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Hale SL, Vanderipe DR, Kloner RA. Continuous heliox breathing and the extent of anatomic zone of noreflow and necrosis following ischemia/reperfusion in the rabbit heart. Open Cardiovasc Med J. 2014;8:1-5doi: 10.2174/1874192401408010001.
Hale, S. L., Vanderipe, D. R., & Kloner, R. A. (2013). Continuous heliox breathing and the extent of anatomic zone of noreflow and necrosis following ischemia/reperfusion in the rabbit heart. The open cardiovascular medicine journal, 81-5. https://doi.org/10.2174/1874192401408010001
Hale, Sharon L, et al. "Continuous heliox breathing and the extent of anatomic zone of noreflow and necrosis following ischemia/reperfusion in the rabbit heart." The open cardiovascular medicine journal vol. 8 (2013): 1-5. doi: https://doi.org/10.2174/1874192401408010001
Hale SL, Vanderipe DR, Kloner RA. Continuous heliox breathing and the extent of anatomic zone of noreflow and necrosis following ischemia/reperfusion in the rabbit heart. Open Cardiovasc Med J. 2014 Jan 24;8:1-5. doi: 10.2174/1874192401408010001. eCollection 2013. PMID: 24587834; PMCID: PMC3937439.
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Open Cardiovasc Med J. 2014 Jan 24;8:1-5. doi: 10.2174/1874192401408010001. eCollection 2013.

Continuous heliox breathing and the extent of anatomic zone of noreflow and necrosis following ischemia/reperfusion in the rabbit heart.

The open cardiovascular medicine journal

Sharon L Hale, Donald R Vanderipe, Robert A Kloner

Affiliations

  1. The Heart Institute of Good Samaritan Hospital, Los Angeles, CA, USA.
  2. The Heart Institute of Good Samaritan Hospital, Los Angeles, CA, USA ; Keck School of Medicine, Division of Cardiovascular Medicine, University of Southern California, Los Angeles, CA, USA.

PMID: 24587834 PMCID: PMC3937439 DOI: 10.2174/1874192401408010001

Abstract

BACKGROUND: Nitrogen may contribute to reperfusion injury. Some studies have shown that helium as a replacement for nitrogen in breathing gas (heliox) reduces cell necrosis after ischemia/reperfusion when used in a preconditioning fashion (intermittent heliox exposure). Our aim was to test whether heliox, breathed continuously throughout the ischemic and reperfusion periods, reduced necrosis and a marker of reperfusion injury, the no-reflow phenomenon.

METHODS AND RESULTS: Anesthetized, open-chest rabbits received 30 min coronary artery occlusion/3 hrs reperfusion. Before CAO rabbits were randomized to heliox (30% oxygen + 70% helium, n=8) or air supplemented with oxygen to achieve blood gas values within physiologic range (n = 8). Rabbits received the appropriate mix during ischemic and reperfusion periods. Infarct size (% risk zone) and no-reflow defect were measured at the end of the reperfusion period. The ischemic risk zone was similar in both groups (28% of left ventricle in heliox and 29% in control). Heliox breathing did not reduce necrosis; infarct size, expressed as a percentage of the risk region was 44±4% in the heliox group and 49±5% in controls, p = 0.68. The extent of the no-reflow defect was not altered by heliox, either expressed as a percent of the risk region (29±4% in heliox and 28±3% in control) or as a percent of the necrotic zone (65±5% in heliox and 59±8% in control).Heliox treatment had no effect on hemodynamic parameters or arterial blood gas values.

CONCLUSION: Continuous heliox breathing does not appear to be cardioprotective in the setting of acute myocardial infarction in the rabbit model. Heliox respiration administered during 30 minutes of ischemia and 180 minutes of reperfusion did not alter infarct size or the extent of no-reflow.

Keywords: heliox; infarct size; no-reflow phenomenon; rabbit

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