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- W2806500511 abstract "To the Editor We read with interest the report by Behmenburg et al1 describing the influence of baseline anesthesia on remote ischemic preconditioning (RIPC) in rat hearts in situ. RIPC was produced by 4 cycles of 5 minutes of limb occlusion, interspersed with 5 minutes of reperfusion before a prolonged (25 minutes) left anterior descending coronary artery occlusion and 2 hours of reperfusion.1 RIPC decreased myocardial infarct size (triphenyltetrazolium chloride staining) during pentobarbital or sevoflurane–remifentanil anesthesia, but not when a propofol–remifentanil anesthetic technique was used. The findings provided further evidence that propofol inhibits, whereas sevoflurane preserves, myocardial protection afforded by RIPC. Reductions in troponin I release produced by RIPC were previously shown to occur only during isoflurane–sufentanil but not propofol–sufentanil anesthesia in patients undergoing coronary artery surgery,2 most likely because propofol inhibits activation of signal transducer and activator of transcription 5 (STAT5),3 a critical mediator of RIPC-induced protection against ischemic injury in human myocardium.4 It is noteworthy that STAT5 activation also mediates classical ischemic preconditioning.4 Whether STAT5 activation is also involved in volatile anesthetic-induced preconditioning is unknown, but this assertion seems likely because ischemic preconditioning and anesthetic-induced preconditioning share virtually indistinguishable intracellular mechanisms. From our perspective, the current and previous results are particularly interesting because they may provide an additional explanation for differences in cardiovascular outcome between volatile- and propofol-based anesthetic techniques in patients undergoing cardiac surgery.4 Several clinical trials and a number of meta-analyses showed that the use of a volatile anesthetic decreases myocardial necrosis and preserves left ventricular function compared with propofol-based anesthesia in cardiac surgery patients. These findings were interpreted as clinical evidence for volatile anesthetic-induced myocardial protection, providing a rationale for the use of volatile anesthetics in these patients.4 The current results by Behmenburg et al1 and others suggest that a detrimental effect of propofol (mediated through STAT5 inhibition) may also have made a contribution to the findings. Paul S. Pagel, MD, PhDAnesthesia ServiceClement J. Zablocki Veterans Affairs Medical CenterMilwaukee, Wisconsin[email protected] George J. Crystal, PhDDepartment of AnesthesiologyThe University of Illinois College of MedicineChicago, Illinois" @default.
- W2806500511 created "2018-06-13" @default.
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- W2806500511 date "2018-08-01" @default.
- W2806500511 modified "2023-09-26" @default.
- W2806500511 title "Propofol and Remote Ischemic Preconditioning" @default.
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- W2806500511 doi "https://doi.org/10.1213/ane.0000000000003519" @default.
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