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 language | English |
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Pages (from-to) | 642-651 |
Number of pages | 10 |
Journal | Journal of Surgical Research |
Volume | 193 |
Issue number | 2 |
DOIs | |
Publication status | Published - Feb 1 2015 |
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Keywords
- Histologic image analysis
- Ischemia
- Liver diseases
- Microcirculation
- Remote perconditioning
- Reperfusion injury
ASJC Scopus subject areas
- Surgery
- Medicine(all)
Cite this
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 journal › Article
}
TY - JOUR
T1 - Neural elements behind the hepatoprotection of remote perconditioning
AU - Czigány, Zoltán
AU - Turóczi, Zsolt
AU - Kleiner, Dénes
AU - Lotz, G.
AU - Homeyer, André
AU - Harsányi, László
AU - Szijártó, Attila
PY - 2015/2/1
Y1 - 2015/2/1
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
UR - http://www.scopus.com/inward/record.url?scp=84916910787&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84916910787&partnerID=8YFLogxK
U2 - 10.1016/j.jss.2014.08.046
DO - 10.1016/j.jss.2014.08.046
M3 - Article
C2 - 25266602
AN - SCOPUS:84916910787
VL - 193
SP - 642
EP - 651
JO - Journal of Surgical Research
JF - Journal of Surgical Research
SN - 0022-4804
IS - 2
ER -