A P-31 Nuclear Magnetic Resonance Evaluation of Various Cardioplegie Solutions

Pernot, Anne Catherine; Ingwall, I. S.; Menasche, P.; Grousset, Christian; Bercot, M; Mollet, M.; Piwnica, A; Fossel, Eric T.

doi:10.1007/978-3-642-68016-8_10

Cited by 2 publications

(2 citation statements)

References 3 publications

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“…Previous observations following ischemia in isolated hearts showed variable results. Similar to our findings, some investigators reported a 30% reduction of adenosine triphosphate by 14-25 rnin after ischemia (2,8). A maximal reduction of 40% was seen after 1 h of ischemia (2), but these isolated rat hearts were observed during hypothermia.…”

Section: Fig 2 Temporal Changes Of Adenosing Triphosphate (P-atp)supporting

confidence: 93%

In vivoevaluation of intracellular pH and high‐energy phosphate metabolities during regional myocardial ischemia in cats using³¹P nuclear magnetic resonance

Stein

Goldstein

Sabbah

et al. 1986

Magnetic Resonance in Med

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Phosphorus-31 nuclear magnetic resonance spectroscopy (31P NMR) was used to assess the temporal changes of high-energy phosphate metabolites in the region of acute myocardial ischemia of open-chest cats. Eight anesthetized cats were studied following ligation of the left anterior descending coronary artery. Creatine phosphate showed a 79 +/- 16% (mean +/- SD) reduction by 4 min after the onset of ischemia. Prominent qualitative reductions of the spectral peak of creatine phosphate occurred by 40 s after ischemia. Adenosine triphosphate measured under the beta spectral peak (beta-ATP) decreased 37 +/- 9% by 20-25 min after ligation of the left anterior descending coronary artery. These reductions developed more slowly and were of smaller magnitude than those of creatine phosphate. Intracellular pH decreased from 7.39 +/- 0.07 to 7.13 +/- 0.09 units by 40 s after ischemia. By 30 min, pH decreased to 6.07 +/- 0.40 units. The study shows, therefore, the temporal changes of high-energy phosphate metabolites during ischemia in localized regions of the myocardium of open-chest animals.

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Section: Fig 2 Temporal Changes Of Adenosing Triphosphate (P-atp)supporting

confidence: 93%

In vivoevaluation of intracellular pH and high‐energy phosphate metabolities during regional myocardial ischemia in cats using³¹P nuclear magnetic resonance

Stein

Goldstein

Sabbah

et al. 1986

Magnetic Resonance in Med

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“…Flaherty et al (17) observed partial recovery of ATP after 60 rnin of cold cardioplegic arrest in perfused rabbit hearts. Pernot et al (18) found no recovery, but rather continued decline of ATP during reperfusion after 60 rnin of cardioplegic arrest of perfused rat hearts. Ferrari et al (38) observed no recovery of ATP during reperfusion after 60 rnin of global ischemia in rabbit hearts, although interestingly, ATP recovery was detected when hearts were treated with nifedipine prior to ischemia.…”

Section: "P Magnetic Resonance Spectroscopymentioning

confidence: 97%

Characterization of high‐energy phosphate compounds during reperfusion of the irreversibly injured myocardium using ³¹P MRS

Wendland¹,

White²,

Derugin³

et al. 1988

Magnetic Resonance in Med

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Phosphorus-31 magnetic resonance spectroscopy (MRS) was used to monitor regional changes in high-energy phosphorus compounds and intracellular pH during 60 min of acute regional ischemia (acute occlusion of left anterior descending artery) and reperfusion in open-chest cats using a 1.2-cm two-turn coil sutured to the myocardium. During the 60-min ischemic phase, phosphocreatine (PCr) intensity was reduced to 47 +/- 4.9% (mean +/- SE) of control (p less than 0.01) by 15 min postocclusion while adenosine triphosphate (ATP) intensity decreased more slowly with the decrease (66 +/- 5.6%) achieving significance (p less than 0.05) only at 60 min postocclusion. Inorganic phosphate (Pi) increased to a maximum of 397 +/- 42% of control (p less than 0.01) while the pH decreased progressively from 7.36 +/- 0.02 to 6.02 +/- 0.14 (p less than 0.01). After release of occlusion PCr intensity recovered to 86 +/- 12% of the initial control value at 15 min postreperfusion but showed a subsequent downward trend to 79 +/- 8.8%. The ATP did not recover but tended to decline further during reperfusion. The Pi intensity decreased to 260 +/- 38% of control while the pH increased to 7.01 +/- 0.23 by 15 min postreperfusion. Thus, the reperfused irreversibly injured myocardium is characterized by persistent depletion of PCr and ATP and elevation of Pi. Phosphorus-31 MRS provides a nondestructive method for characterizing the reperfused irreversibly damaged myocardium.

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A P-31 Nuclear Magnetic Resonance Evaluation of Various Cardioplegie Solutions

Cited by 2 publications

References 3 publications

In vivoevaluation of intracellular pH and high‐energy phosphate metabolities during regional myocardial ischemia in cats using³¹P nuclear magnetic resonance

In vivoevaluation of intracellular pH and high‐energy phosphate metabolities during regional myocardial ischemia in cats using³¹P nuclear magnetic resonance

Characterization of high‐energy phosphate compounds during reperfusion of the irreversibly injured myocardium using ³¹P MRS

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A P-31 Nuclear Magnetic Resonance Evaluation of Various Cardioplegie Solutions

Cited by 2 publications

References 3 publications

In vivoevaluation of intracellular pH and high‐energy phosphate metabolities during regional myocardial ischemia in cats using31P nuclear magnetic resonance

In vivoevaluation of intracellular pH and high‐energy phosphate metabolities during regional myocardial ischemia in cats using31P nuclear magnetic resonance

Characterization of high‐energy phosphate compounds during reperfusion of the irreversibly injured myocardium using 31P MRS

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In vivoevaluation of intracellular pH and high‐energy phosphate metabolities during regional myocardial ischemia in cats using³¹P nuclear magnetic resonance

In vivoevaluation of intracellular pH and high‐energy phosphate metabolities during regional myocardial ischemia in cats using³¹P nuclear magnetic resonance

Characterization of high‐energy phosphate compounds during reperfusion of the irreversibly injured myocardium using ³¹P MRS