Abstract
Myocardial infarction (MI), which occurs often due to acute ischemia followed by reflow, is associated with irreversible loss (death) of cardiomyocytes. If left untreated, MI will lead to progressive loss of viable cardiomyocytes, deterioration of cardiac function, and congestive heart failure. While supplemental oxygen therapy has long been in practice to treat acute MI, there has not been a clear scientific basis for the observed beneficial effects. Further, there is no rationale for the amount or duration of administration of supplemental oxygenation for effective therapy. The goal of the present study was to determine an optimum oxygenation protocol that can be clinically applicable for treating acute MI. Using EPR oximetry, we studied the effect of exposure to supplemental oxygen cycling (OxCy) administered by inhalation of 21–100% oxygen for brief periods (15–90 min), daily for 5 days, using a rat model of acute MI. Myocardial oxygen tension (pO2), cardiac function and pro-survival/apoptotic signaling molecules were used as markers of treatment outcome. OxCy resulted in a significant reduction of infarct size and improvement of cardiac function. An optimal condition of 30-min OxCy with 95% oxygen + 5% CO2 under normobaric conditions was found to be effective for cardioprotection.
Highlights
A myocardial infarction (MI) or a “heart attack,” in which there is an obstruction of blood flow to the coronary arteries, is commonly followed by ischemia-reperfusion (I-R) injury upon restoration of circulation
We have previously reported that brief periods of hyperbaric oxygen cycling (OxCy; 100% O2; 2 ATA pressure; 90 min/day; 5 days/week for 4 weeks) enhanced the retention of transplanted mesenchymal stem cells and improved cardiac function in a rat model of MI induced by ischemia-reperfusion [14]
Using EPR oximetry, we determined the effect of increasing concentrations of inspired oxygen on myocardial pO2 in healthy rats
Summary
A myocardial infarction (MI) or a “heart attack,” in which there is an obstruction of blood flow to the coronary arteries, is commonly followed by ischemia-reperfusion (I-R) injury upon restoration of circulation. This “one-two punch” often results in widespread cardiac tissue damage and irreversible loss of cardiomyocytes (heart muscle cells), which can lead to cardiac dysfunction and eventual heart failure. Some guidelines recommended regular administration of oxygen for the treatment of MI [2, 3] This position has changed, so that continued treatment with oxygen is only recommended under certain circumstances and not for cases of uncomplicated MI [1, 4]. Hyperoxygenation of patients with acute MI results in a rise in arterial blood pressure and a reduction in cardiac output [5, 6]
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