Anesthesia and analgesia
-
Anesthesia and analgesia · Apr 2006
Case ReportsAccidental epidural administration of succinylcholine.
We report a case of accidental epidural of succinylcholine injection. A prolonged onset and a longer duration of neuromuscular blockade were observed compared with IV administration. No neurological or cardiovascular side effects or other symptoms of local or systemic toxicity were observed.
-
Anesthesia and analgesia · Apr 2006
Comparative StudyLocal anesthetic-induced protection against lipopolysaccharide-induced injury in endothelial cells: the role of mitochondrial adenosine triphosphate-sensitive potassium channels.
Lidocaine attenuates cell injury induced by ischemic-reperfusion and inflammation, although the protective mechanisms are not understood. We hypothesized that lidocaine and other amide local anesthetics protect against endothelial cell injury through activation of the mitochondrial adenosine triphosphate-sensitive potassium (mitoK(ATP)) channels. We determined the effects of amide local anesthetics (lidocaine, ropivacaine, and bupivacaine), ester local anesthetics (tetracaine and procaine), one amide analog (YWI), and two non-amide local anesthetic analogs (JDA and ICM) on viability of human microvascular endothelial cells after exposure to lipopolysaccharide (LPS) in the absence or presence of the mitoK(ATP) channel antagonist 5-hydroxydecaonate. ⋯ In conclusion, amide local anesthetics and the amide analog (YWI) attenuate LPS-induced cell injury, in part, through activation of mitoK(ATP) channels. In contrast, tetracaine and procaine had no protective effects and inhibited activation of mitoK(ATP) channels. The non-amide local anesthetic analogs induced protection but through mechanisms independent of mitoK(ATP) channels.
-
Anesthesia and analgesia · Apr 2006
Comparative StudyThe antiproliferative effect of lidocaine on human tongue cancer cells with inhibition of the activity of epidermal growth factor receptor.
Local anesthetics suppress proliferation in several cancer cells. The mechanism of the suppression, however, is unknown. Our previous study shows that lidocaine, at the level of tissue concentration under topical or local administration, has a direct inhibitory effect on the activity of epidermal growth factor receptor (EGFR), which is a potential target for antiproliferation in cancer cells. ⋯ A larger concentration of lidocaine (4000 microM) showed cytotoxicity with an antiproliferative effect. We suggest that the inhibition of EGF-stimulated EGFR activity is one of the mechanisms of the antiproliferative effect of lidocaine on CAL27 cells. Lidocaine administered topically within the oral cavity for cancer pain relief may suppress the proliferation of human tongue cancer cells.
-
Anesthesia and analgesia · Apr 2006
Comparative StudyAnesthetic requirements and stress hormone responses in spinal cord-injured patients undergoing surgery below the level of injury.
Neuraxial anesthesia decreases the minimum alveolar concentration. We determined the effects of spinal cord injury (SCI) on sevoflurane requirements and stress hormone response. Twenty-two chronic SCI patients undergoing surgery below the level of the injury were enrolled in the study, and 15 patients without cord injury served as control patients. ⋯ In the control group, plasma norepinephrine and cortisol concentrations were significantly increased during and 1 h after surgery compared with awake baseline values. In the SCI group, the sympathoadrenal and cortisol responses were virtually abolished. We conclude that SCI reduces the anesthetic requirement by 20%-39% during surgery below the level of injury, in association with blunted sympathoadrenal and cortisol responses.
-
Anesthesia and analgesia · Apr 2006
Comparative StudyEtomidate depresses lumbar dorsal horn neuronal responses to noxious thermal stimulation in rats.
Etomidate is a widely used IV anesthetic, but little is known about its analgesic properties, in particular, its effects on spinal cord neuronal responses to noxious stimuli. We hypothesized that etomidate would depress lumbar neuronal responses to noxious heat. Rats (n = 15) were anesthetized with isoflurane (1.2%) and laminectomy was performed to record single unit activity. ⋯ The responses quickly recovered, usually by the 10-min period postinjection. Similar responses were obtained in decerebrate, isoflurane-free rats administered etomidate and in isoflurane-anesthetized rats administered propofol. These data demonstrate that etomidate depresses spinal cord neuronal responses to noxious stimulation and is a possible mechanism by which this drug might produce analgesia.