Anesthesia and analgesia
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Anesthesia and analgesia · Oct 2003
The acute myotoxic effects of bupivacaine and ropivacaine after continuous peripheral nerve blockades.
Bupivacaine causes muscle damage. However, the myotoxic potency of ropivacaine is still unexplored. Therefore, we performed this study to compare the effects of bupivacaine and ropivacaine on skeletal muscle tissue in equipotent concentrations. Femoral nerve catheters were inserted into anesthetized minipigs, and 20 mL of either bupivacaine (5 mg/mL) or ropivacaine (7.5 mg/mL) was injected. Subsequently, bupivacaine (2.5 mg/mL) and ropivacaine (3.75 mg/mL) were continuously infused over 6 h. Control animals were treated with corresponding volumes of normal saline. Finally, muscle samples were dissected at injection sites. After processing and staining, histological patterns of muscle damage were blindly examined, scored (0 = no damage to 3 = myonecrosis), and statistically analyzed. After normal saline, only interstitial edema was found. Bupivacaine treatment caused severe tissue damage (score, 2.3 +/- 0.7), whereas ropivacaine induced fiber injury of a significantly smaller extent (score, 1.3 +/- 0.8). Furthermore, bupivacaine, but not ropivacaine, induced apoptosis in muscle fibers. In summary, both drugs induce muscle damage with similar histological patterns. Compared with bupivacaine, which induces both necrosis and apoptosis, the tissue damage caused by ropivacaine is significantly less severe. We conclude that ropivacaine's myotoxic potential is more moderate in comparison with that of bupivacaine. ⋯ After continuous peripheral nerve blockades, the long-acting local anesthetics bupivacaine and ropivacaine both induce fiber necrosis in porcine skeletal muscle tissue. In comparison with ropivacaine, bupivacaine causes tissue damage of a significantly larger extent and additionally induces apoptosis in skeletal muscle cells.
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Anesthesia and analgesia · Oct 2003
Behavioral monitoring and urine toxicology testing in patients receiving long-term opioid therapy.
No study has examined the role of urine toxicology in addition to behavioral monitoring in patients receiving opioid therapy for chronic pain. All patients maintained on chronic opioid therapy by the two senior authors at two university pain management centers were monitored for 3 yr with urine toxicology testing and for behaviors suggestive of inappropriate medication use. We retrospectively extracted demographic information, aberrant drug-taking behaviors, and urine toxicology information from the medical record. For 122 patients maintained on chronic opioid therapy, 43% (n = 53) had a "problem" (either positive urine toxicology or one or more aberrant drug-taking behaviors). Of patients with no behavioral issues, 21% (n = 26) had a positive urine screen for either an illicit drug or a nonprescribed controlled medication. Of patients with a negative urine screen, 14% (n = 17) had one or more behavioral issues. Monitoring both urine toxicology and behavioral issues captured more patients with inappropriate drug-taking behavior than either alone. Requiring a report of behavioral issues and urine toxicology screens for patients receiving chronic opioids creates a more comprehensive monitoring system than either alone. ⋯ Monitoring both urine toxicology and aberrant behavior in chronic-pain patients treated with opioids identified more problem patients than by monitoring either alone. The authors recommend routine urine testing on all patients prescribed opioids for noncancer pain and as a required element in all opioid analgesic studies.
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Anesthesia and analgesia · Oct 2003
The effect of sevoflurane and propofol on cerebral neurotransmitter concentrations during cerebral ischemia in rats.
Sevoflurane and propofol are neuroprotective possibly by attenuating central or peripheral catecholamines. We evaluated the effect of these anesthetics on circulating catecholamines and brain neurotransmitters during ischemia in rats. Forty male Sprague-Dawley rats were randomly assigned to one of the following treatment groups: fentanyl and N(2)O/O(2) (control), 2.0% sevoflurane, 0.8-1.2 mg x kg(-1) x min(-1) of propofol, and sham-operated rats with fentanyl and N(2)O/O(2). Ischemia (30 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension to a mean arterial blood pressure of 32 +/- 2 mm Hg. Pericranial temperature, arterial blood gases, and pH value were maintained constant. Cerebral catecholamine and glutamate concentrations, sampled by microdialysis, and plasma catecholamine concentrations were analyzed using high-pressure liquid chromatography. During ischemia, circulating catecholamines were almost completely suppressed by propofol but only modestly decreased with sevoflurane. Sevoflurane and propofol suppressed brain norepinephrine concentration increases by 75% and 58%, respectively, compared with controls. Intra-ischemia cerebral glutamate concentration was decreased by 60% with both sevoflurane and propofol. These results question a role of circulating catecholamines as a common mechanism for cerebral protection during sevoflurane and propofol. A role of brain tissue catecholamines in mediating ischemic injury is consistent with our results. ⋯ During incomplete cerebral ischemia, the neuroprotective anesthetics sevoflurane and propofol suppressed cerebral increases in norepinephrine and glutamate concentrations. In contrast, propofol, but not sevoflurane, suppressed the ischemia-induced increase in circulating catecholamines to baseline levels. The results question a role for plasma catecholamines in cerebral ischemic injury.
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Anesthesia and analgesia · Oct 2003
Comment Letter Comparative StudyComparing the ProSeal laryngeal mask airway with the laryngeal tube airway.