Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect

H. Yokoyama, D. M. Lingle, J. A. Crestanello, J. Kamelgard, B. R. Kott, R. Momeni, J. Millili, S. A. Mortensen, Glenn Whitman

Research output: Contribution to journalArticle

Abstract

Background. Cardiac ischemia reperfusion (I/R) injury causes coronary vascular dysfunction. Coenzyme Q10 (CoQ, which preserves cardiac mechanical function after I/R, recently has been recognized as a free radical scavenger. We hypothesized that CoQ protects coronary vascular reactivity after I/R via an antioxidant mechanism. Methods. Rats were pretreated with either CoQ (20 mg/kg intramuscular and 10 mg/kg intraperitoneal [CoQ group]) or a vehicle (Control) before the experiment. Isolated perfused rat hearts were subjected to 25 minutes of global normothermic ischemia and 40 minutes of reperfusion. The reperfusion-induced oxidative burst was directly assessed by lucigenin enhanced chemiluminescence. Coronary flow was measured at equilibration and after reperfusion with or without bradykinin, an endothelium-dependent vasodilator, and sodium nitroprusside (SNP), an endothelium-independent vasodilator. The effect of intracoronary infusion of hydrogen peroxide (H2O2 0.1 μmol/gm body weight given over 5 minutes), simulating the free radical burst after I/R, also was evaluated. Results. I/R decreased the bradykinin-induced change in coronary flow (-5% ± 4% versus 26% ± 3% at equilibration; p <0.05) and the SNP-induced change (+20% ± 6% versus +56% ± 5% at equilibration; p <0.05). The coronary vasculature after H2O2 infusion revealed a similar loss in vasodilatory responsiveness (+4% ± 4% in response to bradykinin, +35% ± 8% in response to SNP; p <0.05 versus equilibration). Pretreatment with CoQ improved BK-induced vasorelaxation after I/R (+12% ± 2%; p <0.05 versus control I/R) or H2O2 infusion (18% ± 4%; p <0.05 versus control I/R) but failed to improve SNP-induced vasorelaxation. The CoQ pretreatment decreased the I/R-induced maximal free radical burst (9.3 ± 0.8 x 103 cpm versus 11.5 ± 1.1 x 103 cpm; p <0.05) during the early period of reperfusion. Conclusions. Endothelium-dependent vasorelaxation is more sensitive than endothelium-independent relaxation to I/R injury. Via a direct antioxidant effect, CoQ preserved endothelium-dependent vasorelaxation by improving tolerance to I/R injury.

Original languageEnglish (US)
Pages (from-to)189-196
Number of pages8
JournalSurgery
Volume120
Issue number2
StatePublished - 1996
Externally publishedYes

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coenzyme Q10
Reperfusion Injury
Reperfusion
Antioxidants
Ischemia
Nitroprusside
Vasodilation
Endothelium
Bradykinin
Free Radicals
Blood Vessels

ASJC Scopus subject areas

  • Surgery

Cite this

Yokoyama, H., Lingle, D. M., Crestanello, J. A., Kamelgard, J., Kott, B. R., Momeni, R., ... Whitman, G. (1996). Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect. Surgery, 120(2), 189-196.

Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect. / Yokoyama, H.; Lingle, D. M.; Crestanello, J. A.; Kamelgard, J.; Kott, B. R.; Momeni, R.; Millili, J.; Mortensen, S. A.; Whitman, Glenn.

In: Surgery, Vol. 120, No. 2, 1996, p. 189-196.

Research output: Contribution to journalArticle

Yokoyama, H, Lingle, DM, Crestanello, JA, Kamelgard, J, Kott, BR, Momeni, R, Millili, J, Mortensen, SA & Whitman, G 1996, 'Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect', Surgery, vol. 120, no. 2, pp. 189-196.
Yokoyama H, Lingle DM, Crestanello JA, Kamelgard J, Kott BR, Momeni R et al. Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect. Surgery. 1996;120(2):189-196.
Yokoyama, H. ; Lingle, D. M. ; Crestanello, J. A. ; Kamelgard, J. ; Kott, B. R. ; Momeni, R. ; Millili, J. ; Mortensen, S. A. ; Whitman, Glenn. / Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect. In: Surgery. 1996 ; Vol. 120, No. 2. pp. 189-196.
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abstract = "Background. Cardiac ischemia reperfusion (I/R) injury causes coronary vascular dysfunction. Coenzyme Q10 (CoQ, which preserves cardiac mechanical function after I/R, recently has been recognized as a free radical scavenger. We hypothesized that CoQ protects coronary vascular reactivity after I/R via an antioxidant mechanism. Methods. Rats were pretreated with either CoQ (20 mg/kg intramuscular and 10 mg/kg intraperitoneal [CoQ group]) or a vehicle (Control) before the experiment. Isolated perfused rat hearts were subjected to 25 minutes of global normothermic ischemia and 40 minutes of reperfusion. The reperfusion-induced oxidative burst was directly assessed by lucigenin enhanced chemiluminescence. Coronary flow was measured at equilibration and after reperfusion with or without bradykinin, an endothelium-dependent vasodilator, and sodium nitroprusside (SNP), an endothelium-independent vasodilator. The effect of intracoronary infusion of hydrogen peroxide (H2O2 0.1 μmol/gm body weight given over 5 minutes), simulating the free radical burst after I/R, also was evaluated. Results. I/R decreased the bradykinin-induced change in coronary flow (-5{\%} ± 4{\%} versus 26{\%} ± 3{\%} at equilibration; p <0.05) and the SNP-induced change (+20{\%} ± 6{\%} versus +56{\%} ± 5{\%} at equilibration; p <0.05). The coronary vasculature after H2O2 infusion revealed a similar loss in vasodilatory responsiveness (+4{\%} ± 4{\%} in response to bradykinin, +35{\%} ± 8{\%} in response to SNP; p <0.05 versus equilibration). Pretreatment with CoQ improved BK-induced vasorelaxation after I/R (+12{\%} ± 2{\%}; p <0.05 versus control I/R) or H2O2 infusion (18{\%} ± 4{\%}; p <0.05 versus control I/R) but failed to improve SNP-induced vasorelaxation. The CoQ pretreatment decreased the I/R-induced maximal free radical burst (9.3 ± 0.8 x 103 cpm versus 11.5 ± 1.1 x 103 cpm; p <0.05) during the early period of reperfusion. Conclusions. Endothelium-dependent vasorelaxation is more sensitive than endothelium-independent relaxation to I/R injury. Via a direct antioxidant effect, CoQ preserved endothelium-dependent vasorelaxation by improving tolerance to I/R injury.",
author = "H. Yokoyama and Lingle, {D. M.} and Crestanello, {J. A.} and J. Kamelgard and Kott, {B. R.} and R. Momeni and J. Millili and Mortensen, {S. A.} and Glenn Whitman",
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T1 - Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect

AU - Yokoyama, H.

AU - Lingle, D. M.

AU - Crestanello, J. A.

AU - Kamelgard, J.

AU - Kott, B. R.

AU - Momeni, R.

AU - Millili, J.

AU - Mortensen, S. A.

AU - Whitman, Glenn

PY - 1996

Y1 - 1996

N2 - Background. Cardiac ischemia reperfusion (I/R) injury causes coronary vascular dysfunction. Coenzyme Q10 (CoQ, which preserves cardiac mechanical function after I/R, recently has been recognized as a free radical scavenger. We hypothesized that CoQ protects coronary vascular reactivity after I/R via an antioxidant mechanism. Methods. Rats were pretreated with either CoQ (20 mg/kg intramuscular and 10 mg/kg intraperitoneal [CoQ group]) or a vehicle (Control) before the experiment. Isolated perfused rat hearts were subjected to 25 minutes of global normothermic ischemia and 40 minutes of reperfusion. The reperfusion-induced oxidative burst was directly assessed by lucigenin enhanced chemiluminescence. Coronary flow was measured at equilibration and after reperfusion with or without bradykinin, an endothelium-dependent vasodilator, and sodium nitroprusside (SNP), an endothelium-independent vasodilator. The effect of intracoronary infusion of hydrogen peroxide (H2O2 0.1 μmol/gm body weight given over 5 minutes), simulating the free radical burst after I/R, also was evaluated. Results. I/R decreased the bradykinin-induced change in coronary flow (-5% ± 4% versus 26% ± 3% at equilibration; p <0.05) and the SNP-induced change (+20% ± 6% versus +56% ± 5% at equilibration; p <0.05). The coronary vasculature after H2O2 infusion revealed a similar loss in vasodilatory responsiveness (+4% ± 4% in response to bradykinin, +35% ± 8% in response to SNP; p <0.05 versus equilibration). Pretreatment with CoQ improved BK-induced vasorelaxation after I/R (+12% ± 2%; p <0.05 versus control I/R) or H2O2 infusion (18% ± 4%; p <0.05 versus control I/R) but failed to improve SNP-induced vasorelaxation. The CoQ pretreatment decreased the I/R-induced maximal free radical burst (9.3 ± 0.8 x 103 cpm versus 11.5 ± 1.1 x 103 cpm; p <0.05) during the early period of reperfusion. Conclusions. Endothelium-dependent vasorelaxation is more sensitive than endothelium-independent relaxation to I/R injury. Via a direct antioxidant effect, CoQ preserved endothelium-dependent vasorelaxation by improving tolerance to I/R injury.

AB - Background. Cardiac ischemia reperfusion (I/R) injury causes coronary vascular dysfunction. Coenzyme Q10 (CoQ, which preserves cardiac mechanical function after I/R, recently has been recognized as a free radical scavenger. We hypothesized that CoQ protects coronary vascular reactivity after I/R via an antioxidant mechanism. Methods. Rats were pretreated with either CoQ (20 mg/kg intramuscular and 10 mg/kg intraperitoneal [CoQ group]) or a vehicle (Control) before the experiment. Isolated perfused rat hearts were subjected to 25 minutes of global normothermic ischemia and 40 minutes of reperfusion. The reperfusion-induced oxidative burst was directly assessed by lucigenin enhanced chemiluminescence. Coronary flow was measured at equilibration and after reperfusion with or without bradykinin, an endothelium-dependent vasodilator, and sodium nitroprusside (SNP), an endothelium-independent vasodilator. The effect of intracoronary infusion of hydrogen peroxide (H2O2 0.1 μmol/gm body weight given over 5 minutes), simulating the free radical burst after I/R, also was evaluated. Results. I/R decreased the bradykinin-induced change in coronary flow (-5% ± 4% versus 26% ± 3% at equilibration; p <0.05) and the SNP-induced change (+20% ± 6% versus +56% ± 5% at equilibration; p <0.05). The coronary vasculature after H2O2 infusion revealed a similar loss in vasodilatory responsiveness (+4% ± 4% in response to bradykinin, +35% ± 8% in response to SNP; p <0.05 versus equilibration). Pretreatment with CoQ improved BK-induced vasorelaxation after I/R (+12% ± 2%; p <0.05 versus control I/R) or H2O2 infusion (18% ± 4%; p <0.05 versus control I/R) but failed to improve SNP-induced vasorelaxation. The CoQ pretreatment decreased the I/R-induced maximal free radical burst (9.3 ± 0.8 x 103 cpm versus 11.5 ± 1.1 x 103 cpm; p <0.05) during the early period of reperfusion. Conclusions. Endothelium-dependent vasorelaxation is more sensitive than endothelium-independent relaxation to I/R injury. Via a direct antioxidant effect, CoQ preserved endothelium-dependent vasorelaxation by improving tolerance to I/R injury.

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