Poly-ADP-ribose polymerase inhibition reduces mesenteric injury after cardiopulmonary bypass

G. Szabó, L. Seres, P. Soós, C. Flechtenmacher, Z. Zsengellér, F. U. Sack, C. Szabó, S. Hagl

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: We investigated the effects of PARS inhibition on intestinal injury in a canine model of cardiopulmonary bypass (CPB). Methods: Twelve dogs underwent 90 minutes of hypothermic CPB. 6 dogs received 5 mg/kg PJ34, a selective PARP inhibitor during CPB, 6 vehicle-treated animals served as controls. Mesenteric blood flow (MBF) and mesenteric vascular resistance (MVR) were measured before and 60 minutes after weaning from CPB. Endothelium- dependent vasorelaxation to acetylcholine (ACH) and endothelium-independent vasorelaxation to sodium-nitroprussid (SNP) were expressed as percent change of MVR. In addition, mesenteric creatinkinase (CK) and lactate release were determined. Results: Baseline hemodynamics, MBF, response to ACH (- 41 ± 3 vs. - 55 ± 6%) and SNP (- 60 ± 2 vs. - 56 ± 4%) did not differ significantly between the groups. The response to ACH decreased significantly in the control group while it remained unchanged in the PJ34 group (- 29 ± 5 vs. - 46 ± 9%, p <0.05). The response to SNP did not change. Mesenteric CK release (325 ± 99 vs. 16 ± 10 U/l, p <0.05) and lactate production (0.96 ± 0.17 vs. 0.4 ± 0.2 mmol/l, p <0.05) were significantly lower in the PJ34 group. Conclusion: PARP inhibition prevents CPB-induced mesenteric endothelial dysfunction and tissue damage.

Original languageEnglish
Pages (from-to)338-343
Number of pages6
JournalThoracic and Cardiovascular Surgeon
Volume52
Issue number6
DOIs
Publication statusPublished - Dec 2004

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Poly(ADP-ribose) Polymerases
Cardiopulmonary Bypass
Wounds and Injuries
Acetylcholine
Endothelium
Sodium
Vasodilation
Vascular Resistance
Lactic Acid
Dogs
Weaning
Canidae
Hemodynamics
Control Groups
N-(oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide hydrochloride

Keywords

  • Cardiopulmonary bypass
  • Mesenteric injury
  • Poly (ADP-ribose) polymerase

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Poly-ADP-ribose polymerase inhibition reduces mesenteric injury after cardiopulmonary bypass. / Szabó, G.; Seres, L.; Soós, P.; Flechtenmacher, C.; Zsengellér, Z.; Sack, F. U.; Szabó, C.; Hagl, S.

In: Thoracic and Cardiovascular Surgeon, Vol. 52, No. 6, 12.2004, p. 338-343.

Research output: Contribution to journalArticle

Szabó, G. ; Seres, L. ; Soós, P. ; Flechtenmacher, C. ; Zsengellér, Z. ; Sack, F. U. ; Szabó, C. ; Hagl, S. / Poly-ADP-ribose polymerase inhibition reduces mesenteric injury after cardiopulmonary bypass. In: Thoracic and Cardiovascular Surgeon. 2004 ; Vol. 52, No. 6. pp. 338-343.
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AB - Background: We investigated the effects of PARS inhibition on intestinal injury in a canine model of cardiopulmonary bypass (CPB). Methods: Twelve dogs underwent 90 minutes of hypothermic CPB. 6 dogs received 5 mg/kg PJ34, a selective PARP inhibitor during CPB, 6 vehicle-treated animals served as controls. Mesenteric blood flow (MBF) and mesenteric vascular resistance (MVR) were measured before and 60 minutes after weaning from CPB. Endothelium- dependent vasorelaxation to acetylcholine (ACH) and endothelium-independent vasorelaxation to sodium-nitroprussid (SNP) were expressed as percent change of MVR. In addition, mesenteric creatinkinase (CK) and lactate release were determined. Results: Baseline hemodynamics, MBF, response to ACH (- 41 ± 3 vs. - 55 ± 6%) and SNP (- 60 ± 2 vs. - 56 ± 4%) did not differ significantly between the groups. The response to ACH decreased significantly in the control group while it remained unchanged in the PJ34 group (- 29 ± 5 vs. - 46 ± 9%, p <0.05). The response to SNP did not change. Mesenteric CK release (325 ± 99 vs. 16 ± 10 U/l, p <0.05) and lactate production (0.96 ± 0.17 vs. 0.4 ± 0.2 mmol/l, p <0.05) were significantly lower in the PJ34 group. Conclusion: PARP inhibition prevents CPB-induced mesenteric endothelial dysfunction and tissue damage.

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