Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2013
ReviewPresurgical evaluation of patients with epilepsy: the role of the anesthesiologist.
Patients with medically refractory epilepsy when referred for surgical treatment often undergo extensive investigations to determine whether surgical treatment is feasible. Surgical feasibility is determined by identifying the location and number of seizure foci and their relationship to eloquent areas of the brain. ⋯ Understanding of the principles of seizure localization and of the effects of anesthetic drugs on the various preoperative investigations is essential for patient management. In this review article, we discuss the role of the anesthesiologist in patient management during many of these investigations and the role of anesthetic drugs to aid in the localization of the seizure focus and of determining eloquent brain function.
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Anesthesia and analgesia · Apr 2013
Ketamine enhances human neural stem cell proliferation and induces neuronal apoptosis via reactive oxygen species-mediated mitochondrial pathway.
Growing evidence indicates that ketamine causes neurotoxicity in a variety of developing animal models, leading to a serious concern regarding the safety of pediatric anesthesia. However, if and how ketamine induces human neural cell toxicity is unknown. Recapitulation of neurogenesis from human embryonic stem cells (hESCs) in vitro allows investigation of the toxic effects of ketamine on neural stem cells (NSCs) and developing neurons, which is impossible to perform in humans. In the present study, we assessed the influence of ketamine on the hESC-derived NSCs and neurons. ⋯ These data for the first time demonstrate that (1) ketamine increases NSC proliferation and causes neuronal apoptosis; (2) mitochondria are involved in ketamine-induced neuronal toxicity, which can be prevented by Trolox; and (3) the stem cell-associated neurogenesis system may provide a simple and promising in vitro model for rapidly screening anesthetic neurotoxicity and studying the underlying mechanisms as well as prevention strategies to avoid this toxic effect.
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Anesthesia and analgesia · Apr 2013
General anesthesia with sevoflurane decreases myocardial blood volume and hyperemic blood flow in healthy humans.
Preservation of myocardial perfusion during general anesthesia is likely important in patients at risk for perioperative cardiac complications. Data related to the influence of general anesthesia on the normal myocardial circulation are limited. In this study, we investigated myocardial microcirculatory responses to pharmacological vasodilation and sympathetic stimulation during general anesthesia with sevoflurane in healthy humans immediately before surgical stimulation. ⋯ In otherwise healthy subjects who are not subjected to surgical stimulation, MBF at rest and after sympathetic stimulation is preserved during sevoflurane anesthesia despite a decrease in myocardial blood volume. However, sevoflurane anesthesia reduces hyperemic MBF, and thus MBF reserve, in these subjects.
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Anesthesia and analgesia · Apr 2013
Occurrence of rapid eye movement sleep deprivation after surgery under regional anesthesia.
Sleep disturbances after general surgery have been described. In this study, we assessed rapid eye movement (REM) sleep in patients undergoing knee replacement surgery using a regional anesthetic technique. ⋯ Postoperative reduction of REM sleep also occurs after surgery and regional anesthesia.
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Anesthesia and analgesia · Apr 2013
Propofol increases vascular relaxation in aging rats chronically treated with the angiotensin-converting enzyme inhibitor captopril.
Both propofol use and advanced age are predictors of intraoperative hypotension. We previously demonstrated that propofol enhances vasodilation in mesenteric arteries from aged rats, partly due to increased nitric oxide (NO) bioavailability. Patients chronically treated with angiotensin-converting enzyme (ACE) inhibitors may exhibit refractory hypotension under general anesthesia. We hypothesized that propofol enhances NO-mediated vasodilation in arteries from aged rats chronically treated with ACE inhibitors. ⋯ Our results show that mesenteric arterial relaxation in response to propofol, both by direct stimulation and through modulation of endothelium-dependent mechanisms, is, in part, NO-dependent. In captopril-treated rats, propofol further increased arterial relaxation through a non-NO-dependent vasodilating pathway (e.g., endothelium-derived hyperpolarizing factor), which may account for enhanced vasodilation during propofol exposure in patients treated with ACE inhibitors.