coronary artery surgery. ⋯ Doppler assessment of PCWP was neither sensitive nor specific enough to be clinically useful in anesthetized patients with mechanical ventilation. The fixed curve pattern of the interatrial septum was the best predictor of raised PCWP.
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Randomized Controlled Trial
A Randomized Controlled Trial of ACE-inhibition for Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease.
Skeletal muscle impairment is a recognized complication of COPD, predicting mortality in severe disease. Increasing evidence implicates the renin-angiotensin system in control of muscle phenotype. We hypothesized that angiotensin-converting enzyme (ACE) inhibition would improve quadriceps function and exercise performance in COPD. ⋯ This randomized controlled trial found that ACE inhibition, using fosinopril for 3 months, did not improve quadriceps function or exercise performance in patients with COPD with quadriceps weakness.
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Anesthesia and analgesia · Oct 2014
Glycogen Synthase Kinase-3β Inhibition Prevents Remifentanil-Induced Postoperative Hyperalgesia via Regulating the Expression and Function of AMPA Receptors.
Many studies have confirmed that brief remifentanil exposure can enhance pain sensitivity. We previously reported that activation of glycogen synthase kinase-3β (GSK-3β) contributes to remifentanil-induced hyperalgesia via regulating N-methyl-D-aspartate receptor plasticity in the spinal dorsal horn. In this study, we demonstrated that GSK-3β inhibition prevented remifentanil-induced postoperative hyperalgesia via regulating α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) expression and function in the spinal dorsal horn. ⋯ These results indicate that amelioration of remifentanil-induced postoperative hyperalgesia by GSK-3β inhibition is attributed to downregulated AMPAR GluR1 expression in the membrane fraction and inhibition of AMPAR function via altering pGluR1 and Rab5 expression in the spinal dorsal horn.