Anesthesia and analgesia
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Anesthesia and analgesia · Dec 2003
Propofol suppresses the cortical somatosensory evoked potential in rats.
The dose-response curve for the effect of volatile anesthetics on the somatosensory evoked potential (SEP) is well described, but for propofol, the large dose segment of the curve is undefined. We describe the effect of increasing plasma concentrations of propofol on cortical SEPs in 18 rats. After surgical preparation under ketamine anesthesia, a remifentanil infusion was begun at 2.5, 5, or 10 microg x kg(-1) x min(-1). After 20 min, the propofol infusion was initiated at 20 mg x kg(-1) x h(-1) and was increased to 40, 60, and 80 mg x kg(-1) x h(-1) at 20-min intervals. SEP was recorded before remifentanil infusion, before propofol infusion rate changes, and 30 min after discontinuing propofol infusion. In six additional rats, the plasma concentrations of propofol after each 20-min infusion were measured using gas chromatography. Remifentanil did not have a significant effect, but propofol significantly depressed the SEP amplitude and prolonged the latency at infusion rates of 40 mg x kg(-1) x h(-1) and more. Propofol's effect was dose-dependent, but even at 80 mg x kg(-1) x h(-1) with an estimated plasma concentration of 31.6 +/- 3.4 microg/mL (10.8 50% effective concentration), a measurable response was present in 44.5% of rats. These results suggest that even at large doses, propofol and remifentanil provide adequate conditions for SEP monitoring. ⋯ Rats demonstrate dose-dependent somatosensory evoked potential (SEP) suppression with propofol but not with remifentanil. However, SEP suppression by 50% occurred only at large (1.5 EC(50)) concentrations of propofol, and a measurable SEP was present in 8 of 18 rats, even at 10.8 EC(50).
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Anesthesia and analgesia · Dec 2003
Clinical TrialMonitoring renal oxygen supply in critically-ill patients using urinary oxygen tension.
Critically-ill patients are at risk of developing renal disorders as a consequence of systemic hypoperfusion. Ischemic acute tubular necrosis and resulting acute renal failure are caused by hypotension or therapeutic management. In this study, we tested the change of O(2) availability induced by fenoldopam mesylate using the continuous measurement of urinary oxygen tension (PuO(2)), a relatively noninvasive technique that could provide potentially important real-time data regarding renal oxygenation in intensive care unit patients. Fenoldopam was administered at different doses (0.03, 0.06, and 0.09 microg x kg(-1) x min(-1)) to 50 stable critically-ill patients. Urine output was collected every hour to assess volume and urinary electrolytes. Heart rate, mean arterial blood pressure, cardiac output, pulmonary artery occlusion pressure, arterial oxygen delivery index, and oxygen consumption index were analyzed after fenoldopam dose modifications and at infusion end. PaO(2) and PuO(2) continuous measurements were obtained through two sensors inserted in the radial artery and in the bladder. After a fenoldopam dose increase, PuO(2) significantly increased (P < 0.05), whereas PaO(2) remained unchanged. During the study, heart rate, mean arterial blood pressure, cardiac output, central venous pressure, pulmonary artery occlusion pressure, arterial oxygen delivery index, and oxygen consumption remained unchanged. Dose-dependent PuO(2) increases, unrelated to indexes of systemic perfusion and cardiac function, demonstrate that fenoldopam affects the balance between renal oxygen supply and demand in stable critically-ill patients. ⋯ Acute renal failure in critically-ill patients is associated with frequent mortality. Prolonged renal hypoperfusion cannot be detected by current systemic hemodynamic indexes. Using continuous measurement of urinary oxygen tension, which could indirectly provide real-time data regarding renal oxygenation, our study showed that fenoldopam increases the ratio between oxygen supply and demand.
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Anesthesia and analgesia · Dec 2003
The effects of thoracic epidural anesthesia on hepatic perfusion and oxygenation in healthy pigs during general anesthesia and surgical stress.
Perioperative liver injury due to decreased perfusion may be an underlying mechanism behind the development of systemic inflammatory response syndrome. We designed this animal study to assess whether thoracic epidural anesthesia (TEA) impairs liver oxygenation due to induced hypotension. After ethical approval, 19 anesthetized and acutely instrumented pigs were randomly assigned to 3 groups (control and TEA alone versus TEA plus volume loading). ⋯ Volume loading before TEA did not relevantly affect total hepatic blood flow; it even decreased oxygen supply to the liver by hemodilution. We conclude that, despite decreased mean arterial blood pressure, TEA did not affect liver oxygenation. There was no clinically relevant effect of volume loading on total hepatic perfusion.