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1 Department of Pediatrics, University of Washington, Seattle, WA, USA; Department of Anesthesiology, University of Washington, Seattle, WA, USA; Department of Bioengineering, University of Washington, Seattle, WA, USA
2 Department of Bioengineering, University of Washington, Seattle, WA, USA
3 Pediatrics, Children's Hospital and Regional Medical Center, Seattle, WA, USA
4 Department of Physiology and Biophysics, University of Washington, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: ken.schenkman{at}seattlechildrens.org.
Myocardial mean myoglobin oxygen saturation was determined spectroscopically from isolated guinea pig hearts perfused with red blood cells during increasing hypoxia. These experiments were undertaken to compare intracellular myoglobin oxygen saturation in isolated hearts perfused with a modest concentration of red blood cells (5% hematocrit) with intracellular myoglobin saturation previously reported from traditional buffer-perfused hearts. Studies were performed at 37 °C with hearts paced at 240 bpm and constant perfusion pressure of 80 cm water pressure. It was found that during perfusion with a hematocrit of 5%, baseline mean myoglobin saturation was 93% compared with 72% during buffer perfusion. Mean myoglobin saturation, ventricular function and oxygen consumption remained fairly constant for arterial perfusate oxygen tensions above 100 mmHg, then decreased precipitously below 100 mmHg. In contrast, mean myoglobin saturation, ventricular function and oxygen consumption began to decrease even at high oxygen tension with buffer perfusion. The present results demonstrate that perfusion with 5% red blood cells in the perfusate increases the baseline mean myoglobin saturation, and better preserves cardiac function at low oxygen tension relative to buffer perfusion. These results suggest that caution should be used in extrapolating intracellular oxygen dynamics from buffer-perfused to blood perfused hearts.
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