Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2004
Amiodarone decreases heat, cold, and mechanical hyperalgesia in a rat model of neuropathic pain.
Lidocaine is effective in controlling ventricular dysrhythmia and neuropathic pain. Amiodarone, like lidocaine, has sodium channel blocking properties. In the present study we explore whether amiodarone has a similar effect as lidocaine on the heat, cold, and mechanical hyperalgesia seen in the rat model of neuropathic pain. Ten male Sprague-Dawley rats were anesthetized. Four loose ligatures were placed on the sciatic nerve of the right hindpaw. A sham operation was performed on the contralateral hindpaw (control). Heat hyperalgesia was determined by comparing each paw withdrawal latency to heat stimulation (radiant heat source, 50 degrees C). Cold hyperalgesia was assessed with acetone application. Mechanical hyperalgesia was determined by comparing the mechanical threshold in the ligated and control hind paws using calibrated von Frey filaments. Amiodarone was intraperitoneally administered at doses of 1, 5, 10, 20, 50, and 100 mg/kg after the development of hyperalgesia. The animals were tested for hyperalgesia before and 1, 3, and 24 h after the administration of a single dose of amiodarone. Intrathecal catheters were implanted in 5 new rats, and amiodarone 5 mg/kg was injected. Testing for heat, mechanical, and cold hyperalgesia was performed similarly in the intrathecal amiodarone administration group. Amiodarone produces statistically significant decreases of heat, cold, and mechanical hyperalgesia after intraperitoneal administration. Results are statistically significant at 10 mg/kg (heat hyperalgesia), 20 mg/kg (mechanical hyperalgesia), and 100 mg/kg (cold hyperalgesia) intraperitoneally. Hyperalgesia returns 24 h after a dose. The intrathecal administration of amiodarone produces a nonstatistically significant reduction of hyperalgesia. Amiodarone seems to have a similar effect as lidocaine on the hyperalgesia seen in the rat model of neuropathic pain. As the half-life of amiodarone is significantly longer that that of lidocaine (mean, 53 days versus 90 min) in humans, it may have the potential to provide a longer lasting (and perhaps more effective) effect than lidocaine on neuropathic pain states. ⋯ Amiodarone was found to produce a statistically significant decrease in heat, cold, and mechanical hyperalgesia in a rat model of neuropathic pain after intraperitoneal injection. Considering its long half-life in humans, amiodarone has the potential to provide long lasting pain relief in neuropathic pain states.
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Anesthesia and analgesia · Jan 2004
Clinical TrialCorrelation of bispectral index and Guedel's stages of ether anesthesia.
Bispectral index (BIS) analysis is a method of electroencephalograph (EEG) analysis based on the interfrequency phase relationships of the EEG, designed to quantify anesthetic hypnosis. The BIS was created after concurrent collection of EEG and clinical data from a large number of patients anesthetized with various drugs over a prolonged period and then performing a Fourier analysis followed by a bispectral calculation. The clinical stages of anesthetic depth are very well demonstrated in etherized patients. In this study, we studied the BIS changes during various stages of ether anesthesia and quantified the hypnotic depth during the surgical stage of ether anesthesia. The values for BIS under various stages and planes of ether anesthesia were recorded in 21 patients listed for short surgical procedures. During diethyl ether anesthesia, BIS initially increased and subsequently decreased. During surgical anesthesia, a BIS value of 30 was observed. ⋯ For the first time, bispectral index (BIS) has been studied in patients being anesthetized solely with ether. Ether both causes an increase and decrease in BIS during induction and emergence. The index observed during the surgical stage of ether anesthesia is probably the correct value for the depth of hypnosis because no other volatile anesthetic can produce the true anesthetic state when used alone. This value could be taken as the value to be attained when balanced anesthesia is being practiced.
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Anesthesia and analgesia · Jan 2004
Alaris AEP monitor's "Click Detection" does not help to detect inadvertent disconnection of headphones during anesthesia.
Auditory evoked potentials (AEP) can be suppressed by anesthetics dose dependently, but may fail to be registered because of the absence of adequate auditory stimuli. The Alaris AEP monitor includes the "Click Detection" (CD) (generating the message "NO AEP" or "LOW AEP") to detect the loss of auditory stimuli. We investigated the accuracy of the CD in 17 patients awake (AWAKE) and during anesthesia (ANESTHESIA) with accurately placed headphones (HP) and after disconnected HP (No HP) over 5 min each, respectively. Alaris AEP ARX index, CD, and Bispectral Index were recorded each minute. Changes were evaluated with the Friedman and Wilcoxon test. Sensitivity (SEN) and specificity (SPE) and receiver operating characteristic curve were analyzed for the accuracy of the CD. During AWAKE after disconnection of the HP, Alaris AEP ARX index decreased significantly (P < 0.05). The CD was able to detect No HP after 2 min with a SEN of 88% and a SPE of 97%. During ANESTHESIA, no changes were found after HP disconnection. CD detected No HP with a SEN of 100% and a SPE of 20%. The CD of the Alaris AEP monitor is not able to detect unnoticed disconnection of HP during ANESTHESIA. ⋯ Signal transmission of auditory evoked potentials can be suppressed by anesthetics, but also by disconnection of headphones. In the present study, we demonstrate that even the Alaris AEP monitor with the very new feature "Click Detection" was not able to detect the loss of headphones during general anesthesia with propofol and remifentanil.
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Anesthesia and analgesia · Jan 2004
Reduction in [D-Ala2, NMePhe4, Gly-ol5]enkephalin-induced peripheral antinociception in diabetic rats: the role of the L-arginine/nitric oxide/cyclic guanosine monophosphate pathway.
To test our hypothesis that the abnormally small efficacy of mu-opioid agonists in diabetic rats may be due to functional changes in the L-arginine/nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) pathway, we evaluated the effects of N-iminoethyl-L-ornithine, methylene blue, and 3-morpholino-sydnonimine on [D-Ala(2), NMePhe(4), Gly-ol(5)]enkephalin (DAMGO)-induced antinociception in both streptozotocin (STZ)-diabetic and nondiabetic rats. Animals were rendered diabetic by an injection of STZ (60 mg/kg intraperitoneally). Antinociception was evaluated by the formalin test. The mu-opioid receptor agonist DAMGO (1 microg per paw) suppressed the agitation response in the second phase. The antinociceptive effect of DAMGO in STZ-diabetic rats was significantly less than in nondiabetic rats. N-Iminoethyl-L-ornithine (100 microg per paw), an NO synthase inhibitor, or methylene blue (500 microg per paw), a guanylyl cyclase inhibitor, significantly decreased DAMGO-induced antinociception in both diabetic and nondiabetic rats. Furthermore, 3-morpholino-sydnonimine (200 microg per paw), an NO donor, enhanced the antinociceptive effect of DAMGO in nondiabetic rats but did not change in diabetic rats. These results suggest that the peripheral antinociceptive effect of DAMGO may result from activation of the L-arginine/NO/cGMP pathway and dysfunction of this pathway; also, events that are followed by cGMP activation may have contributed to the demonstrated poor antinociceptive response of diabetic rats to mu-opioid agonists. ⋯ This is the first study on the role of the nitric oxide (NO)/cyclic guanosine monophosphate pathway on [D-Ala(2), NMePhe(4), Gly-ol(5)]enkephalin (DAMGO)-induced peripheral antinociception and the effect of diabetes on this pathway. The study suggests a possible role of DAMGO as a peripherally-acting analgesic drug.
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Anesthesia and analgesia · Jan 2004
Comment Letter Comparative StudyComparison between level 1 and rapid infusion system.