Year-end Sale % OFF 
Abstract
Remote ischemic preconditioning (RIPC) by repeated brief cycles of limb ischemia/reperfusion may reduce myocardial ischemia/reperfusion injury and improve patients‘ prognosis after elective coronary artery bypass graft (CABG) surgery. The signal transducer and activator of transcription (STAT)5 activation in left ventricular myocardium is associated with RIPC´s cardioprotection. Cytokines and growth hormones typically activate STATs and could therefore act as humoral transfer factors of RIPC´s cardioprotection. We here determined arterial plasma concentrations of 25 different cytokines, growth hormones, and other factors which have previously been associated with cardioprotection, before (baseline)/after RIPC or placebo (n = 23/23), respectively, and before/after ischemic cardioplegic arrest in CABG patients. RIPC-induced protection was reflected by a 35% reduction of serum troponin I release. With the exception of interleukin-1α, none of the humoral factors changed in their concentrations after RIPC or placebo, respectively. Interleukin-1α, when normalized to baseline, increased after RIPC (280 ± 56%) but not with placebo (97 ± 15%). The interleukin-1α concentration remained increased until after ischemic cardioplegic arrest and was also higher than with placebo in absolute concentrations (25 ± 6 versus 16 ± 3 pg/mL). Only interleukin-1α possibly fulfills the criteria which would be expected from a substance to be released in response to RIPC and to protect the myocardium during ischemic cardioplegic arrest.
Highlights
Remote ischemic conditioning (RIC) by brief episodes of ischemia/reperfusion in parenchymal organs or limbs before or during sustained myocardial ischemia and subsequent reperfusion is a non-invasive strategy to protect the myocardium from irreversible ischemia/reperfusion injury
We have quantified the arterial concentration of a number of humoral factors, which may potentially activate signal transducer and activator of transcription (STAT) and the survival activating factor enhancement pathway, in a cohort of consecutive patients undergoing coronary artery bypass graft (CABG) surgery under isoflurane anesthesia before and after Remote ischemic preconditioning (RIPC)/placebo, respectively, and before and after ischemic cardioplegic arrest: chemokines/cytokines, i.e. erythropoietin (EPO)[52], interleukin-(IL-)1α53, IL-1β54, IL-255, IL-656, IL-857, IL-1058, IL-1555, IL-1759, IL-3360, stromal cell-derived factor-1α (SDF-1α)[61], tumor necrosis factor-α (TNF-α)[62] and growth hormones, i.e. growth hormone (GH)[63,64], growth differentiation factor-11 (GDF-11)[65], growth hormone releasing hormone (GHRH)[66], growth hormone-releasing peptide (GHRP)[67]
The troponin I (TnI) concentration area under the curve (AUC) over 72 h was decreased by RIPC, indicating cardioprotection (190 ± 16 versus 543 ± 145 ng/mL × 72 h, p = 0.015; Fig. 1)
Summary
Remote ischemic conditioning (RIC) by brief episodes of ischemia/reperfusion in parenchymal organs or limbs before (remote ischemic preconditioning; RIPC) or during (remote ischemic perconditioning) sustained myocardial ischemia and subsequent reperfusion is a non-invasive strategy to protect the myocardium from irreversible ischemia/reperfusion injury. In patients undergoing cardiac surgery, only some of the potential humoral transfer factors (amino acids, circulating RNase-1, cytokines/chemokines) have been associated with the RIC procedure[26,30,31,40], but only in two studies there was a reduction of myocardial injury by RIC30,31, and one of these studies was in infants[30]. We have quantified the arterial concentration of a number of humoral factors, which may potentially activate STAT and the survival activating factor enhancement pathway, in a cohort of consecutive patients undergoing CABG surgery under isoflurane anesthesia before and after RIPC/placebo, respectively, and before and after ischemic cardioplegic arrest: chemokines/cytokines, i.e. erythropoietin (EPO)[52], interleukin-(IL-)1α53, IL-1β54, IL-255, IL-656, IL-857, IL-1058, IL-1555, IL-1759, IL-3360, stromal cell-derived factor-1α (SDF-1α)[61], tumor necrosis factor-α (TNF-α)[62] and growth hormones, i.e. growth hormone (GH)[63,64], growth differentiation factor-11 (GDF-11)[65], growth hormone releasing hormone (GHRH)[66], growth hormone-releasing peptide (GHRP)[67]. We determined a few other factors which have been reported before in association with cardioprotection and/or STAT activation, i.e. Apo-A138,39, GLP-141, HIF-1α68,69, leptin[70,71], pentraxin-372, prolactin[73], RNase-140, survivin[74,75] and thymosin-β476,77
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
