Effects of fluorocarbons with and without oxygen supplementation on cardiac hemodynamics and energetics
Because of uncertainty about the mechanism by which fluorocarbons ameliorate myocardial ischemia, the effects of a fluorocarbon emulsion, perfluorodecalin and perfluorotripropylamine (Fluosol-DA 20% ™) with and without 100% O 2 inhalation, on cardiac hemodynamics and energetics were studied in the a...
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Published in | The American journal of cardiology Vol. 54; no. 7; pp. 880 - 883 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Inc
01.10.1984
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Because of uncertainty about the mechanism by which fluorocarbons ameliorate myocardial ischemia, the effects of a fluorocarbon emulsion, perfluorodecalin and perfluorotripropylamine (Fluosol-DA 20%
™) with and without 100% O
2 inhalation, on cardiac hemodynamics and energetics were studied in the anesthetized dog. Left ventricular (LV) intramural partial pressure of oxygen (P
mO
2) was measured by mass spectrometry before and after intravenous infusion of Fluosol-DA 20% (40 ml/kg), and was compared with measurements made in another group of dogs receiving the volume expander dextran (36 ml/kg). Both groups of dogs were then ventilated with 100% O
2 and repeat measurements were performed.
In the 11 animals receiving fluorocarbons, there were increases in left atrial pressure, LV myocardial blood flow, and LV myocardial O
2 consumption (MV̇O
2) compatible with volume expansion. After 100% O
2, LV MV̇O
2 decreased to control values, while P
mO
2 increased to 127 ± 48 mm Hg (p <0.001). There were no significant changes in heart rate, arterial pressure or first derivative of LV pressure (dP/dt) during the study. In 10 dogs treated with dextran there was no change in heart rate or dP/dt, but arterial and left atrial pressures were higher after dextran infusion and remained elevated after 100% O
2 inhalation. LV MVO
2 increased with volume expansion, and remained increased after 100% O
2. P
mO
2 (66 ± 18 mm Hg) after 100% O
2 was lower (p <0.02) than in the fluorocarbon-treated dogs after O
2 inhalation.
Thus, the acute hemodynamic effects of Fluosol-DA 20% are similar to those of a volume expander alone, but elevated left atrial pressure and LV MV̇O
2 tend to be shorter lived than in dogs treated with dextran. After 100% O
2, LV MV̇O
2 remained elevated in the dogs treated with dextran, but not in the fluorocarbon group. The extraordinarily high P
mO
2 attained in dogs treated with fluorocarbon-O
2 is greater than that produced by volume expansion alone, and is not due to a measurable decrease in LV myocardial O
2 demand. Thus, any beneficial effect of this fluorocarbon preparation on myocardial ischemia is likely due to enhanced O
2 delivery rather than to reduced O
2 demand. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0002-9149 1879-1913 |
DOI: | 10.1016/S0002-9149(84)80225-8 |