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Comparison of effects of propofol and midazolam at sedative concentrations on sympathetic tone generation in the isolated spinal cord of neonatal rats
Author(s) -
Ho C.M.,
Tarng G.W.,
Su C.K.
Publication year - 2007
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.2007.01333.x
Subject(s) - propofol , midazolam , medicine , anesthesia , splanchnic , splanchnic nerves , spinal cord , sedative , sedation , sympathetic nervous system , pharmacology , hemodynamics , blood pressure , stimulation , psychiatry
Background: Propofol and midazolam are common sedatives for critically ill patients. Little is known about the effects of propofol and midazolam on central sympathetic activity when drug concentrations in extracellular milieu are under precise control. Previous work using an in vitro neonatal rat splanchnic nerve–spinal cord preparation has demonstrated that tonic sympathetic activity is generated spontaneously in the thoracic spinal cord. The aim of this study was to investigate the concentration effects of propofol and midazolam on spinally generated sympathetic activity. Methods: Using an in vitro neonatal rat splanchnic nerve–spinal cord preparation that allows the precise control of drug concentrations, the central sympathetic effects elicited by the application of propofol (10–640 μ m ) and midazolam (10–640 μ m ) were compared. Results: There was a prompt decrease in sympathetic activity on application of propofol or midazolam in a concentration‐dependent manner. A significant decrease in sympathetic activity was observed on application of propofol at 80–640 μ m ; however, the application of propofol at 10–40 μ m caused only a slight alteration in activity. The sympathetic activity was not altered significantly by 10 μ m of midazolam, but the application of midazolam at 20–640 μ m caused a significant decrease in activity. Thus, in these experimental conditions, the minimum concentration of propofol causing a significant decrease in sympathetic activity was 80 μ m and that of midazolam was 20 μ m . Conclusions: The current findings suggest that the administration of 9–19 μ m of propofol or 0.7–0.9 μ m of midazolam, the clinically relevant concentrations for sedation, does not alter central sympathetic outflow at the spinal cord level. However, propofol at a concentration of 86 μ m , which could be achieved by a single‐bolus loading dose to induce sedation, depresses central sympathetic activity.