Perfusate sodium during ischemia modifies post-ischemic functional and metabolic recovery in the rabbit heart

Dale G. Renlund, Gary Gerstenblith, Edward G. Lakatta, William E. Jacobus, Clayton H. Kallman, Myron L. Weisfeldt

Research output: Contribution to journalArticlepeer-review

Abstract

Metabolic and functional recovery following 60 minutes of low flow (0.1 ml/min) ischemia were compared in rabbit hearts perfused with normal sodium and potassium, low sodium (120 mm NaCl replaced by 120 mm LiCl), or zero potassium perfusate during ischemia. During the control, pre-ischemic, and reperfusion periods, all hearts were perfused identically with normal sodium and potassium. 31P NMR was used to monitor intracellular pH (pHi), ATP, and phosphocreatine (PCr). Developed pressure, end diastolic pressure, pHi, and the integrated areas of ATP and PCr were equivalent in the three groups in the pre-ischemic period. The fall in pHi, PCr, ATP, and developed pressure and the rise in end diastolic pressure during 60 min ischemia also did not differ among the three groups. In contrast to the lack of an effect of perfusate sodium and potassium on the decline in parameters of metabolism and function during ischemia, there was a marked difference in the recovery of these indices during reperfusion. Hearts perfused with low sodium during ischemia exhibited the best recovery (expressed as percent of control) of developed pressure (95±4%), PCr (106±6%), and ATP (51±2%) and the smallest rise in end diastolic pressure (229±50%); hearts perfused with normal sodium and potassium during ischemia had intermediate recovery values for developed pressure (53±10%), PCr (78±9%), ATP (45±4%) and end diastolic pressure (487±73%) and the hearts perfused with zero potassium solution during ischemia exhibited the poorest recovery of developed pressure (23±6%), PCr (49±6%), ATP (39±5%) and end diastolic pressure (968±185%). These results indicate that interventions which do not alter PCr, ATP or pHi during ischemia but which can diminish or enhance intracellular sodium accumulation can respectively improve or impair metabolic and functional recovery during reperfusion. The most likely mechanism to explain these findings is a sodium-dependent calcium influx occurring during reperfusion. This suggests that interventions which lower intracellular sodium or inhibit or reverse the direction of sodium-calcium exchange at the onset of reperfusion may lessen injury following reperfusion of ischemic myocardium.

Original languageEnglish (US)
Pages (from-to)795-801
Number of pages7
JournalJournal of Molecular and Cellular Cardiology
Volume16
Issue number9
DOIs
StatePublished - Sep 1984

Keywords

  • Intracellular pH
  • Ischemia
  • Myocardial energy metabolism
  • Reperfusion of ischemic myocardium
  • Sodium-dependent calcium influx

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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