Anesthesia and analgesia
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Anesthesia and analgesia · Dec 2002
Influence of rate and volume of infusion on the kinetics of 0.9% saline and 7.5% saline/6.0% dextran 70 in sheep.
We examined whether volume kinetic variables obtained during infusion of a short bolus of 0.9% saline (NS) or 7.5% saline/6.0% dextran 70 (HSD) predict the dilution-time curve resulting from a 20-min infusion of the same fluid. Each of six conscious, splenectomized sheep (mean body weight, 36 +/- 3 kg), on 4 different days, in a random order, received each of 4 IV boluses: NS at a rate of 1.2 mL. kg(-1). min(-1) over 5 min or 20 min or 4.0 mL/kg of HSD over 2 min or 20 min. One, 2, and 3-volume kinetic models were fitted to the dilution of the arterial hemoglobin concentration and the urinary excretion as sampled during 180 min. The maximum dilution of arterial plasma at the end of the 5-min and 20-min infusions of NS was approximately 10% and 22%, respectively, and after the 2-min and 20-min infusions of HSD, maximum dilution was 24% and 21%, respectively. The median absolute performance error was virtually identical when the mean variable estimates from the 5-min infusion of NS were used to predict the individual dilution-time curves of the 5-min (mean, 0.027 dilution units) and 20-min (mean, 0.027) infusions and when the 2-min infusion of HSD was used to predict the dilution during the individual 2-min (mean, 0.050) and 20-min infusions (mean, 0.047). Computer simulations indicated that the difference at the end of infusion between the volume effects of NS and HSD is larger after longer infusions. We concluded that the volume kinetic variables obtained during a short infusion can be used to predict the outcome of a longer one, even if the longer infusion also delivers a larger volume. ⋯ Kinetic analysis of a short infusion of 7.5% saline/6% dextran or 0.9% saline accurately predicts the effects of a longer infusion of the same volume (7.5% saline/6% dextran) or of a larger volume (0.9% saline).
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Anesthesia and analgesia · Dec 2002
Needle electrodes can be used for bispectral index monitoring of sedation in burn patients.
We present the results of a study examining the agreement of bispectral index values obtained using original sensor and subdermal needle electrodes in burn patients. Both types of electrodes can be used interchangeably to monitor depth of sedation.
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Anesthesia and analgesia · Dec 2002
The effects of intrathecal administration of an antagonist for prostaglandin E receptor subtype EP(1) on mechanical and thermal hyperalgesia in a rat model of postoperative pain.
Despite substantial advances in understanding acute pain mechanisms and in the treatment of pain, postoperative pain, especially mechanically evoked pain (incident pain), is generally not effectively treated. Tissue injury and inflammation increase the release of prostaglandin E(2) in the spinal cord, contributing to the development of hyperalgesia. We designed the present study to determine whether the intrathecal administration of an antagonist for prostaglandin E(2) receptor subtype EP(1), ONO-8711, has an analgesic effect on incision-induced mechanical and thermal hyperalgesia. A 1-cm longitudinal skin incision was made in the plantar aspect of the rat foot. The withdrawal threshold to mechanical stimulation and the withdrawal latency to thermal stimulation applied adjacent to the wound of the hindpaw were investigated. Both mechanical and thermal hyperalgesia were observed at 2 h and 24 h after the incision had been made. ONO-8711 (50, 80, 100 micro g) or saline was administered intrathecally. ONO-8711 significantly increased the withdrawal thresholds to mechanical stimulation, but not to thermal stimulation, in a dose- and time-dependent manner. We conclude that EP(1) receptor-mediated sensitization of the spinal dorsal horn may contribute to the generation of mechanical, but not thermal, hyperalgesia and that an EP(1) receptor antagonist administered intrathecally is a potential analgesic for postoperative pain, especially mechanically evoked pain (incident pain). ⋯ We examined the effects of an intrathecally administered selective EP(1) receptor antagonist on mechanical and thermal hyperalgesia in a postoperative pain model. The intrathecal EP(1) receptor antagonist inhibited the mechanical, but not thermal, hyperalgesia, indicating the potential for an EP(1) receptor antagonist to be used as an analgesic for postoperative pain, especially incident pain.
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Anesthesia and analgesia · Dec 2002
Acetylcholine receptors and thresholds for convulsions from flurothyl and 1,2-dichlorohexafluorocyclobutane.
There are acetylcholine receptors throughout the central nervous system, and they may mediate some forms and aspects of convulsive activity. Most high-affinity binding sites on nicotinic acetylcholine receptors for nicotine, cytisine, and epibatidine in the brain contain the beta2 subunit of the receptor. Transitional inhaled compounds (compounds less potent than predicted from their lipophilicity and the Meyer-Overton hypothesis) and nonimmobilizers (compounds that do not produce immobility despite a lipophilicity that suggests anesthetic qualities as predicted from the Meyer-Overton hypothesis) can produce convulsions. The nonimmobilizer flurothyl [di-(2,2,2,-trifluoroethyl)ether] blocks the action of gamma-aminobutyric acid on gamma-aminobutyric acid(A) receptors, whereas the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (2N, also called F6) does not. 2N can block the action of acetylcholine on nicotinic acetylcholine receptors. We examined the relative capacities of these compounds to cause convulsions in mice having and lacking the beta2 subunit of the acetylcholine receptor. The partial pressure causing convulsions in half the mice (the 50% effective concentration [EC(50)]) was the same as in control mice. For the knockout mice, the EC(50) for flurothyl was 0.00170 +/- 0.00030 atm (mean +/- SD), and for 2N, it was 0.0345 +/- 0.0041 atm. For the control mice, the respective values were 0.00172 +/- 0.00057 atm and 0.0341 +/- 0.0048 atm. The ratio of the 2N to flurothyl EC(50) values was 20.8 +/- 3.5 for the knockout mice and 21.7 +/- 7.0 for the control mice. These results do not support the notion that acetylcholine receptors are important mediators of the capacity of 2N or flurothyl to cause convulsions. However, we also found that both nonimmobilizers inhibit rat alpha4beta2 neuronal nicotinic acetylcholine receptors at EC(50) partial pressures (0.00091 atm and 0.062 atm for flurothyl and 2N, respectively) that approximate those that produce convulsions (0.0015 atm and 0.04 atm). ⋯ The results from the present study provide conflicting data concerning the notion that acetylcholine receptors mediate the capacity of nonimmobilizers to produce convulsions.