Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction

J. Richard Spears, Cassandra Henney, Petar Prcevski, Rui Xu, Li Li, Giles J. Brereton, Marcello DiCarli, Ali Spanta, Richard Crilly, Abdulbaset M. Sulaiman, Samir Hadeed, Steven Lavine, William R. Patterson, Jeffrey Creech, Richard Vander Heide

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Objectives. The purpose of the study was to test the hypothesis that intracoronary aqueous oxygen (AO) hyperbaric reperfusion reduces myocardial injury after prolonged coronary occlusion. Background. Attenuation of ischemia/reperfusion injury by the use of hyperbaric oxygen (HBO) administered during reperfusion has been demonstrated for a wide variety of tissues, including myocardium. We have recently developed a more practical, catheter-based, site-specific method for delivery of oxygen at hyperbaric levels with aqueous oxygen infusion. Methods. Following a 60-minute balloon occlusion of the left anterior descending coronary artery in swine, intracoronary AO hyperoxemic perfusion (50 mL blood/minute; 1.5 mL AO/minute; mean pO2 = 834 ± 104 mmHg) was performed for 90 minutes after a 15-minute period of normoxemic autoreperfusion (physiologic reperfusion). Control groups consisted of autoreperfusion alone; active normoxemic perfusion (50 mL/minute) for 90 minutes; and hyperoxemic perfusion with a hollow fiber oxygenator (HFO) for 90 minutes. Results. A significant improvement in left ventricular ejection fraction was noted by ventriculography at 105 minutes of reperfusion (ANOVA, p <0.05), compared to the 15-minute autoreperfusion period, only in the AO and HFO groups. Mean percent infarct size (area of necrosis)/(area at risk), quantitative post-mortem hemorrhage score, and myocardial myeloperoxidase levels at 3 hours of reperfusion were significantly less in the AO group (ANOVA, p <0.05), but not in the HFO group, compared to normoxemic groups. Conclusions. The results demonstrate that intracoronary hyperbaric reperfusion with AO, but not with a membrane oxygenator, attenuates myocardial ischemia/reperfusion injury.

Original languageEnglish (US)
Pages (from-to)160-166
Number of pages7
JournalJournal of Invasive Cardiology
Volume14
Issue number4
StatePublished - 2002
Externally publishedYes

Fingerprint

Reperfusion
Swine
Myocardial Infarction
Oxygen
Oxygenators
Myocardial Reperfusion Injury
Perfusion
Reperfusion Injury
Analysis of Variance
Membrane Oxygenators
Balloon Occlusion
Coronary Occlusion
Stroke Volume
Peroxidase
Myocardial Ischemia
Coronary Vessels
Myocardium
Necrosis
Catheters
Hemorrhage

Keywords

  • Infarction
  • Ischemia
  • Oxygen
  • Reperfusion

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Spears, J. R., Henney, C., Prcevski, P., Xu, R., Li, L., Brereton, G. J., ... Vander Heide, R. (2002). Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction. Journal of Invasive Cardiology, 14(4), 160-166.

Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction. / Spears, J. Richard; Henney, Cassandra; Prcevski, Petar; Xu, Rui; Li, Li; Brereton, Giles J.; DiCarli, Marcello; Spanta, Ali; Crilly, Richard; Sulaiman, Abdulbaset M.; Hadeed, Samir; Lavine, Steven; Patterson, William R.; Creech, Jeffrey; Vander Heide, Richard.

In: Journal of Invasive Cardiology, Vol. 14, No. 4, 2002, p. 160-166.

Research output: Contribution to journalArticle

Spears, JR, Henney, C, Prcevski, P, Xu, R, Li, L, Brereton, GJ, DiCarli, M, Spanta, A, Crilly, R, Sulaiman, AM, Hadeed, S, Lavine, S, Patterson, WR, Creech, J & Vander Heide, R 2002, 'Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction', Journal of Invasive Cardiology, vol. 14, no. 4, pp. 160-166.
Spears JR, Henney C, Prcevski P, Xu R, Li L, Brereton GJ et al. Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction. Journal of Invasive Cardiology. 2002;14(4):160-166.
Spears, J. Richard ; Henney, Cassandra ; Prcevski, Petar ; Xu, Rui ; Li, Li ; Brereton, Giles J. ; DiCarli, Marcello ; Spanta, Ali ; Crilly, Richard ; Sulaiman, Abdulbaset M. ; Hadeed, Samir ; Lavine, Steven ; Patterson, William R. ; Creech, Jeffrey ; Vander Heide, Richard. / Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction. In: Journal of Invasive Cardiology. 2002 ; Vol. 14, No. 4. pp. 160-166.
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abstract = "Objectives. The purpose of the study was to test the hypothesis that intracoronary aqueous oxygen (AO) hyperbaric reperfusion reduces myocardial injury after prolonged coronary occlusion. Background. Attenuation of ischemia/reperfusion injury by the use of hyperbaric oxygen (HBO) administered during reperfusion has been demonstrated for a wide variety of tissues, including myocardium. We have recently developed a more practical, catheter-based, site-specific method for delivery of oxygen at hyperbaric levels with aqueous oxygen infusion. Methods. Following a 60-minute balloon occlusion of the left anterior descending coronary artery in swine, intracoronary AO hyperoxemic perfusion (50 mL blood/minute; 1.5 mL AO/minute; mean pO2 = 834 ± 104 mmHg) was performed for 90 minutes after a 15-minute period of normoxemic autoreperfusion (physiologic reperfusion). Control groups consisted of autoreperfusion alone; active normoxemic perfusion (50 mL/minute) for 90 minutes; and hyperoxemic perfusion with a hollow fiber oxygenator (HFO) for 90 minutes. Results. A significant improvement in left ventricular ejection fraction was noted by ventriculography at 105 minutes of reperfusion (ANOVA, p <0.05), compared to the 15-minute autoreperfusion period, only in the AO and HFO groups. Mean percent infarct size (area of necrosis)/(area at risk), quantitative post-mortem hemorrhage score, and myocardial myeloperoxidase levels at 3 hours of reperfusion were significantly less in the AO group (ANOVA, p <0.05), but not in the HFO group, compared to normoxemic groups. Conclusions. The results demonstrate that intracoronary hyperbaric reperfusion with AO, but not with a membrane oxygenator, attenuates myocardial ischemia/reperfusion injury.",
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T1 - Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction

AU - Spears, J. Richard

AU - Henney, Cassandra

AU - Prcevski, Petar

AU - Xu, Rui

AU - Li, Li

AU - Brereton, Giles J.

AU - DiCarli, Marcello

AU - Spanta, Ali

AU - Crilly, Richard

AU - Sulaiman, Abdulbaset M.

AU - Hadeed, Samir

AU - Lavine, Steven

AU - Patterson, William R.

AU - Creech, Jeffrey

AU - Vander Heide, Richard

PY - 2002

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N2 - Objectives. The purpose of the study was to test the hypothesis that intracoronary aqueous oxygen (AO) hyperbaric reperfusion reduces myocardial injury after prolonged coronary occlusion. Background. Attenuation of ischemia/reperfusion injury by the use of hyperbaric oxygen (HBO) administered during reperfusion has been demonstrated for a wide variety of tissues, including myocardium. We have recently developed a more practical, catheter-based, site-specific method for delivery of oxygen at hyperbaric levels with aqueous oxygen infusion. Methods. Following a 60-minute balloon occlusion of the left anterior descending coronary artery in swine, intracoronary AO hyperoxemic perfusion (50 mL blood/minute; 1.5 mL AO/minute; mean pO2 = 834 ± 104 mmHg) was performed for 90 minutes after a 15-minute period of normoxemic autoreperfusion (physiologic reperfusion). Control groups consisted of autoreperfusion alone; active normoxemic perfusion (50 mL/minute) for 90 minutes; and hyperoxemic perfusion with a hollow fiber oxygenator (HFO) for 90 minutes. Results. A significant improvement in left ventricular ejection fraction was noted by ventriculography at 105 minutes of reperfusion (ANOVA, p <0.05), compared to the 15-minute autoreperfusion period, only in the AO and HFO groups. Mean percent infarct size (area of necrosis)/(area at risk), quantitative post-mortem hemorrhage score, and myocardial myeloperoxidase levels at 3 hours of reperfusion were significantly less in the AO group (ANOVA, p <0.05), but not in the HFO group, compared to normoxemic groups. Conclusions. The results demonstrate that intracoronary hyperbaric reperfusion with AO, but not with a membrane oxygenator, attenuates myocardial ischemia/reperfusion injury.

AB - Objectives. The purpose of the study was to test the hypothesis that intracoronary aqueous oxygen (AO) hyperbaric reperfusion reduces myocardial injury after prolonged coronary occlusion. Background. Attenuation of ischemia/reperfusion injury by the use of hyperbaric oxygen (HBO) administered during reperfusion has been demonstrated for a wide variety of tissues, including myocardium. We have recently developed a more practical, catheter-based, site-specific method for delivery of oxygen at hyperbaric levels with aqueous oxygen infusion. Methods. Following a 60-minute balloon occlusion of the left anterior descending coronary artery in swine, intracoronary AO hyperoxemic perfusion (50 mL blood/minute; 1.5 mL AO/minute; mean pO2 = 834 ± 104 mmHg) was performed for 90 minutes after a 15-minute period of normoxemic autoreperfusion (physiologic reperfusion). Control groups consisted of autoreperfusion alone; active normoxemic perfusion (50 mL/minute) for 90 minutes; and hyperoxemic perfusion with a hollow fiber oxygenator (HFO) for 90 minutes. Results. A significant improvement in left ventricular ejection fraction was noted by ventriculography at 105 minutes of reperfusion (ANOVA, p <0.05), compared to the 15-minute autoreperfusion period, only in the AO and HFO groups. Mean percent infarct size (area of necrosis)/(area at risk), quantitative post-mortem hemorrhage score, and myocardial myeloperoxidase levels at 3 hours of reperfusion were significantly less in the AO group (ANOVA, p <0.05), but not in the HFO group, compared to normoxemic groups. Conclusions. The results demonstrate that intracoronary hyperbaric reperfusion with AO, but not with a membrane oxygenator, attenuates myocardial ischemia/reperfusion injury.

KW - Infarction

KW - Ischemia

KW - Oxygen

KW - Reperfusion

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