Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2004
Randomized Controlled Trial Clinical TrialThe influence of ambulation time on the incidence of transient neurologic symptoms after lidocaine spinal anesthesia.
The cause of transient neurologic symptoms (TNSs) after lidocaine spinal anesthesia remains unclear. It has been proposed that early ambulation after spinal anesthesia contributes to the development of TNSs. We evaluated the influence of ambulation time on the occurrence of TNSs after spinal anesthesia with 50 mg of 2% plain lidocaine for knee arthroscopy. One-hundred-twenty patients undergoing knee arthroscopy (ASA physical status 1-2) were randomized into 3 groups, i.e., early (Group E), 6-h (Group 6-h), or late ambulation (Group L) groups. In Group E, ambulation was allowed as early as possible after regression of spinal block (on average 229 +/- 21 min; range, 135-247 min). In Group 6-h, the patients remained in bed for approximately 6 h after the block and in Group L until the next morning. The patient groups were comparable with respect to demographic, anesthetic, and surgical variables. The overall incidence of TNSs was 16%. TNSs occurred in 3 patients of Group E (7.5%), in 11 patients of Group 6-h (28%), and in 5 patients of Group L (13%). No significant differences were detected between the patients with and without TNSs. Early ambulation was not found to be a risk factor for TNSs after spinal anesthesia with 50 mg of 2% lidocaine. ⋯ This study shows that early ambulation time does not increase the incidence of transient neurologic symptoms after spinal anesthesia with 50 mg of 2% lidocaine for elective knee arthroscopy.
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Anesthesia and analgesia · Mar 2004
Intracellular calcium increases in growth cones exposed to tetracaine.
Neurotoxicity of local anesthetics has been reported for both matured and growing neurons. In the present study, we examined if tetracaine increases Ca(2+) concentration during growth cone collapse. Intracellular Ca(2+) concentration was measured by fura 2/AM after exposure to tetracaine. Tetracaine (1-2 mM) induced increases in intra-growth cone Ca(2+) concentration (P < 0.01). The Ca(2+) hot spot was expanded into the neurite from the periphery towards the cell body. When tetracaine was applied to growth cones in Ca(2+) free media, the increase was minor. However, tetracaine induced growth cone collapse even in the culture media, which did not contain Ca(2+). Ni(2+) (100 microM; a general Ca(2+) channel inhibitor) and BAPTA-AM (5 microM; intracellular Ca(2+) chelator) could not inhibit growth cone collapse induced by 1-2 mM tetracaine. Tetracaine (>1 mM) induces collapse and Ca(2+) increase at growth cones simultaneously; however, these two phenomena might be provoked independently. ⋯ Tetracaine induced intracellular Ca(2+) increases and growth cone collapse in dorsal root ganglion neurons. The Ca(2+) hot spot in the growth cone expanded into the neurite from periphery towards the cell body.
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Anesthesia and analgesia · Mar 2004
Clinical TrialContinuous parasacral sciatic block: a radiographic study.
Parasacral sciatic blockade results in anesthesia of the entire sacral plexus. In this study we sought to determine the spread of the local anesthetic injected through a parasacral catheter, the anatomical location of the inserted catheters, and the extent and reliability of the blockade. In this study, 87 consecutive patients undergoing major lower limb surgery were enrolled. After placement of the catheter and injection of 8 mL of radio-opaque contrast dye, radiographic images were evaluated for dispersion of the injectate. Sensory and motor evaluations were also performed. Radiographic analysis of the injectates revealed that nearly all catheters (86 catheters, 99%) were in the correct anatomical position. The mean volume of local anesthetic injection was 21 +/- 3 mL. All patients developed a full sensory block of all three major components of the sciatic plexus (tibial, common peroneal, and posterior cutaneous nerve of the thigh). We conclude that the parasacral sciatic block results in frequent success of blockade of all three major components of the sciatic plexus and it has a small risk of complications. Contrast radiography can be used to document the catheter placement. ⋯ The parasacral sciatic block results in a frequent success rate of blockade of all three major components of the sciatic plexus (tibial, common peroneal, and cutaneous nerve of thigh). A contrast radiography can be used to confirm the proper position of the catheter.
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Anesthesia and analgesia · Mar 2004
Amplification by hyperoxia of coronary vasodilation induced by propofol.
We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10-300 microM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (PaO(2) = 137 +/- 16 mm Hg, n = 12) or in the presence (PaO(2) = 541 +/- 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (-13% +/- 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 microM) and cromakalim (0.5 microM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (-16% +/- 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 micro M both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia. ⋯ Propofol induced a coronary vasodilation that was amplified in the presence of hyperoxia. This phenomenon does not seem to be related to previous coronary vasoconstriction. The myocardial effects of propofol were not significantly modified in the presence of hyperoxia.
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Anesthesia and analgesia · Mar 2004
Vasodilation increases the threshold for bupivacaine-induced convulsions in rats.
Bupivacaine affects the vascular resistance by peripheral and central nervous system (CNS) mechanisms. As vasoconstrictors increase the CNS toxicity of IV bupivacaine, vasodilators may decrease its CNS toxicity. We examined the hypothesis that vasodilators decrease the CNS toxicity of bupivacaine in awake, spontaneously breathing rats. Male Sprague-Dawley rats were randomly divided into control (C), nicardipine (N), and phentolamine (P) groups (n = 12 in each group). Racemic bupivacaine was administered IV at 1 mg/kg/min until tonic/clonic convulsions occurred. Saline, nicardipine (0.4 microg/min), and phentolamine (10 microg/min within 5 min, 50 microg/min thereafter) were simultaneously administered with bupivacaine in groups C, N, and P, respectively. Mean arterial blood pressure was significantly increased by infusion of bupivacaine in group C and was maintained at baseline levels before the onset of convulsions in groups N and P. The convulsive dose of bupivacaine in group C was 5.8 +/- 1.5 mg/kg, but was significantly larger in groups N and P (7.6 +/- 1.5 and 8.1 +/- 1.1 mg/kg, P = 0.02 and 0.001, respectively). However, there were no differences in total or protein-unbound plasma concentration of bupivacaine or in concentration of bupivacaine in the brain at the onset of convulsions among the 3 groups. We conclude that nicardipine and phentolamine increase the cumulative dose but do not affect the threshold plasma or brain concentrations required for bupivacaine-induced convulsions. ⋯ Bupivacaine, a long-acting local anesthetic, induces central nervous system toxicity when its plasma concentration is increased. Nicardipine and phentolamine increased the cumulative dose but did not affect the threshold plasma concentrations, required for bupivacaine-induced convulsions, suggesting that both nicardipine and phentolamine inhibited the increase in the plasma concentration of bupivacaine by inducing peripheral vasodilation.