Regulation of oxygen delivery during induced polycythemia in exercising dogs
Autor: | Victoria L. Travis, John V. Weil, Lawrence D. Horwitz, JoAnn Lindenfeld |
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Rok vydání: | 2005 |
Předmět: |
medicine.medical_specialty
Cardiac output Physiology medicine.medical_treatment Physical Exertion Blood viscosity Exchange transfusion Blood Pressure Polycythemia Hematocrit Muscle Smooth Vascular Methemoglobin Dogs Oxygen Consumption hemic and lymphatic diseases Physiology (medical) Internal medicine medicine Animals Lactic Acid Cardiac Output medicine.diagnostic_test business.industry Hemodynamics Blood Viscosity Methylene Blue Oxygen Blood pressure medicine.anatomical_structure Anesthesia Cardiology Vascular resistance Blood Gas Analysis Erythrocyte Transfusion Cardiology and Cardiovascular Medicine business Packed red blood cells |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 289:H1821-H1825 |
ISSN: | 1522-1539 0363-6135 |
DOI: | 10.1152/ajpheart.01016.2004 |
Popis: | Previous studies have concluded that polycythemia decreases oxygen delivery primarily because of a large fall in cardiac output associated with a rise in systemic vascular resistance that has been attributed to increased blood viscosity. However, because other studies have shown that polycythemia may not reduce oxygen delivery, an alternative hypothesis is that cardiac output falls in response to a rising oxygen content, thereby maintaining oxygen delivery constant. To determine whether oxygen content participates in the regulation of cardiac output during polycythemia, we studied eight chronically instrumented dogs trained to exercise on a treadmill. The dogs underwent exchange transfusion with packed red blood cells containing methemoglobin, which caused an increase in hematocrit from 35 ± 1 to 50 ± 1% and in viscosity, with little change in oxygen content. The expected fall in exercise cardiac output failed to occur after exchange transfusion with red blood cells containing methemoglobin (7.5 ± 4 vs. 6.8 ± 0.5 l/min; P = not significant), and there was no rise in systemic vascular resistance. Methylene blue was then administered intravenously to facilitate conversion of methemoglobin to oxyhemoglobin, which increased oxygen content (12.8 ± 0.9 vs. 18.4 ± 0.9 vol%; P < 0.01) with no change in hematocrit or viscosity. Resting cardiac output did not change significantly, but there was a significant decrease in exercise output (6.8 ± 0.5 vs. 5.8 ± 0.4 l/min; P < 0.05). Thus we conclude that the fall in cardiac output seen in acute polycythemia results in part from the regulation of oxygen delivery and is not due solely to increased blood viscosity. |
Databáze: | OpenAIRE |
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