Anesthesiology
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Randomized Controlled Trial Clinical Trial
Effects of combining propofol and alfentanil on ventilation, analgesia, sedation, and emesis in human volunteers.
Propofol and alfentanil frequently are administered together for intravenous sedation. This study investigated pharmacokinetic and pharmacodynamic interactions between propofol and alfentanil, at sedative concentrations, with specific regard to effects on ventilation, analgesia, sedation, and nausea. ⋯ The combination of propofol and alfentanil produced greater sedation and analgesia than that with either drug alone. Propofol offset the emetic effects of alfentanil. Equivalent depression of the carbon dioxide response curve, and elevation of end-tidal carbon dioxide occurred with propofol/alfentanil combined and alfentanil.
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Randomized Controlled Trial Comparative Study Clinical Trial
Propofol fails to attenuate the cardiovascular response to rapid increases in desflurane concentration.
A rapid increase in desflurane concentration to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating catecholamine concentration. Because propofol decreases sympathetic outflow, it was hypothesized that propofol would blunt these responses. ⋯ Although able to blunt the increase in epinephrine concentration, propofol 2 mg.kg-1 propofol does no attenuate the transient cardiovascular response to a rapid increase in desflurane concentration to greater than 1 MAC.
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Comparative Study Clinical Trial
Electroencephalogram bispectral analysis predicts the depth of midazolam-induced sedation.
The electroencephalogram (EEG) has been used to study the effects of anesthetic and analgesic drugs on central nervous system function. A prospective study was designed to evaluate the accuracy of various EEG parameters for assessing midazolam-induced sedation during regional anesthesia. ⋯ The EEG-BI appears to be a useful parameter for assessing midazolam-induced sedation and can predict the likelihood of a patient responding to verbal commands or to shaking of the head during midazolam-induced sedation.
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Comparative Study
Intravenous opioids stimulate norepinephrine and acetylcholine release in spinal cord dorsal horn. Systematic studies in sheep and an observation in a human.
Opioids produce analgesia by direct effects as well as by activating neural pathways that release nonopioid transmitters. This study tested whether systematically administered opioids activate descending spinal noradrenergic and cholinergic pathways. ⋯ These results support functional studies that indicate that systematically administered opioids cause spinal norepinephrine and acetylcholine release by a naloxone-sensitive mechanism. Idazoxan blockade of morphine's effects on cerebrospinal fluid norepinephrine was unexpected, and suggests that both norepinephrine and acetylcholine release in the spinal cord may be regulated by alpha 2-adrenoceptors. Microdialysis experiments suggest increased norepinephrine and acetylcholine levels in cerebrospinal fluid resulted from intravenous morphine-induced activation of bulbospinal pathways.
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Animal studies show that airway receptors responsible for eliciting respiratory protective reflexes are not uniformly distributed in the airways. Based on this information, it is possible that the protective reflex responses to airway irritation in humans may vary, depending on the site of stimulation. The purpose of this study is to examine whether the protective reflex responses evoked from the larynx are different from those evoked from the lower airways and to see how change in depth of anesthesia modifies the protective reflex responses evoked from individual sites. ⋯ The respiratory reflex responses evoked by injection of water vary, depending on the site of stimulation. The incidence of various reflex responses was not affected by the changing depth of anesthesia. The sensitivity to airway irritation seems to be greater at the larynx and trachea than at the more peripheral airways.