Anesthesia and analgesia
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Anesthesia and analgesia · Nov 2013
Observational StudyFIBTEM PLUS Provides an Improved Thromboelastometry Test for Measurement of Fibrin-Based Clot Quality in Cardiac Surgery Patients.
The viscoelastic functional fibrinogen (FF) and FIBTEM assays measure the contribution of fibrin to clot strength. Inhibition of platelet function is a necessary precondition for these tests to work. We investigated a novel test for measuring fibrin-based clotting, FIBTEM PLUS, in cardiac surgery and compared it with FF and FIBTEM. ⋯ The FIBTEM PLUS assay produces precise results. At baseline, it provides greater inhibition of platelets than FIBTEM, but there is no meaningful difference between FIBTEM PLUS and FIBTEM in patients with low platelet counts.
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Anesthesia and analgesia · Nov 2013
The Effect of Endoplasmic Reticulum Stress on Neurotoxicity Caused by Inhaled Anesthetics.
The mechanisms by which inhaled anesthetics cause neurotoxicity are not well clarified. Exposure to inhaled anesthetics induces a release of Ca from the endoplasmic reticulum (ER) into the cytosol. Aberrant Ca mobilization may alter the protein-folding environment in the ER, causing ER stress. Binding immunoglobulin protein (BiP) is an ER chaperone that is critical to ER functions. Because ER stress leads to cellular dysfunction and apoptotic cell death, leading to diverse human disorders such as neurodegenerative diseases, we hypothesized ER stress may play a role in neurotoxicity caused by inhaled anesthetics. ⋯ Sevoflurane exposure may cause ER stress, which is tolerated to some extent in wild-type cells. When this tolerance is limited, like in cells with mutant BiP, the exposure leads to cell death in the brain, suggesting that ER stress may partially mediate neurotoxicity caused by inhaled anesthetics. This study suggests that patients with certain conditions sensitive to ER stress such as ischemia, hypoxia, developing brain, or neurodegenerative diseases may be vulnerable to inhaled anesthetics.
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Anesthesia and analgesia · Nov 2013
The Distinct Effects of Lipid Emulsions Used for "Lipid Resuscitation" on Gating and Bupivacaine-Induced Inhibition of the Cardiac Sodium Channel Nav1.5.
Systemic administration of lipid emulsions is an established treatment for local anesthetic intoxication. However, it is unclear by which mechanisms lipids achieve this function. The high cardiac toxicity of the lipophilic local anesthetic bupivacaine probably results from a long-lasting inhibition of the cardiac Na channel Nav1.5. In this study, we sought to determine whether lipid emulsions functionally interact with Nav1.5 or counteract inhibition by bupivacaine. ⋯ Our data indicate that lipid emulsions reduce rather than increase availability of Nav1.5. However, both Intralipid and Lipofundin partly relieve Nav1.5 from block by bupivacaine. These effects are likely to involve not only a direct interaction of lipids with Nav1.5 but also the ability of lipid emulsions to absorb bupivacaine and thus reduce its effective concentration.
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Anesthesia and analgesia · Nov 2013
Remifentanil Has a Minimal Direct Effect on Sinoatrial Node Pacemaker Activity in the Guinea Pig Heart.
Whereas remifentanil administration is associated with severe bradycardia, it has yet to be fully investigated whether the negative chronotropic action of remifentanil is mediated by its direct action on sinoatrial (SA) node pacemaker activity in the heart versus indirect results of enhanced vagal activity. ⋯ Clinically relevant concentrations (nanomolar order concentrations) of remifentanil do not produce significant direct effects on intrinsic cardiac automaticity; thus, suggesting that remifentanil-induced bradycardia in the clinical setting is independent of its direct cardiac effects.