Anesthesiology
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Clinical Trial
Characterization of prothrombin activation during cardiac surgery by hemostatic molecular markers.
Prothrombin activation represents the key regulatory step in the hemostatic process. Once formed, thrombin contributes to the generation of fibrin as well as the activation of platelets and fibrinolysis. Failure to suppress thrombin formation during cardiac surgery could result in disorders of hemostasis and thrombosis in the perioperative period. The aim of this study was to determine the time course for prothrombin activation during the perioperative period associated with cardiac surgery. ⋯ These data clearly demonstrate the occurrence of prothrombin activation and thrombin activity during CPB despite heparin concentrations adequate to maintain the activated clotting time greater than 400 s. Hemostatic markers for the activation of prothrombin demonstrated peak concentrations 3 h after completion of CPB with a return to baseline concentrations by the morning after surgery. Markers for thrombin activity, however, suggest the presence of active thrombin through the morning after surgery. Further investigations will be necessary to determine the role of hemostatic activation in thrombotic complications after cardiac surgery.
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Randomized Controlled Trial Comparative Study Clinical Trial
Midlatency auditory evoked potentials and explicit and implicit memory in patients undergoing cardiac surgery.
A high incidence of intraoperative awareness during cardiac surgery has been reported. Midlatency auditory evoked potentials (MLAEP) have been used recently as an indicator of awareness. In the current study, memory for information presented during anesthesia was investigated using MLAEP as one experimental indicator in 45 patients scheduled for elective cardiac surgery. ⋯ When the early cortical potentials of MLAEP are preserved during general anesthesia, auditory information may be processed and remembered postoperatively by an implicit memory task.
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Randomized Controlled Trial Clinical Trial
Humans anesthetized with sevoflurane or isoflurane have similar arrhythmic response to epinephrine.
Anesthetics can alter the dose of exogenously administered epinephrine that causes cardiac arrhythmias. The purpose of this study was to test the hypothesis that in humans anesthetized with sevoflurane, the arrhythmic response to epinephrine is not different from the response in humans anesthetized with isoflurane. ⋯ Sevoflurane and isoflurane do not differ in their sensitization of the human myocardium to the arrhythmogenic effect of exogenously administered epinephrine.
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Surface membrane dihydropyridine receptor Ca2+ channels may play a role in the response of malignant hyperthermia-susceptible skeletal muscle to volatile anesthetics. ⋯ Volatile anesthetics inhibit the binding of PN200-110 to skeletal muscle membranes by decreasing the number of functionally active dihydropyridine receptor proteins. This inhibition is similar for membranes isolated from both normal and malignant hyperthermia-susceptible muscle, thus providing no evidence for a halothane-induced functional defect in this protein in malignant hyperthermia-susceptible muscle. However, the results of this study also indicate that the mechanism by which volatile anesthetics decrease surface membrane Ca2+ currents in skeletal muscle is by reducing the number of functional dihydropyridine receptor Ca2+ channels.