Superoxide generation during cardiopulmonary bypass: Is there a role for vitamin E?

Nicholas C. Cavarocchi, Michael D. England, John F. O'Brien, Eduardo Solis, Pierantonio Russo, Hartzell V Schaff, Thomas A. Orszulak, James R. Pluth, Michael P. Kaye

Research output: Contribution to journalArticle

90 Citations (Scopus)

Abstract

The cytotoxic metabolites of oxygen [superoxide (O2 -), hydrogen peroxide (H2O2), and hydroxyl (OH)] have been demonstrated to be involved in the peroxidation of membrane lipids consequently altering membrane composition, morphology, and function. Of all the lines of defense adopted by living organisms against toxic oxygen free radicals, vitamin E is most effective in the prevention of membrane damage. Cardiopulmonary bypass (CPB) has been shown to activate complement and cause sequestration of leukocytes which can recruit, adhere, and stimulate release of cytotoxic oxygen radicals. A prospective study of 30 patients evaluated the effects of CPB with and without an exogenous free radical scavenger (Group I, N = 20, control) and (Group II, N = 10, vitamin E) on H2O2 (a marker of oxygen free radicals) malonaldehyde (a marker of lipid peroxidation), transpulmonary leukosequestration, and plasma levels of vitamins E and C. Group I showed a progressive increase in H2O2 during CPB from 65 ± 6 to 130 ± 11 μm/ml (P < 0.0001); plasma vitamin E decreased from 15 ± 3 to 6 ± 1 mg/liter (P < 0.0001) while vitamin C increased from 1.6 ±.3 to 2.3 ±.3 mg/dl (P < 0.0001). Group II showed no significant increase in H2O2 (from 78 ± 8 to 93 ± 5 μm/ml) during CPB and a significant reduction in H2O2 levels compared to Group I (P < 0.001); plasma vitamins E and C did not change significantly in Group II. Transpulmonary leukosequestration, expressed as median cell difference (MCD), occurred in Group I (MCD = 1700) and Group II (MCD = 1900) (P < 0.001 vs pre-CPB). We conclude that (1) cytotoxic oxygen radicals liberated during CPB can be reduced by pretreatment with vitamin E despite complement activation and pulmonary sequestration of white blood cells. (2) Vitamin E pretreatment prevented a clinically overt vitamin E deficiency during CPB. (3) The rise in vitamin C post-CPB demonstrates the direct effect on oxidized vitamin E by vitamin C in vivo.

Original languageEnglish (US)
Pages (from-to)519-527
Number of pages9
JournalJournal of Surgical Research
Volume40
Issue number6
DOIs
StatePublished - 1986

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Cardiopulmonary Bypass
Vitamin E
Superoxides
Ascorbic Acid
Reactive Oxygen Species
Free Radicals
Leukocytes
Vitamin E Deficiency
Bronchopulmonary Sequestration
Free Radical Scavengers
Membranes
Complement Activation
Poisons
Membrane Lipids
Malondialdehyde
Hydroxyl Radical
Hydrogen Peroxide
Lipid Peroxidation
Prospective Studies
Oxygen

ASJC Scopus subject areas

  • Surgery

Cite this

Cavarocchi, N. C., England, M. D., O'Brien, J. F., Solis, E., Russo, P., Schaff, H. V., ... Kaye, M. P. (1986). Superoxide generation during cardiopulmonary bypass: Is there a role for vitamin E? Journal of Surgical Research, 40(6), 519-527. https://doi.org/10.1016/0022-4804(86)90093-4

Superoxide generation during cardiopulmonary bypass : Is there a role for vitamin E? / Cavarocchi, Nicholas C.; England, Michael D.; O'Brien, John F.; Solis, Eduardo; Russo, Pierantonio; Schaff, Hartzell V; Orszulak, Thomas A.; Pluth, James R.; Kaye, Michael P.

In: Journal of Surgical Research, Vol. 40, No. 6, 1986, p. 519-527.

Research output: Contribution to journalArticle

Cavarocchi, NC, England, MD, O'Brien, JF, Solis, E, Russo, P, Schaff, HV, Orszulak, TA, Pluth, JR & Kaye, MP 1986, 'Superoxide generation during cardiopulmonary bypass: Is there a role for vitamin E?', Journal of Surgical Research, vol. 40, no. 6, pp. 519-527. https://doi.org/10.1016/0022-4804(86)90093-4
Cavarocchi, Nicholas C. ; England, Michael D. ; O'Brien, John F. ; Solis, Eduardo ; Russo, Pierantonio ; Schaff, Hartzell V ; Orszulak, Thomas A. ; Pluth, James R. ; Kaye, Michael P. / Superoxide generation during cardiopulmonary bypass : Is there a role for vitamin E?. In: Journal of Surgical Research. 1986 ; Vol. 40, No. 6. pp. 519-527.
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abstract = "The cytotoxic metabolites of oxygen [superoxide (O2 -), hydrogen peroxide (H2O2), and hydroxyl (OH•)] have been demonstrated to be involved in the peroxidation of membrane lipids consequently altering membrane composition, morphology, and function. Of all the lines of defense adopted by living organisms against toxic oxygen free radicals, vitamin E is most effective in the prevention of membrane damage. Cardiopulmonary bypass (CPB) has been shown to activate complement and cause sequestration of leukocytes which can recruit, adhere, and stimulate release of cytotoxic oxygen radicals. A prospective study of 30 patients evaluated the effects of CPB with and without an exogenous free radical scavenger (Group I, N = 20, control) and (Group II, N = 10, vitamin E) on H2O2 (a marker of oxygen free radicals) malonaldehyde (a marker of lipid peroxidation), transpulmonary leukosequestration, and plasma levels of vitamins E and C. Group I showed a progressive increase in H2O2 during CPB from 65 ± 6 to 130 ± 11 μm/ml (P < 0.0001); plasma vitamin E decreased from 15 ± 3 to 6 ± 1 mg/liter (P < 0.0001) while vitamin C increased from 1.6 ±.3 to 2.3 ±.3 mg/dl (P < 0.0001). Group II showed no significant increase in H2O2 (from 78 ± 8 to 93 ± 5 μm/ml) during CPB and a significant reduction in H2O2 levels compared to Group I (P < 0.001); plasma vitamins E and C did not change significantly in Group II. Transpulmonary leukosequestration, expressed as median cell difference (MCD), occurred in Group I (MCD = 1700) and Group II (MCD = 1900) (P < 0.001 vs pre-CPB). We conclude that (1) cytotoxic oxygen radicals liberated during CPB can be reduced by pretreatment with vitamin E despite complement activation and pulmonary sequestration of white blood cells. (2) Vitamin E pretreatment prevented a clinically overt vitamin E deficiency during CPB. (3) The rise in vitamin C post-CPB demonstrates the direct effect on oxidized vitamin E by vitamin C in vivo.",
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N2 - The cytotoxic metabolites of oxygen [superoxide (O2 -), hydrogen peroxide (H2O2), and hydroxyl (OH•)] have been demonstrated to be involved in the peroxidation of membrane lipids consequently altering membrane composition, morphology, and function. Of all the lines of defense adopted by living organisms against toxic oxygen free radicals, vitamin E is most effective in the prevention of membrane damage. Cardiopulmonary bypass (CPB) has been shown to activate complement and cause sequestration of leukocytes which can recruit, adhere, and stimulate release of cytotoxic oxygen radicals. A prospective study of 30 patients evaluated the effects of CPB with and without an exogenous free radical scavenger (Group I, N = 20, control) and (Group II, N = 10, vitamin E) on H2O2 (a marker of oxygen free radicals) malonaldehyde (a marker of lipid peroxidation), transpulmonary leukosequestration, and plasma levels of vitamins E and C. Group I showed a progressive increase in H2O2 during CPB from 65 ± 6 to 130 ± 11 μm/ml (P < 0.0001); plasma vitamin E decreased from 15 ± 3 to 6 ± 1 mg/liter (P < 0.0001) while vitamin C increased from 1.6 ±.3 to 2.3 ±.3 mg/dl (P < 0.0001). Group II showed no significant increase in H2O2 (from 78 ± 8 to 93 ± 5 μm/ml) during CPB and a significant reduction in H2O2 levels compared to Group I (P < 0.001); plasma vitamins E and C did not change significantly in Group II. Transpulmonary leukosequestration, expressed as median cell difference (MCD), occurred in Group I (MCD = 1700) and Group II (MCD = 1900) (P < 0.001 vs pre-CPB). We conclude that (1) cytotoxic oxygen radicals liberated during CPB can be reduced by pretreatment with vitamin E despite complement activation and pulmonary sequestration of white blood cells. (2) Vitamin E pretreatment prevented a clinically overt vitamin E deficiency during CPB. (3) The rise in vitamin C post-CPB demonstrates the direct effect on oxidized vitamin E by vitamin C in vivo.

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