Anesthesiology
-
Comparative Study Clinical Trial
Amniotic fluid removal during cell salvage in the cesarean section patient.
Cell salvage has been used in obstetrics to a limited degree because of a fear of amniotic fluid embolism. In this study, cell salvage was combined with blood filtration using a leukocyte depletion filter. A comparison of this washed, filtered product was then made with maternal central venous blood. ⋯ Leukocyte depletion filtering of cell-salvaged blood obtained from cesarean section significantly reduces particulate contaminants to a concentration equivalent to maternal venous blood.
-
Clinical Trial
Pain relief in complex regional pain syndrome due to spinal cord stimulation does not depend on vasodilation.
Spinal cord stimulation (SCS) is known to relieve pain in patients with complex regional pain syndrome (CRPS) and, in general, to cause vasodilation. The vasodilatory effect of SCS is hypothesized to be secondary to inhibition of sympathetically mediated vasoconstriction, or through antidromic impulses resulting in release of vasoactive substances. The aim of the present study was to assess whether pain relief in CRPS after SCS is, in fact, dependent on vasodilation. In addition, we tried to determine which of the potential mechanisms may cause the vasodilatory effect that is generally found after SCS. ⋯ The current study failed to show that SCS influences skin microcirculation in patients with CRPS and a low sympathetic tone. Therefore, we may conclude that pain relief in CRPS due to SCS is possible without vasodilation. Because sympathetic activity was greatly decreased in our patients, these results support the hypothesis that the vasodilation that is normally found with SCS is due to an inhibitory effect on sympathetically maintained vasoconstriction.
-
Erythrocytes are transfused to prevent or treat inadequate oxygen delivery resulting from insufficient hemoglobin concentration. Previous studies failed to find evidence of inadequate systemic oxygen delivery at a hemoglobin concentration of 5 g/dl. However, in those studies, sensitive, specific measures of critical organ function were not used. This study tested the hypothesis that acute severe decreases of hemoglobin concentration alters human cognitive function. ⋯ Acute reduction of hemoglobin concentration to 7 g/dl does not produce detectable changes in human cognitive function. Further reduction of hemoglobin level to 6 and 5 g/dl produces subtle, reversible increases in reaction time and impaired immediate and delayed memory. These are the first prospective data to demonstrate subtle degraded human function with acute anemia of hemoglobin concentrations of 6 and 5 g/dl. This reversibility of these decrements with erythrocyte transfusion suggests that our model can be used to test the efficacy of erythrocytes, oxygen therapeutics, or other treatments for acute anemia.
-
Comparative Study
Isoflurane, but not halothane, induces protection of human myocardium via adenosine A1 receptors and adenosine triphosphate-sensitive potassium channels.
Volatile anesthetics produce differing degrees of myocardial protection in animal models of ischemia. The purpose of the current investigation was to determine the influence of isoflurane and halothane on myocardial protection in a human model of simulated ischemia and the role of adenosine A1 receptors and adenosine triphosphate-sensitive potassium (KATP) channels in the anesthetic pathway. ⋯ This study demonstrates the cardioprotective effects of isoflurane in contrast to the effects of halothane. Furthermore, A1 receptors and KATP channels seem to mediate the beneficial effects of anoxia and isoflurane in human myocardium.
-
Volatile anesthetic-induced preconditioning is mediated by adenosine triphosphate-dependent potassium (KATP) channels; however, the subcellular location of these channels is unknown. The authors tested the hypothesis that desflurane reduces experimental myocardial infarct size by activation of specific sarcolemmal and mitochondrial KATP channels. ⋯ Desflurane reduces myocardial infarct size in vivo, and the results further suggest that both sarcolemmal and mitochondrial KATP channels could be involved.