Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury

Jeffrey T. Cope, David Banks, Victor E. Laubach, Oliver A.R. Binns, R. Christopher King, R. Mark Richardson, Kimberly S. Shockey, Curtis G. Tribble, Irving L. Kron

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Background. The role of nitric oxide in myocardial ischemia-reperfusion is controversial. Although many studies claim that nitric oxide ameliorates reperfusion injury, others suggest that it exacerbates such injury, possibly through peroxynitrite production. These discordant results may be attributable to a dose-dependent phenomenon. Methods. Isolated rabbit hearts sustained sequential periods of blood perfusion (20 minutes), warm ischemia (30 minutes), and reperfusion (20 minutes). During reperfusion, four groups underwent intracoronary infusion of saline solution (n = 6), or the nitric oxide donor sodium nitroprusside (100 nm/min [SNP100, n = 6], 1 nmol · L- 1/min-1 [SNP1, n = 6], or 0.01 nmol · L-1 · min-1 [SNP0.01]). Left ventricular-developed pressure and oxygen consumption were measured after preischemic perfusion and reperfusion. Levels of myocardial nitrotyrosine, a marker for peroxynitrite, were measured after reperfusion with an immunoradiochemical assay. Results. Postischemic-developed pressure and myocardial oxygen consumption were significantly higher in the saline group than all nitroprusside-reperfused groups (p < 0.01 for both parameters). However, there were no differences in either parameter between SNP100, SNP1, or SNP0.01. Nitrotyrosine levels were similar among the four groups (p = 0.43). Conclusions. Nitroprusside exacerbates myocardial ischemia-reperfusion injury over a wide range of doses, although the mechanism does not appear to be mediated by peroxynitrite.

Original languageEnglish (US)
Pages (from-to)1656-1660
Number of pages5
JournalAnnals of Thoracic Surgery
Volume64
Issue number6
DOIs
StatePublished - Dec 1 1997
Externally publishedYes

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Myocardial Reperfusion Injury
Nitroprusside
Reperfusion Injury
Reperfusion
Peroxynitrous Acid
Myocardial Ischemia
Oxygen Consumption
Nitric Oxide
Perfusion
Warm Ischemia
Myocardial Reperfusion
Nitric Oxide Donors
Ventricular Pressure
Sodium Chloride
Rabbits
Pressure
Wounds and Injuries
3-nitrotyrosine

ASJC Scopus subject areas

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

Cope, J. T., Banks, D., Laubach, V. E., Binns, O. A. R., King, R. C., Richardson, R. M., ... Kron, I. L. (1997). Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury. Annals of Thoracic Surgery, 64(6), 1656-1660. https://doi.org/10.1016/S0003-4975(97)01089-8

Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury. / Cope, Jeffrey T.; Banks, David; Laubach, Victor E.; Binns, Oliver A.R.; King, R. Christopher; Richardson, R. Mark; Shockey, Kimberly S.; Tribble, Curtis G.; Kron, Irving L.

In: Annals of Thoracic Surgery, Vol. 64, No. 6, 01.12.1997, p. 1656-1660.

Research output: Contribution to journalArticle

Cope, JT, Banks, D, Laubach, VE, Binns, OAR, King, RC, Richardson, RM, Shockey, KS, Tribble, CG & Kron, IL 1997, 'Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury', Annals of Thoracic Surgery, vol. 64, no. 6, pp. 1656-1660. https://doi.org/10.1016/S0003-4975(97)01089-8
Cope JT, Banks D, Laubach VE, Binns OAR, King RC, Richardson RM et al. Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury. Annals of Thoracic Surgery. 1997 Dec 1;64(6):1656-1660. https://doi.org/10.1016/S0003-4975(97)01089-8
Cope, Jeffrey T. ; Banks, David ; Laubach, Victor E. ; Binns, Oliver A.R. ; King, R. Christopher ; Richardson, R. Mark ; Shockey, Kimberly S. ; Tribble, Curtis G. ; Kron, Irving L. / Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury. In: Annals of Thoracic Surgery. 1997 ; Vol. 64, No. 6. pp. 1656-1660.
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abstract = "Background. The role of nitric oxide in myocardial ischemia-reperfusion is controversial. Although many studies claim that nitric oxide ameliorates reperfusion injury, others suggest that it exacerbates such injury, possibly through peroxynitrite production. These discordant results may be attributable to a dose-dependent phenomenon. Methods. Isolated rabbit hearts sustained sequential periods of blood perfusion (20 minutes), warm ischemia (30 minutes), and reperfusion (20 minutes). During reperfusion, four groups underwent intracoronary infusion of saline solution (n = 6), or the nitric oxide donor sodium nitroprusside (100 nm/min [SNP100, n = 6], 1 nmol · L- 1/min-1 [SNP1, n = 6], or 0.01 nmol · L-1 · min-1 [SNP0.01]). Left ventricular-developed pressure and oxygen consumption were measured after preischemic perfusion and reperfusion. Levels of myocardial nitrotyrosine, a marker for peroxynitrite, were measured after reperfusion with an immunoradiochemical assay. Results. Postischemic-developed pressure and myocardial oxygen consumption were significantly higher in the saline group than all nitroprusside-reperfused groups (p < 0.01 for both parameters). However, there were no differences in either parameter between SNP100, SNP1, or SNP0.01. Nitrotyrosine levels were similar among the four groups (p = 0.43). Conclusions. Nitroprusside exacerbates myocardial ischemia-reperfusion injury over a wide range of doses, although the mechanism does not appear to be mediated by peroxynitrite.",
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AU - Cope, Jeffrey T.

AU - Banks, David

AU - Laubach, Victor E.

AU - Binns, Oliver A.R.

AU - King, R. Christopher

AU - Richardson, R. Mark

AU - Shockey, Kimberly S.

AU - Tribble, Curtis G.

AU - Kron, Irving L.

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N2 - Background. The role of nitric oxide in myocardial ischemia-reperfusion is controversial. Although many studies claim that nitric oxide ameliorates reperfusion injury, others suggest that it exacerbates such injury, possibly through peroxynitrite production. These discordant results may be attributable to a dose-dependent phenomenon. Methods. Isolated rabbit hearts sustained sequential periods of blood perfusion (20 minutes), warm ischemia (30 minutes), and reperfusion (20 minutes). During reperfusion, four groups underwent intracoronary infusion of saline solution (n = 6), or the nitric oxide donor sodium nitroprusside (100 nm/min [SNP100, n = 6], 1 nmol · L- 1/min-1 [SNP1, n = 6], or 0.01 nmol · L-1 · min-1 [SNP0.01]). Left ventricular-developed pressure and oxygen consumption were measured after preischemic perfusion and reperfusion. Levels of myocardial nitrotyrosine, a marker for peroxynitrite, were measured after reperfusion with an immunoradiochemical assay. Results. Postischemic-developed pressure and myocardial oxygen consumption were significantly higher in the saline group than all nitroprusside-reperfused groups (p < 0.01 for both parameters). However, there were no differences in either parameter between SNP100, SNP1, or SNP0.01. Nitrotyrosine levels were similar among the four groups (p = 0.43). Conclusions. Nitroprusside exacerbates myocardial ischemia-reperfusion injury over a wide range of doses, although the mechanism does not appear to be mediated by peroxynitrite.

AB - Background. The role of nitric oxide in myocardial ischemia-reperfusion is controversial. Although many studies claim that nitric oxide ameliorates reperfusion injury, others suggest that it exacerbates such injury, possibly through peroxynitrite production. These discordant results may be attributable to a dose-dependent phenomenon. Methods. Isolated rabbit hearts sustained sequential periods of blood perfusion (20 minutes), warm ischemia (30 minutes), and reperfusion (20 minutes). During reperfusion, four groups underwent intracoronary infusion of saline solution (n = 6), or the nitric oxide donor sodium nitroprusside (100 nm/min [SNP100, n = 6], 1 nmol · L- 1/min-1 [SNP1, n = 6], or 0.01 nmol · L-1 · min-1 [SNP0.01]). Left ventricular-developed pressure and oxygen consumption were measured after preischemic perfusion and reperfusion. Levels of myocardial nitrotyrosine, a marker for peroxynitrite, were measured after reperfusion with an immunoradiochemical assay. Results. Postischemic-developed pressure and myocardial oxygen consumption were significantly higher in the saline group than all nitroprusside-reperfused groups (p < 0.01 for both parameters). However, there were no differences in either parameter between SNP100, SNP1, or SNP0.01. Nitrotyrosine levels were similar among the four groups (p = 0.43). Conclusions. Nitroprusside exacerbates myocardial ischemia-reperfusion injury over a wide range of doses, although the mechanism does not appear to be mediated by peroxynitrite.

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