Effects of amiloride on metabolism and contractility during reoxygenation in perfused rat hearts

Research output: Contribution to journalArticle

Abstract

Myocardial recovery after hypoxia may be determined not only by the extent of metabolic depression during the hypoxic period but also by changes in cation contents as well. Calcium overload during reoxygenation, mediated in part by Na-Ca exchange and supported by the rise in cell sodium during hypoxia, may be one factor. The effects of amiloride (0.1 mM), a diuretic that inhibits Na+-H+ and Na-Ca exchanges in cardiac sarcolemma and mitochondria preparations, were studied during hypoxia-reoxygenation in the isovolumic, isolated rat heart. During hypoxia, cell sodium, measured using potassium ethylenediamine tetraacetate cobaltate as an extracellular marker, increased in amiloride and amiloride-free hearts, but there was no increase in cell calcium (3.3 ± 0.3 vs. 3.6 ± 0.9 μmol/g dry wt; p = NS). Amiloride did not alter developed pressure (DP), end-diastolic pressure (EDP), pH, or integrated areas of adenosine triphosphate (ATP) and phosphocreatine (PCr) (determined by phosphorus-31-nuclear magnetic resonance copy) during hypoxia or normal perfusion conditions. Forty minutes after reoxygenation, however, cell calcium was significantly lower in the amiloride (5.1 ± 1.3 μmol/g dry wt) than in the amiloride-free group (10.4 ± 1.8 μmol/g dry wt; p

Original languageEnglish (US)
Pages (from-to)1012-1022
Number of pages11
JournalCirculation Research
Volume66
Issue number4
StatePublished - 1990

Fingerprint

Amiloride
ethylenediamine
Calcium
Sodium
Sarcolemma
Phosphocreatine
Diuretics
Phosphorus
Cations
Potassium
Mitochondria
Magnetic Resonance Spectroscopy
Perfusion
Adenosine Triphosphate
Hypoxia
Blood Pressure
Pressure

Keywords

  • P-NMR
  • amiloride
  • hypoxia
  • Na-Ca exchange
  • reoxygenation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Effects of amiloride on metabolism and contractility during reoxygenation in perfused rat hearts",
abstract = "Myocardial recovery after hypoxia may be determined not only by the extent of metabolic depression during the hypoxic period but also by changes in cation contents as well. Calcium overload during reoxygenation, mediated in part by Na-Ca exchange and supported by the rise in cell sodium during hypoxia, may be one factor. The effects of amiloride (0.1 mM), a diuretic that inhibits Na+-H+ and Na-Ca exchanges in cardiac sarcolemma and mitochondria preparations, were studied during hypoxia-reoxygenation in the isovolumic, isolated rat heart. During hypoxia, cell sodium, measured using potassium ethylenediamine tetraacetate cobaltate as an extracellular marker, increased in amiloride and amiloride-free hearts, but there was no increase in cell calcium (3.3 ± 0.3 vs. 3.6 ± 0.9 μmol/g dry wt; p = NS). Amiloride did not alter developed pressure (DP), end-diastolic pressure (EDP), pH, or integrated areas of adenosine triphosphate (ATP) and phosphocreatine (PCr) (determined by phosphorus-31-nuclear magnetic resonance copy) during hypoxia or normal perfusion conditions. Forty minutes after reoxygenation, however, cell calcium was significantly lower in the amiloride (5.1 ± 1.3 μmol/g dry wt) than in the amiloride-free group (10.4 ± 1.8 μmol/g dry wt; p",
keywords = "P-NMR, amiloride, hypoxia, Na-Ca exchange, reoxygenation",
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T1 - Effects of amiloride on metabolism and contractility during reoxygenation in perfused rat hearts

AU - Weiss, Robert George

AU - Lakatta, Edward

AU - Gerstenblith, Gary

PY - 1990

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N2 - Myocardial recovery after hypoxia may be determined not only by the extent of metabolic depression during the hypoxic period but also by changes in cation contents as well. Calcium overload during reoxygenation, mediated in part by Na-Ca exchange and supported by the rise in cell sodium during hypoxia, may be one factor. The effects of amiloride (0.1 mM), a diuretic that inhibits Na+-H+ and Na-Ca exchanges in cardiac sarcolemma and mitochondria preparations, were studied during hypoxia-reoxygenation in the isovolumic, isolated rat heart. During hypoxia, cell sodium, measured using potassium ethylenediamine tetraacetate cobaltate as an extracellular marker, increased in amiloride and amiloride-free hearts, but there was no increase in cell calcium (3.3 ± 0.3 vs. 3.6 ± 0.9 μmol/g dry wt; p = NS). Amiloride did not alter developed pressure (DP), end-diastolic pressure (EDP), pH, or integrated areas of adenosine triphosphate (ATP) and phosphocreatine (PCr) (determined by phosphorus-31-nuclear magnetic resonance copy) during hypoxia or normal perfusion conditions. Forty minutes after reoxygenation, however, cell calcium was significantly lower in the amiloride (5.1 ± 1.3 μmol/g dry wt) than in the amiloride-free group (10.4 ± 1.8 μmol/g dry wt; p

AB - Myocardial recovery after hypoxia may be determined not only by the extent of metabolic depression during the hypoxic period but also by changes in cation contents as well. Calcium overload during reoxygenation, mediated in part by Na-Ca exchange and supported by the rise in cell sodium during hypoxia, may be one factor. The effects of amiloride (0.1 mM), a diuretic that inhibits Na+-H+ and Na-Ca exchanges in cardiac sarcolemma and mitochondria preparations, were studied during hypoxia-reoxygenation in the isovolumic, isolated rat heart. During hypoxia, cell sodium, measured using potassium ethylenediamine tetraacetate cobaltate as an extracellular marker, increased in amiloride and amiloride-free hearts, but there was no increase in cell calcium (3.3 ± 0.3 vs. 3.6 ± 0.9 μmol/g dry wt; p = NS). Amiloride did not alter developed pressure (DP), end-diastolic pressure (EDP), pH, or integrated areas of adenosine triphosphate (ATP) and phosphocreatine (PCr) (determined by phosphorus-31-nuclear magnetic resonance copy) during hypoxia or normal perfusion conditions. Forty minutes after reoxygenation, however, cell calcium was significantly lower in the amiloride (5.1 ± 1.3 μmol/g dry wt) than in the amiloride-free group (10.4 ± 1.8 μmol/g dry wt; p

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