2. Academic Validation
  3. Anesthetic propofol blunts remote preconditioning of trauma-induced cardioprotection via the TRPV1 receptor

Anesthetic propofol blunts remote preconditioning of trauma-induced cardioprotection via the TRPV1 receptor

  • Biomed Pharmacother. 2019 Oct;118:109308. doi: 10.1016/j.biopha.2019.109308.
Junma Yu 1,  Ke Chen 2,  Lining Wu 3,  Xuesheng Liu 2,  Yao Lu 4
Affiliations

Affiliations

  • 1 Hefei National Laboratory for Physical Sciences at the Microscale, Department of Biophysics and Neurobiology, University of Science and Technology of China, Hefei, 230027, PR China; Department of Anesthesiology, The Third Affiliated Hospital of Anhui Medical University, Hefei, 230061, PR China.
  • 2 Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, PR China.
  • 3 Department of Anesthesiology, The Third Affiliated Hospital of Anhui Medical University, Hefei, 230061, PR China.
  • 4 Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, PR China. Electronic address: [email protected].
PMID: 31401396 DOI: 10.1016/j.biopha.2019.109308
Abstract

Remote preconditioning of trauma (RPCT) by surgical incision is an effective cardioprotective strategy via the transient receptor potential vanilloid 1 (TRPV1) channel as a form of remote ischemic preconditioning (RIPC). However, cardioprotection by RIPC has been shown to be completely blocked by propofol. We thus hypothesized that propofol may interfere with RPCT induced cardioprotection, and that RPCT induces cardioprotection via the cardiac TRPV1 channel. Male Sprague-Dawley rats were subjected to 30 min of myocardial ischemia followed by 2 h of reperfusion. RPCT was achieved by a transverse abdominal incision. Additionally, propofol or the TRPV1 receptor inhibitor capsazepine (CPZ) was given before RPCT. Infarct size was assessed by triphenyltetrazolium staining. Heart TRPV1 expression was detected by Western blot and immunofluorescence. RPCT significantly reduced infarct size compared to control treatment (45.6 ± 4% versus 65.4 ± 2%, P < 0.01). This protective effect of RPCT was completely abolished by propofol and CPZ. TRPV1 channels are present in the heart. Therefore, cardioprotection by RPCT is also abolished by propofol, and cardiac TRPV1 mediates this cardioprotection.

Keywords

Incision; Myocardial infarction; Propofol; Remote preconditioning; TRPV1.

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