Comparison of effects of propofol pretreatment and ischemic preconditioning on ischemia-reperfusion injury in the isolated rat heart
Jing Wu
Abstract
Jing Wu
Abstract
Objective:To compare the effects of propofol pretreatment and ischemic preconditioning on ischemia-reperfusion injury in the isolated rat heart and to determine whether propofol shared the same mechanism of IPC, which is related to mitochondrial K ATP channels. Method: Male rat hearts were isolated and perfused with oxygenated Krebs-Hensleit (K-H) in a Langendorff apparatus, then randomly divided into 6 groups. All isolated hearts were subjected to 30 min of no-flow global ischemia followed by 120 min reperfusion, after a treatment period consisting of no intervention after the pretreatment without (group A, n=8) or with 5-HD(100 μmol/L, group D, n=8), 10 min propofol (50 μmol/L) followed by a 10-min washout period without (group B, n=6) or with 5-HD (100 μmol/L, group E, n=6), or two times of 5 min of ischemia followed by 5 min reperfusion after the pretreatment without (group C, n=6) or with 5-HD(100 μmol/L, group F, n=7).The hemodynamic index and coronary flow were monitored continuously, an arrhythmia score was used to quantify the arrhythmias during reperfusion and TTC staining was used to determine infarct size.Result:During reperfusion, compared with group A, hemodynamic values, coronary flow, arrhythmia score and infarct size were significantly improved in group B、C、E, especially in group C (P0.01 or 0.05). Conclusion:Both propofol pretreatment and ischemic preconditioning improve function of the isolated rat heart after ischemia-reperfusion injury, attenuate the reperfusion arrhythmias and reduce infarct size. Propofol pretreatment shows less protection than ischemic preconditioning and is independent of mitochondrial K ATP channels.
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Objective:To compare the effects of propofol pretreatment and ischemic preconditioning on ischemia-reperfusion injury in the isolated rat heart and to determine whether propofol shared the same mechanism of IPC, which is related to mitochondrial K ATP channels. Method: Male rat hearts were isolated and perfused with oxygenated Krebs-Hensleit (K-H) in a Langendorff apparatus, then randomly divided into 6 groups. All isolated hearts were subjected to 30 min of no-flow global ischemia followed by 120 min reperfusion, after a treatment period consisting of no intervention after the pretreatment without (group A, n=8) or with 5-HD(100 μmol/L, group D, n=8), 10 min propofol (50 μmol/L) followed by a 10-min washout period without (group B, n=6) or with 5-HD (100 μmol/L, group E, n=6), or two times of 5 min of ischemia followed by 5 min reperfusion after the pretreatment without (group C, n=6) or with 5-HD(100 μmol/L, group F, n=7).The hemodynamic index and coronary flow were monitored continuously, an arrhythmia score was used to quantify the arrhythmias during reperfusion and TTC staining was used to determine infarct size.Result:During reperfusion, compared with group A, hemodynamic values, coronary flow, arrhythmia score and infarct size were significantly improved in group B、C、E, especially in group C (P0.01 or 0.05). Conclusion:Both propofol pretreatment and ischemic preconditioning improve function of the isolated rat heart after ischemia-reperfusion injury, attenuate the reperfusion arrhythmias and reduce infarct size. Propofol pretreatment shows less protection than ischemic preconditioning and is independent of mitochondrial K ATP channels.
Key concepts: Medicine, Propofol, Ischemia, Reperfusion injury, Hemodynamics, Anesthesia, Ischemic preconditioning, Cardiology