PubMed · 7702176
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D R Ball. 1995. Sevoflurane.. https://doi.org/10.1111/j.1365-2044.1995.tb04546.x
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A high-performance liquid chromatographic (HPLC) method for the determination of oxolinic acid (OA) in the plasma of seabass (Dicentrarchus labrax) anaesthetized with 2-phenoxyethanol is described. The samples were extracted and cleaned up by a solid-phase extraction procedure using C18 extraction cartridges. After the eluent was evaporated, the dry residue was dissolved in 1/15 M phosphate buffer. OA was determined by using an isocratic HPLC method with UV detection at 340 nm. Seabass drug-free plasma samples were spiked with OA at 0.2, 1.0, 5.0 and 25.0 microg/ml. Validation of the method showed good precision and accuracy. The mean recovery was 92.2%, with a relative standard deviation lower than 5%. The quantification limit was 0.2 microg/ml. The method was tested on 300 plasma samples of OA-treated seabass.
Thermodynamic analysis of anesthetic effects on Ca2+-ATPase activity was performed to evaluate the feasibility of anesthetic binding and gain insight into the molecular events underlying the anesthetic-enzyme interactions. The Ca2+-ATPases, integral membrane proteins vital in cellular Ca2+ regulation, are suitable models for investigation of the mechanism of anesthetic action on membrane proteins that are targeted by the anesthetics. Ca2+-ATPase of plasma membrane, PMCA, and SERCA1 in the intracellular sarcoplasmic reticulum membrane were used to study two general anesthetics: halothane, a halogenated two-carbon alkane; and propofol, an intravenous, strongly lipophilic-substituted phenol. Interactions of both anesthetics result in a negative Gibbs free energy change, which in both enzymes is more favorable for the more lipophilic propofol than halothane. Temperature dependence (more negative change in Gibbs free energy at increased temperature) is in agreement with predominantly nonpolar interactions. The interactions are entropy-driven, characterized by positive enthalpy which is overcompensated by positive entropy changes. This is in contrast to the reported in literature enthalpy-driven anesthetic binding to soluble proteins. The possible contributions to the observed positive entropy change are discussed including displacement of ordered water molecules by anesthetic binding in nonpolar cavities in the membrane proteins and subtle structural rearrangements.
After cardioversion of chronic atrial fibrillation to sinus rhythm, there is a gradual increase of 56% in cardiac output over 4 weeks. The increase is caused by the gradual return and increasing strength of left atrial mechanical activity as the atrial myopathy of chronic atrial fibrillation subsides. Cardiac output decreases after cardioversion of atrial fibrillation in more than a third of patients, and the decrease may last a week. Acute pulmonary edema is uncommon; 50% of cases occur within 3 hours of cardioversion, with a mortality of 18%. The reduced cardiac performance after cardioversion most likely results from the combination of heart disease and cardiac depressant effects of anesthetic drugs used. Pulmonary and/or coronary artery emboli and the resumption of right atrial mechanical activity before left atrial mechanical activity may be additional factors in the pathogenesis of pulmonary edema after cardioversion. Anticoagulant therapy should be continued for a month or longer after cardioversion in those patients who maintain sinus rhythm to prevent thromboembolism.