Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2002
The feasibility of transesophageal echocardiograph-guided right and left ventricular oximetry in hemodynamically stable patients undergoing coronary artery bypass grafting.
There are no techniques available for continuous noninvasive measurement of the oxygen saturation of blood flowing through the heart. We assessed the feasibility and accuracy of transesophageal echocardiograph (TEE)-guided left ventricular (SpO2 LV) and right ventricular (SpO2 RV) oximetry. Twenty hemodynamically stable, well-oxygenated anesthetized patients (ASA physical status III, aged 51-75 yr) undergoing coronary artery bypass grafting were studied. A TEE probe was modified by attaching a single-use pediatric reflectance pulse oximeter just proximal to the ultrasound transducer. The TEE probe was directed toward the LV by using the transgastric mid-short axis view or toward the RV by using the transgastric RV inflow view, in random order. Readings were taken every 30 s for 10 min during a hemodynamically stable period of anesthesia. Simultaneous blood samples were taken from the radial artery and pulmonary artery to determine arterial oxygen saturation (SaO2) and mixed venous oxygen saturation (SvO2), respectively. During SpO2 LV readings, simultaneous finger pulse oximetry (SpO2 finger) was also recorded. SpO2 LV was feasible in 20 of 20 patients, and SpO2 RV was feasible in 19 of 20 patients. The mean +/- SD (range) oxygen saturation for each method was the following: SpO2 LV, 98.7% +/- 0.6% (97%-100%); SaO2, 98.7% +/- 0.6% (96.6%-99.4%); SpO2 finger, 98.1% +/- 1.2% (97%-100%); SpO2 RV, 73.9% +/- 4.7% (64%-85%); and SvO2, 74.5% +/- 4.4% (66.8%-82.6%). SpO2 LV agreed closely with SaO2 (mean difference, 0.072%). SpO2 RV agreed closely with SvO2 (mean difference, 0.65%). SpO2 LV agreed more closely with SaO2 than finger oximetry (mean difference, -0.072 vs -0.692). TEE-guided SpO2 LV and SpO2 RV are feasible in hemodynamically stable anesthetized patients and provide similar readings to arterial and mixed venous blood samples. The technique merits further investigation. ⋯ Transesophageal echocardiograph-guided left and right ventricular oximetry is feasible in hemodynamically stable anesthetized patients and provides similar readings to arterial and mixed venous blood samples.
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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.