Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2002
Randomized Controlled Trial Multicenter Study Clinical TrialPreserved gastric tonometric variables in cardiac surgical patients administered intravenous perflubron emulsion.
Low gastric intramucosal pH (pHi) and an increased gastric-arterial PCO2 difference (CO2 gap) are markers of tissue hypoperfusion. Perfluorocarbons (PFCs) have a large oxygen-carrying capacity and release oxygen when encountering low tissue oxygen tension. Nine cardiac surgical patients instrumented for gastric tonometry were enrolled as part of a multicenter, randomized, single-blinded study of a PFC emulsion (perflubron emulsion [Oxygent]). Patients were randomized to receive PFC (n = 4) or placebo (n = 5) after intraoperative autologous blood harvesting by acute normovolemic hemodilution. At baseline there were no intergroup differences in tonometric-, hemodynamic-, or oxygen delivery-derived variables, e.g., Control group (pHi, 7.37 +/- 0.06; CO2 gap, 6.4 +/- 1.3 mm Hg) versus PFC group (pHi, 7.38 +/- 0.06; CO2 gap, 6.7 +/- 1.5 mm Hg). After acute normovolemic hemodilution, pHi was significantly lower (P < 0.01) in the Control group (7.22 +/- 0.25) than in the PFC group (7.44 +/- 0.25), and CO2 gap was significantly higher (P < 0.001) in the Control group (23.4 +/- 5.1 mm Hg) than in the PFC group (1.8 +/- 0.8 mm Hg). These differences in tonometric variables persisted during surgery. The PFC group showed a significantly (P < 0.007) shorter time to first bowel movement postoperatively (2.0 +/- 0.8 vs 5.4 +/- 1.6 days). Time to consumption of solid food was also shorter in the PFC group and almost achieved statistical significance (P = 0.056). ⋯ This study suggests that the administration of perflubron emulsion prevents gastrointestinal tract ischemia in cardiac surgical patients and may preserve postoperative gastrointestinal tract function.
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Anesthesia and analgesia · Apr 2002
Motor-evoked potential facilitation during progressive cortical suppression by propofol.
We characterized the effects of various stimulation patterns on motor-evoked potentials (MEPs) elicited by repetitive transcranial magnetoelectric stimulation at different levels of cortical suppression by propofol. In 20 patients undergoing lumbar disk surgery, propofol target plasma concentrations (PTPCs) were increased incrementally by target plasma-level controlled infusion during the induction of anesthesia. MEPs were recorded from the muscles of the upper extremities after single, double, and quadruple magnetoelectric stimulation at 500, 200, and 100 Hz. The mean PTPC during loss of responsiveness to verbal instructions (CP50) was 3 microg/mL (CP(95), 5 microg/mL). At PTPCs <3 microg/mL, maximal MEP amplitudes were elicited by quadruple stimulation at 100 Hz. At PTPCs > or =3 microg/mL, four pulses at 200 Hz yielded peak MEP amplitudes. Therefore, quadruple magnetoelectric stimulation at 100 Hz yields peak myogenic responses in awake patients. With progressive cortical suppression resulting from PTPCs beyond 3 microg/mL, the most effective stimulation frequency shifts to 200 Hz. This may be explained by a differential dose-dependent action of propofol on GABAergic cortical interneurons, corresponding to the clinically observed state of vigilance. Recording of spinal cord evoked potentials will aid in further elucidation of the modulatory effects of general anesthesia on intracortical facilitation. ⋯ We investigated the effect of different transcranial magnetoelectric stimulation paradigms on motor-evoked potentials during different levels of cortical suppression by propofol. The most effective stimulation frequency seems to change from 100 to 200 Hz during progressive propofol dose escalation, possibly because of specific interaction with cortical interneurons.
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Anesthesia and analgesia · Apr 2002
The role of mitochondrial and sarcolemmal K(ATP) channels in canine ethanol-induced preconditioning in vivo.
Chronic consumption of small doses of ethanol protects myocardium from ischemic injury. We tested the hypothesis that mitochondrial and sarcolemmal adenosine triphosphate-dependent potassium (K(ATP)) channels mediate these beneficial effects. Dogs (n = 76) were fed with ethanol (1.5 g/kg) or water mixed with dry food bid for 6 or 12 wk, fasted overnight before experimentation, and instrumented for measurement of hemodynamics. Dogs received intracoronary saline (vehicle), 5-hydroxydecanoate (a mitochondrial K(ATP) channel antagonist; 6.75 mg/kg over 45 min), or HMR-1098 (a sarcolemmal K(ATP) channel antagonist; 45 microg/kg over 45 min) and were subjected to a 60 min coronary artery occlusion followed by 3 h of reperfusion. A final group of dogs was pretreated with ethanol and chow for 6 wk before occlusion and reperfusion. Myocardial infarct size and transmural coronary collateral blood flow were measured with triphenyltetrazolium chloride staining and radioactive microspheres, respectively. The area at risk of infarction was similar between groups. A 12-wk pretreatment with ethanol significantly reduced infarct size to 13% +/- 2% (mean +/- SEM; n = 8) of the area at risk compared with control experiments (25% +/- 2%; n = 8), but a 6-wk pretreatment did not (21% +/- 2%; n = 8). 5-hydroxydecanoate and HMR-1098 abolished the protective effects of 12-wk ethanol pretreatment (24% +/- 2% and 29% +/- 3%, respectively; n = 8 for each group) but had no effect in dogs that did not receive ethanol (22% +/- 2% and 23% +/- 4%, respectively; n = 8 for each group). No differences in hemodynamics or transmural coronary collateral blood flow were observed between the groups. The results indicate that mitochondrial and sarcolemmal K(ATP) channels mediate ethanol-induced preconditioning in dogs independent of alterations in systemic hemodynamics or coronary collateral blood flow. ⋯ Mitochondrial and sarcolemmal K(ATP) channels mediate ethanol-induced preconditioning independent of alterations in systemic hemodynamics or coronary collateral perfusion in vivo.