Neural elements behind the hepatoprotection of remote perconditioning

Zoltán Czigány, Zsolt Turóczi, Dénes Kleiner, G. Lotz, André Homeyer, László Harsányi, Attila Szijártó

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background The ability of remote ischemic perconditioning (RIPER) to protect the liver from ischemic-reperfusion (IR) injury has been reported before; however, the mechanism behind the positive effects of RIPER remains unrevealed. Therefore, we aimed to investigate the potential role of neural elements to transfer protective signals evoked by perconditioning.

Materials and methods Male Wistar rats were randomly allocated into six groups (sham, IR, RIPER ± denervation; n = 7 per group). Half of the animals underwent left femoral and sciatic nerve resection. In IR and RIPER groups, normothermic, partial (70%) liver ischemia lasting for 60 min was induced; parallel animals in the RIPER groups received perconditioning treatment (4×5-5 min IR, left femoral artery clamping). Hepatic microcirculation and systemic blood pressure were monitored during the first postischemic hour. After 24 h of reperfusion, liver samples were taken for histology and redox-state analysis. Automated image analysis software was used for necrosis quantification. Serum alanine aminotransferase, aspartate aminotransferase, and bilirubin levels were measured.

Results Microcirculation and blood pressure showed significant improvement during reperfusion after perconditioning. This phenomenon was completely abolished by nerve resection (P <0.05; RIPER versus IR, IR + denervation, and RIPER + denervation).

Results of necrosis quantification showed similar pattern. Besides noncharacteristic changes in aspartate aminotransferase levels, alanine aminotransferase values were significantly lower (P <0.05) in the RIPER group compared with the other IR groups. Mild but significant alterations were observed in liver function assessed by total bilirubin levels. Further supporting results were obtained from analysis of redox homeostasis.

Conclusions Perconditioning was able to reduce liver IR injury in our model via a mechanism most probably involving interorgan neural pathways.

Original languageEnglish
Pages (from-to)642-651
Number of pages10
JournalJournal of Surgical Research
Volume193
Issue number2
DOIs
Publication statusPublished - Feb 1 2015

Fingerprint

Reperfusion
Liver
Denervation
Microcirculation
Aspartate Aminotransferases
Reperfusion Injury
Alanine Transaminase
Bilirubin
Oxidation-Reduction
Necrosis
Blood Pressure
Femoral Nerve
Neural Pathways
Sciatic Nerve
Femoral Artery
Constriction
Wistar Rats
Histology
Homeostasis
Software

Keywords

  • Histologic image analysis
  • Ischemia
  • Liver diseases
  • Microcirculation
  • Remote perconditioning
  • Reperfusion injury

ASJC Scopus subject areas

  • Surgery
  • Medicine(all)

Cite this

Czigány, Z., Turóczi, Z., Kleiner, D., Lotz, G., Homeyer, A., Harsányi, L., & Szijártó, A. (2015). Neural elements behind the hepatoprotection of remote perconditioning. Journal of Surgical Research, 193(2), 642-651. https://doi.org/10.1016/j.jss.2014.08.046

Neural elements behind the hepatoprotection of remote perconditioning. / Czigány, Zoltán; Turóczi, Zsolt; Kleiner, Dénes; Lotz, G.; Homeyer, André; Harsányi, László; Szijártó, Attila.

In: Journal of Surgical Research, Vol. 193, No. 2, 01.02.2015, p. 642-651.

Research output: Contribution to journalArticle

Czigány, Z, Turóczi, Z, Kleiner, D, Lotz, G, Homeyer, A, Harsányi, L & Szijártó, A 2015, 'Neural elements behind the hepatoprotection of remote perconditioning', Journal of Surgical Research, vol. 193, no. 2, pp. 642-651. https://doi.org/10.1016/j.jss.2014.08.046
Czigány, Zoltán ; Turóczi, Zsolt ; Kleiner, Dénes ; Lotz, G. ; Homeyer, André ; Harsányi, László ; Szijártó, Attila. / Neural elements behind the hepatoprotection of remote perconditioning. In: Journal of Surgical Research. 2015 ; Vol. 193, No. 2. pp. 642-651.
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AU - Czigány, Zoltán

AU - Turóczi, Zsolt

AU - Kleiner, Dénes

AU - Lotz, G.

AU - Homeyer, André

AU - Harsányi, László

AU - Szijártó, Attila

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N2 - Background The ability of remote ischemic perconditioning (RIPER) to protect the liver from ischemic-reperfusion (IR) injury has been reported before; however, the mechanism behind the positive effects of RIPER remains unrevealed. Therefore, we aimed to investigate the potential role of neural elements to transfer protective signals evoked by perconditioning.Materials and methods Male Wistar rats were randomly allocated into six groups (sham, IR, RIPER ± denervation; n = 7 per group). Half of the animals underwent left femoral and sciatic nerve resection. In IR and RIPER groups, normothermic, partial (70%) liver ischemia lasting for 60 min was induced; parallel animals in the RIPER groups received perconditioning treatment (4×5-5 min IR, left femoral artery clamping). Hepatic microcirculation and systemic blood pressure were monitored during the first postischemic hour. After 24 h of reperfusion, liver samples were taken for histology and redox-state analysis. Automated image analysis software was used for necrosis quantification. Serum alanine aminotransferase, aspartate aminotransferase, and bilirubin levels were measured.Results Microcirculation and blood pressure showed significant improvement during reperfusion after perconditioning. This phenomenon was completely abolished by nerve resection (P <0.05; RIPER versus IR, IR + denervation, and RIPER + denervation).Results of necrosis quantification showed similar pattern. Besides noncharacteristic changes in aspartate aminotransferase levels, alanine aminotransferase values were significantly lower (P <0.05) in the RIPER group compared with the other IR groups. Mild but significant alterations were observed in liver function assessed by total bilirubin levels. Further supporting results were obtained from analysis of redox homeostasis.Conclusions Perconditioning was able to reduce liver IR injury in our model via a mechanism most probably involving interorgan neural pathways.

AB - Background The ability of remote ischemic perconditioning (RIPER) to protect the liver from ischemic-reperfusion (IR) injury has been reported before; however, the mechanism behind the positive effects of RIPER remains unrevealed. Therefore, we aimed to investigate the potential role of neural elements to transfer protective signals evoked by perconditioning.Materials and methods Male Wistar rats were randomly allocated into six groups (sham, IR, RIPER ± denervation; n = 7 per group). Half of the animals underwent left femoral and sciatic nerve resection. In IR and RIPER groups, normothermic, partial (70%) liver ischemia lasting for 60 min was induced; parallel animals in the RIPER groups received perconditioning treatment (4×5-5 min IR, left femoral artery clamping). Hepatic microcirculation and systemic blood pressure were monitored during the first postischemic hour. After 24 h of reperfusion, liver samples were taken for histology and redox-state analysis. Automated image analysis software was used for necrosis quantification. Serum alanine aminotransferase, aspartate aminotransferase, and bilirubin levels were measured.Results Microcirculation and blood pressure showed significant improvement during reperfusion after perconditioning. This phenomenon was completely abolished by nerve resection (P <0.05; RIPER versus IR, IR + denervation, and RIPER + denervation).Results of necrosis quantification showed similar pattern. Besides noncharacteristic changes in aspartate aminotransferase levels, alanine aminotransferase values were significantly lower (P <0.05) in the RIPER group compared with the other IR groups. Mild but significant alterations were observed in liver function assessed by total bilirubin levels. Further supporting results were obtained from analysis of redox homeostasis.Conclusions Perconditioning was able to reduce liver IR injury in our model via a mechanism most probably involving interorgan neural pathways.

KW - Histologic image analysis

KW - Ischemia

KW - Liver diseases

KW - Microcirculation

KW - Remote perconditioning

KW - Reperfusion injury

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