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Acute volume loading studied in cat myocardium with 31 P Nuclear magnetic resonance
Author(s) -
Osbakken Mary,
Young Marie,
Huddell Judy,
Closter Jeffery,
Prammer Manfred,
Chance Britton
Publication year - 1988
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.1910070203
Subject(s) - cats , phosphocreatine , medicine , chemistry , inferior vena cava , adenosine triphosphate , endocrinology , energy metabolism
To study the effects of acute volume loading on myocardial metabolic and mechanical function, seven cats were volume loaded via anastomosis of the abdominal aorta to the vena cava (A V shunt). Metabolic effects were evaluated with 31 P nuclear magnetic resonance (NMR). Mechanical function was evaluated with heart rate × systolic blood pressure product (HR × SBP). Shunts were opened for 1–2 h during which time phosphocreatine (PCr), adenosine triphosphate (ATP), inorganic phosphate ( P i), and HR × SBP were monitored. High‐energy phosphate energetics as determined by Pi/PCr and PCr/ATP ratios were correlated with HR × SBP. Opening of the AV shunts was associated with an increase (four cats) or a decrease (three cats) in HR × SBP. Pi/PCr ratios increased and PCr/ATP ratios decreased in cats with an increase in HR × SBP. In cats with a decrease in HR × SBP, Pi/PCr and PCr/ATP generally did not change significantly. In summary, acute volume loading could be associated with an increase or decrease in myocardial external work as evaluated by HR × SBP, accompanied by metabolic changes suggestive of appropriate induction of state 3 metabolism (active metabolic state: ADP + Pi → ATP) in those cats with increased mechanical work, and minimal change in bioenergetics in cats with no or minimal increase in mechanical work. These induced metabolic responses to myocardial mechanical loading can be evaluated with 31 P NMR techniques and may provide insight into in vivo metabolic control mechanisms. © 1988 Academic Press, Inc.

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