PubMed · 4188360
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M Isaac, J W Dundee. 1970-01-03. Ethanol infusions.. https://doi.org/10.1016/s0140-6736(70)90546-5
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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.
Excitotoxins are valuable tools in neuroscience research as they can help us to discover the extent to which certain neurones are necessary for different types of behaviour. They have distinctive neurotoxic effects depending on where they are infused, and this study was conducted to delineate the neurotoxic profiles of excitotoxins in the laterodorsal tegmental nucleus (LDTg). Two 0.1 microl infusions of 0.1 M ibotenate, 0.1 M quinolinate, 0.04-0.1 M NMDA, or 0.05-0.015 M AMPA, were made unilaterally into the LDTg under either pentobarbitone or Avertin anaesthesia. The injection needle was oriented at an angle of 24 degrees from vertical in the mediolateral plane. After 23-27 days, sections through the mesopontine tegmentum were processed using standard histological procedures for NADPH-diaphorase histochemistry, tyrosine hydroxylase or 5-hydroxytryptamine immunohistochemistry, and Cresyl violet. Lesions were assessed in terms of the size of the damaged area (identified by reactive gliosis), the extent of cholinergic cell loss in the mesopontine tegmentum (by counting NADPH-diaphorase-positive neurones), and neuronal loss induced in the locus coeruleus and dorsal raphe nucleus. Ibotenate induced compact lesions in the LDTg (more than 80% cholinergic loss) and did little damage to the locus coeruleus and dorsal raphe nucleus. Quinolinate and low doses of AMPA and NMDA made very small lesions with less than 35% cholinergic loss, while at higher doses, AMPA and NMDA induced large areas of reactive gliosis but killed only a proportion of the cholinergic neurones. AMPA appeared to have a particular affinity for noradrenergic neurones in the locus coeruleus, with the 0.015 M dose injected into the LDTg typically destroying the majority of these neurones. The results are discussed in the context of what is known about the mechanisms of excitotoxins and the glutamate receptor profile of mesopontine neurones.