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
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
Review Meta AnalysisInhaled nitric oxide for acute hypoxic respiratory failure in children and adults: a meta-analysis.
We systematically reviewed randomized controlled trials examining inhaled nitric oxide (INO) for the treatment of acute respiratory distress syndrome or acute lung injury in children and adults. Qualitative assessments of identified trials were made, and metaanalyses were performed according to Cochrane methodology. Five randomized controlled trials (n = 535) met entry criteria. ⋯ Other clinical indicators of effectiveness, such as duration of hospital and intensive care stay, were inconsistently reported. Lack of data prevented assessment of all outcomes. If further trials assessing INO in acute respiratory distress syndrome or acute lung injury are to proceed, they should be stratified for primary etiology, incorporate other modalities that may affect outcome, and evaluate clinically relevant outcomes before any benefit of INO can be excluded.
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Anesthesia and analgesia · Oct 2003
Randomized Controlled Trial Clinical TrialContinuous wound infiltration with ropivacaine reduces pain and analgesic requirement after shoulder surgery.
After achieving a reduction of pain scores for 10 h with a single dose wound infiltration after shoulder surgery, we examined in a prospective, placebo-controlled and double-blinded study the analgesic effects of continuous wound infiltration with different concentrations of ropivacaine. Forty-five patients undergoing shoulder surgery were randomly assigned into three groups to receive single dose wound infiltration with 30 mL saline (group S) or ropivacaine 7.5 mg/mL (groups R2 and R3.75) after skin closure. Postoperatively, patients received a continuous wound infiltration with saline (group S), ropivacaine 2 mg/mL (group R2) or ropivacaine 3.75 mg/mL (group R3.75) for 48 h. Supplemental pain relief was provided by IV patient-controlled analgesia with the opioid piritramide. At 1, 2, 3, 4, 24, and 48 h postoperatively visual analogue scale (VAS) values (0-100 mm), piritramide requirements and side effects were registered. Plasma levels of ropivacaine were measured preoperatively and at 24 h and 48 h after surgery. Until 48 h VAS values were smaller in group R3.75 compared with group S (group R3.75, 8 +/- 9 mm; group S, 31 +/- 14 mm; P < 0.005), whereas 4 h and 48 h postoperatively VAS values were even smaller in group R3.75 compared with group R2 (P < 0.05). Cumulative piritramide consumption was always smaller in groups R2 and R3.75 compared with group S (1-24 h, P < 0.005; 48 h, P < 0.05). Plasma ropivacaine levels remained less than the toxic threshold. We conclude that continuous postoperative wound infiltration with ropivacaine, especially using 3.75 mg/mL, provides smaller VAS values and opioid requirement in comparison with saline after shoulder surgery. ⋯ The continuous postoperative wound infiltration after shoulder surgery with different concentrations of ropivacaine, 2 mg/mL and 3.75 mg/mL, results in lower pain scores and opioid requirement compared with infiltration with placebo. Plasma levels of ropivacaine remained less than the toxic threshold.