Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2003
Preconditioning with isoflurane produces dose-dependent neuroprotection via activation of adenosine triphosphate-regulated potassium channels after focal cerebral ischemia in rats.
In this study, we determined whether repeated brief isoflurane (Iso) anesthesia induces ischemic tolerance to focal cerebral ischemia in a dose-response manner and whether the effect is dependent on adenosine triphosphate-regulated potassium channels. In Experiment 1, 40 rats were randomly assigned to 4 groups: control animals received 100% oxygen 1 h/d for 5 days, whereas the isoflurane (Iso)1, Iso2, and Iso3 groups received 0.75%, 1.5%, or 2.25% Iso in oxygen 1 h/d for 5 days. In Experiment 2, 36 rats were randomly assigned to 4 groups: controls received 100% oxygen 1 h/d for 5 days; animals in the Iso and I+G (Iso+glibenclamide) groups received 2% Iso in oxygen 1 h/d for 5 days, and the I+G group received glibenclamide (GLB) (5 mg/kg intraperitoneally) before each Iso pretreatment. Animals in the GLB group received GLB (5 mg/kg intraperitoneally) once a day for 5 days. Twenty-four hours after the last pretreatment, the right middle cerebral artery was occluded for 120 min. Neurologic deficit scores (NDS) and brain infarct volumes were evaluated at 24 h. The NDS and infarct volumes of Iso2 and Iso3 were less than those of the controls (P < 0.05). The infarct volume in Iso3 was smaller than in Iso2 (P < 0.05). The NDS and infarct volume in the Iso group were less than in the control and I+G groups (P < 0.05). There was no statistical difference among the control, I+G, and GLB groups. The study demonstrated that repeated Iso anesthesia induces ischemic tolerance in rats in a dose-response manner. GLB, an adenosine triphosphate-regulated potassium channel blocker, abolished the tolerance induced by Iso. ⋯ Brief isoflurane anesthesia induces ischemic tolerance in the brain. The effect was found to be dose dependent in a rat focal cerebral ischemia model. Ischemic tolerance induced by isoflurane preconditioning is dependent on activation of adenosine triphosphate-regulated potassium channels.
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Anesthesia and analgesia · Jan 2003
Case ReportsDelayed onset of malignant hyperthermia in desflurane anesthesia.
Animal-experimental studies demonstrate desflurane's trigger effect for malignant hyperthermia (MH). In contrast to other anesthetics, the time interval from exposure to the occurrence of symptoms is much longer with desflurane. This case report focuses on MH induced by desflurane alone.
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Anesthesia and analgesia · Jan 2003
Case ReportsHemodynamic response to caudal epidural clonidine in a pediatric cardiac patient.
Postoperative management of sedation and analgesia in pediatric cardiac patients presents many challenges. This case report describes a child who experienced dramatic clinical improvement with the postoperative use of caudal morphine and clonidine after conventional therapy had failed.
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Anesthesia and analgesia · Jan 2003
Validity of arterial and mixed venous oxygen saturation measurements in a canine hemorrhage model after resuscitation with varying concentrations of hemoglobin-based oxygen carrier.
In this study, we evaluated the validity of saturation measurements in mixed venous and arterial blood during posthemorrhagic anemia and resuscitation with varying levels of hemoglobin-based oxygen carrier (Hemoglobin glutamer-200 [bovine]; Oxyglobin [Hb-200]). Nineteen anesthetized, splenectomized, mixed-breed dogs were anesthetized (two were excluded from the data because they did not survive the exsanguination, supporting the validity of the model). Their pulmonary arteries were cannulated with the Abbott QVUE Oximetrix 3 catheter. An 18-gauge catheter was placed in the femoral artery, and a reusable Nellcor probe was applied to the tongue. Mixed venous and arterial samples were drawn at baseline, after 40% hemorrhage (to keep arterial pressure at 50 mm Hg), and postresuscitation with 30 mL/kg of 6% hetastarch in lactated Ringer's solution (n = 4), 10 mL/kg of Hb-200, 20 mL/kg of hetastarch (n = 6), 20 mL/kg of Hb-200, and 10 mL/kg of hetastarch (n = 7). Samples were compared with oxygen content from the LEXO2CON-K oxygen analyzer, and oxygen content was calculated for all values from the monitors. Results were compared by using analysis of variance. There was good correlation (0.97 > or = r > or = 0.92) for the measured versus calculated hemoglobin oxygen saturation values at baseline. After resuscitation, the correlation between calculated and measured values of oxygen content was significantly smaller for all tested instruments. The values of oxygen content calculated from the oxygen saturation monitor and from the oximetric pulmonary artery can deviate by as much as 20% from directly measured values. We conclude that the administration of this oxygen therapeutic may interfere with the values of some monitors. ⋯ This study evaluated oxygen saturation monitors in a canine model of acute blood loss and resuscitation with a blood substitute and found that these may interfere with the monitors' results in a dose-dependent way.
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Anesthesia and analgesia · Jan 2003
Comparative StudyCatheter-associated masses in patients receiving intrathecal analgesic therapy.
A cohort of seven patients receiving intrathecal analgesic drug therapy for chronic intractable pain underwent radiocontrast myelography and computed tomography (CT) scanning to screen for catheter-associated intrathecal masses. Three of seven patients examined had intraspinal masses associated with the tip of the drug infusion catheter after a total of 118 mo of therapy. The index case presented with exacerbation of neuropathic pain and paralysis of the left lower extremity. The two additional cases detected by CT myelography were asymptomatic at the time the catheter-associated mass was assessed. The mean duration of therapy before diagnosis of the catheter-associated mass was 19.6 mo, with a range of 16-25 mo. An intergroup comparison of demographic and treatment variables between patients, with and without catheter-associated masses, demonstrated that patients with masses were younger and were receiving a larger morphine dose than patients without masses. The differences were statistically significant (P = 0.05). In one patient with an asymptomatic catheter-associated intrathecal mass, regression of the mass was observed after cessation of therapy. In a second asymptomatic patient, the mass remained stable over 1 yr of continued treatment after substitution of hydromorphone for morphine without interruption of therapy. Neither asymptomatic patient has subsequently developed additional neurologic findings or injury after detection of occult catheter-associated intrathecal masses and clinical intervention. We suggest that all patients receiving long-term intrathecal analgesia should undergo periodic radiographic surveillance to further define their risk of developing occult catheter-associated masses and to allow intervention before neurologic injury can develop. ⋯ Catheter-associated intrathecal masses were detected in three of seven patients receiving long-term intrathecal analgesia. In the two asymptomatic patients, timely clinical intervention was associated with the avoidance of subsequent neurologic injury and spontaneous resolution of one of the occult masses.